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In Koo Hwang - One of the best experts on this subject based on the ideXlab platform.

  • Ischemia-related changes of fat-mass and obesity-associated protein expression in the gerbil hippocampus
    Metabolic brain disease, 2019
    Co-Authors: Woosuk Kim, Joon Ha Park, Moo-ho Won, Dae Young Yoo, Hyo Young Jung, Min Soo Kang, Tae Hyeong Kim, Jung Hoon Choi, In Koo Hwang
    Abstract:

    Fat-mass and obesity-associated protein (Fto) plays important roles in energy metabolism. It also acts as a demethylase and is most abundantly found in the brain. In the present study, we examined the spatial and temporal changes of Fto immunoreactivity after five minutes of transient forebrain ischemia in the hippocampus. In the control group, Fto immunoreactivity was mainly observed in the nucleus of pyramidal cells in the CA1 and CA3 regions as well as the polymorphic layer, granule cell layer, and subgranular zone of the dentate gyrus. Fto immunoreactivity was transiently, but not significantly, increased in the hippocampal CA3 region and the dentate gyrus two days after ischemia compared to mice without ischemia in the sham-operated group. Four days after ischemia, low Fto immunoreactivity was observed in the Stratum Pyramidale of the CA1 region because of neuronal death, but Fto immunoreactive cells were abundantly detected in the Stratum Pyramidale of the CA3 region, which is relatively resistant to ischemic damage. Thereafter, Fto immunoreactivity progressively decreased in the hippocampal CA1 and CA3 regions and the dentate gyrus until ten days after ischemia. At this time-point, Fto immunoreactivity was significantly lower in the hippocampal CA1 and CA3 regions and the dentate gyrus compared to that in the sham-operated group. The reduction of Fto immunoreactive structures in the hippocampus may be associated with impairments in Fto-related hippocampal function.

  • Differences in neuronal damage and gliosis in the hippocampus between young and adult gerbils induced by long duration of transient cerebral ischemia.
    Journal of the neurological sciences, 2013
    Co-Authors: Bing Chun Yan, Ji Hyeon Ahn, Joon Ha Park, Bai Hui Chen, Jae-chul Lee, Myoung Cheol Shin, Choong Hyun Lee, In Koo Hwang, Taek Geun Ohk, Seung Myung Moon
    Abstract:

    Response to cerebral ischemia in young animals was very different from that in the adult. The aim of this study was to investigate differences in neuronal death and gliosis in the hippocampal CA1 region (CA1) between adult and young gerbils following 5 and 15 min of transient cerebral ischemia. Delayed neuronal death (DND) of pyramidal cells occurred in the CA1 was similar in all the adult gerbils after 5 and 15 min of ischemia: the DND occurred 4 days after ischemia. In the young groups, DND of pyramidal cells in the CA1 region occurred 7 and 3 days after 5 and 15 min of ischemia, respectively. On the other hand, the activation of GFAP-immunoreactive ((+)) astrocytes and Iba-1(+) microglia was different in the young groups from the adult groups after ischemia. The change pattern of GFAP immunoreactivity in the adult groups was similar in both the adult groups after ischemia; in the young groups, the activation of GFAP(+) astrocytes after 5 min of ischemia was much delayed than that after 15 min of ischemia. Activated Iba-1(+) microglia were aggregated in the Stratum Pyramidale 4 days after ischemia in all the adult ischemia-operated groups; in the young groups, activated Iba-1(+) microglia were aggregated in the Stratum Pyramidale 7 days after 5 min of ischemia and 3 days after 15 min of ischemia. These observations indicate that DND in young animals is very different from the adult according to different duration of transient cerebral ischemia and glial activation is very different in young animals after different duration of transient ischemia.

  • ischemia induced ribosomal protein s3 expressional changes and the neuroprotective effect against experimental cerebral ischemic damage
    Journal of Neuroscience Research, 2008
    Co-Authors: In Koo Hwang, Ki-yeon Yoo, Dae Won Kim, So Young Kim, Jun Hong Park, Zae Young Ryoo, Joon Kim, Soo Young Choi, Moo-ho Won
    Abstract:

    Some ribosomal proteins are important regulators of development and DNA repair. However, few studies have been conducted on ribosomal protein S3 (rpS3) in the ischemic hippocampus. In the present study, we investigated ischemia-induced changes in rpS3 immunoreactivity, rpS3 mRNA, and protein levels in the hippocampal CA1 region of Mongolian gerbil after 5 min of transient forebrain ischemia. RpS3 immunoreactivity and its protein level were found to be significantly elevated at 6 hr after ischemia/reperfusion and then continuously decreased with time. RT-PCR analysis also showed that rpS3 mRNA levels were significantly elevated in CA1 at 6 hr after transient ischemia. In addition, during the course of this study, we developed a delivery vector (Pep-1) and its rpS3 fusion protein (Pep-1-rpS3) to elucidate the role of rpS3 in ischemia-induced damage. Pep-1-rpS3 administration to ischemic animals significantly and dose dependently increased neuronal survival in the Stratum Pyramidale of CA1. Moreover, Pep-1-rpS3 treatment reduced terminal deoxynucleotidyl dUTP nick-end labeling-positive CA1 pyramidal cell numbers in the Stratum Pyramidale. To elucidate how Pep-1-rpS3 ameliorates ischemic damage, changes in 4-hydroxy-2-nonnenal (HNE; an indicator of lipid peroxidation) immunoreactivity and protein levels were investigated. HNE levels and immunoreactivities in Pep-1-rpS3-treated ischemic animals were lower than in corresponding Pep-1-treated ischemic animals. These results indicate that rpS3 has a neuroprotective effect in the brain exposed to ischemia.

  • Berberry extract reduces neuronal damage and N-Methyl-D-aspartate receptor 1 immunoreactivity in the gerbil hippocampus after transient forebrain ischemia.
    Biological & pharmaceutical bulletin, 2006
    Co-Authors: Ki-yeon Yoo, In Koo Hwang, Beong Ou Lim, Tae-cheon Kang, Dong-woo Kim, Sang Moo Kim, Hyeon Yong Lee, Jong Dai Kim, Moo-ho Won
    Abstract:

    In the present study, we studied the neuroprotective effects of berberry extract (BE) against ischemic damage and the temporal and spatial alterations of N-methyl-D-aspartate receptor type 1 (NR1) and NR2A/2B immunoreactivities in the gerbil hippocampal CA1 region after transient ischemia to examine anti-ischemic effects and its role in transient forebrain ischemia. In the vehicle-treated group, the percentage of cresyl violet positive pyramidal cells in the CA1 region was about 11.4% compared to the sham-operated group 4 d after ischemic insult. BE showed neuroprotective effects against ischemic damage after ischemia-reperfusion. In the BE-treated groups, about 60-75% of CA1 pyramidal cells were stained with cresyl violet 4 d after ischemic insult. We observed the percentage of berberine (7.45+0.85 mg/g in BE) by HPLC, which is active ingredient of BE. NR1 immunoreactivity in the Stratum Pyramidale of the CA1 region in the vehicle-treated group was significantly increased at 30 min after transient forebrain ischemia, while at this time the NR1 immunoreactivity in the BE-treated groups was significantly low compared to the vehicle-treated group. The pattern of NR2A/B immunoreactivity in the Stratum Pyramidale of the BE-treated group and its protein levels were similar to that in the vehicle-treated group after ischemic insult. These results suggest that BE has potent neuroprotective effects against ischemic damage via the reduction of NR1 activity.

  • Copper chaperone for Cu,Zn-SOD supplement potentiates the Cu,Zn-SOD function of neuroprotective effects against ischemic neuronal damage in the gerbil hippocampus
    Free radical biology & medicine, 2005
    Co-Authors: In Koo Hwang, Ki-yeon Yoo, Dae Won Kim, Jun Hwi Cho, Tae-cheon Kang, J.h Kang, Won Sik Eum, Soo Hyun Choi, Oh-shin Kwon, Soo Young Choi
    Abstract:

    In the present study, we investigated the chronological alterations in SOD1 and its copper chaperone (chaperone for superoxide dismutase, CCS) immunoreactivities and their neuroprotective effects against neuronal damage in the gerbil hippocampus after 5 min of transient forebrain ischemia. SOD1 and CCS immunoreactivities were significantly increased in the Stratum Pyramidale of the CA1 region at 24 and 12 h after ischemic insult, respectively. At 24 h after ischemic insult, the SOD1 and CCS immunoreactivities were colocalized in the CA1 pyramidal cells of the Stratum Pyramidale. Thereafter, their immunoreactivities were significantly decreased in the CA1 region. To elucidate the effects of CCS or CCS/SOD1, we constructed the expression vectors PEP-1-SOD and PEP-1-CCS. In the CCS-treated group and the CCS/SOD1-treated group, 43.9 and 78.9% pyramidal cells, respectively, compared to the sham-operated group, were stained with cresyl violet 5 or 7 days after ischemic insult. The distribution pattern of active astrocytes and microglia in the PEP-CCS/SOD1-treated group 5 days after ischemic insult was similar to that of the sham-operated group. In addition, the SOD activity in the PEP-CCS- or PEP-CCS/SOD1-treated group was maintained by 10 days after ischemic insult. The SOD activity was higher in the PEP-CCS/SOD1-treated group vs the CCS-treated group. These results suggest that the enhanced expression of SOD1 and CCS may be related to compensatory mechanisms against ischemic damage and that cotreatment with CCS and SOD1 has a greater neuroprotective effect than treatment with CCS or SOD1 in isolation.

Joon Ha Park - One of the best experts on this subject based on the ideXlab platform.

  • Age‑dependent alterations in the immunoreactivity of macrophage inflammatory protein‑3α and its receptor CCR6 in the gerbil hippocampus.
    Molecular medicine reports, 2020
    Co-Authors: Ji Hyeon Ahn, Joon Ha Park, Moo-ho Won, Tae‑kyung Lee, Go Eun Yang, Myoung Cheol Shin, Jun Hwi Cho, Choong Hyun Lee
    Abstract:

    Neuroinflammation is a primary characteristic of the aging brain. During normal aging, macrophage inflammatory protein‑3α (MIP‑3α) and its receptor C‑C chemokine receptor type 6 (CCR6) serve pivotal roles in the neuroinflammatory process in the brain. The aim of the present study was to investigate age‑dependent alterations in the immunoreactivity of MIP‑3α and CCR6 in the gerbil hippocampus at postnatal month (PM) 1, 6, 12 and 24 via immunohistochemistry. In the PM 1 group, both MIP‑3α and CCR6 immunoreactivity were observed primarily in the Stratum Pyramidale in the hippocampus proper and in the granule cell layer in the dentate gyrus. In the PM 6 and PM 12 groups, MIP‑3α in the Stratum Pyramidale and granule cell layer was decreased compared with the PM 1 group, and CCR6 immunoreactivity in both layers was faint. In the PM 24 group, MIP‑3α expression in the Stratum Pyramidale and granule cell layer was higher than that in the PM 1 group, and CCR6 immunoreactivity in both layers was increased compared with the PM 12 group; however, it was decreased compared with the PM 1 group. In conclusion, MIP‑3α and CCR6 immunoreactivity were altered in the hippocampus during normal aging. The results of the current study suggested that age‑dependent alterations of MIP‑3α and CCR6 may be associated with age‑related neuroinflammation in the hippocampus.

  • Ischemia-related changes of fat-mass and obesity-associated protein expression in the gerbil hippocampus
    Metabolic brain disease, 2019
    Co-Authors: Woosuk Kim, Joon Ha Park, Moo-ho Won, Dae Young Yoo, Hyo Young Jung, Min Soo Kang, Tae Hyeong Kim, Jung Hoon Choi, In Koo Hwang
    Abstract:

    Fat-mass and obesity-associated protein (Fto) plays important roles in energy metabolism. It also acts as a demethylase and is most abundantly found in the brain. In the present study, we examined the spatial and temporal changes of Fto immunoreactivity after five minutes of transient forebrain ischemia in the hippocampus. In the control group, Fto immunoreactivity was mainly observed in the nucleus of pyramidal cells in the CA1 and CA3 regions as well as the polymorphic layer, granule cell layer, and subgranular zone of the dentate gyrus. Fto immunoreactivity was transiently, but not significantly, increased in the hippocampal CA3 region and the dentate gyrus two days after ischemia compared to mice without ischemia in the sham-operated group. Four days after ischemia, low Fto immunoreactivity was observed in the Stratum Pyramidale of the CA1 region because of neuronal death, but Fto immunoreactive cells were abundantly detected in the Stratum Pyramidale of the CA3 region, which is relatively resistant to ischemic damage. Thereafter, Fto immunoreactivity progressively decreased in the hippocampal CA1 and CA3 regions and the dentate gyrus until ten days after ischemia. At this time-point, Fto immunoreactivity was significantly lower in the hippocampal CA1 and CA3 regions and the dentate gyrus compared to that in the sham-operated group. The reduction of Fto immunoreactive structures in the hippocampus may be associated with impairments in Fto-related hippocampal function.

  • Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia.
    Neural regeneration research, 2016
    Co-Authors: Seung Min Park, Jeong Hwi Cho, Ji Hyeon Ahn, Joon Ha Park, Bai Hui Chen, Bich-na Shin, Chan Woo Park, Tae‑kyeong Lee, Jae-chul Lee, Hyun Jin Tae
    Abstract:

    Ischemic preconditioning (IPC) is a condition of sublethal transient global ischemia and exhibits neuroprotective effects against subsequent lethal ischemic insult. We, in this study, examined the neuroprotective effects of IPC and its effects on immunoreactive changes of antioxidant enzymes including superoxide dismutase (SOD) 1 and SOD2, catalase (CAT) and glutathione peroxidase (GPX) in the gerbil hippocampal CA1 region after transient forebrain ischemia. Pyramidal neurons of the Stratum Pyramidale (SP) in the hippocampal CA1 region of animals died 5 days after lethal transient ischemia without IPC (8.6% (ratio of remanent neurons) of the sham-operated group); however, IPC prevented the pyramidal neurons from subsequent lethal ischemic injury (92.3% (ratio of remanent neurons) of the sham-operated group). SOD1, SOD2, CAT and GPX immunoreactivities in the sham-operated animals were easily detected in pyramidal neurons in the Stratum Pyramidale (SP) of the hippocampal CA1 region, while all of these immunoreactivities were rarely detected in the Stratum Pyramidale at 5 days after lethal transient ischemia without IPC. Meanwhile, their immunoreactivities in the sham-operated animals with IPC were similar to (SOD1, SOD2 and CAT) or higher (GPX) than those in the sham-operated animals without IPC. Furthermore, their immunoreactivities in the Stratum Pyramidale of the ischemia-operated animals with IPC were steadily maintained after lethal ischemia/reperfusion. Results of western blot analysis for SOD1, SOD2, CAT and GPX were similar to immunohistochemical data. In conclusion, IPC maintained or increased the expression of antioxidant enzymes in the Stratum Pyramidale of the hippocampal CA1 region after subsequent lethal transient forebrain ischemia and IPC exhibited neuroprotective effects in the hippocampal CA1 region against transient forebrain ischemia.

  • Time- and cell-type specific changes in iron, ferritin, and transferrin in the gerbil hippocampal CA1 region after transient forebrain ischemia.
    Neural regeneration research, 2016
    Co-Authors: Dae Young Yoo, Joon Ha Park, Ki-yeon Yoo, Hyun Jung Kwon, Hyo Young Jung, Jong Whi Kim, Goang-min Choi, Seung Myung Moon, Dae Won Kim, Yeo Sung Yoon
    Abstract:

    In the present study, we used immunohistochemistry and western blot analysis to examine changes in the levels and cellular localization of iron, heavy chain ferritin (ferritin-H), and transferrin in the gerbil hippocampal CA1 region from 30 minutes to 7 days following transient forebrain ischemia. Relative to sham controls, iron reactivity increased significantly in the Stratum Pyramidale and Stratum oriens at 12 hours following ischemic insult, transiently decreased at 1-2 days and then increased once again within the CA1 region at 4-7 days after ischemia. One day after ischemia, ferritin-H immunoreactivity increased significantly in the Stratum Pyramidale and decreased at 2 days. At 4-7 days after ischemia, ferritin-H immunoreactivity in the glial components in the CA1 region was significantly increased. Transferrin immunoreactivity was increased significantly in the Stratum Pyramidale at 12 hours, peaked at 1 day, and then decreased significantly at 2 days after ischemia. Seven days after ischemia, Transferrin immunoreactivity in the glial cells of the Stratum oriens and radiatum was significantly increased. Western blot analyses supported these results, demonstrating that compared to sham controls, ferritin H and transferrin protein levels in hippocampal homogenates significantly increased at 1 day after ischemia, peaked at 4 days and then decreased. These results suggest that iron overload-induced oxidative stress is most prominent at 12 hours after ischemia in the Stratum Pyramidale, suggesting that this time window may be the optimal period for therapeutic intervention to protect neurons from ischemia-induced death.

  • Monocarboxylate transporter 4 plays a significant role in the neuroprotective mechanism of ischemic preconditioning in transient cerebral ischemia
    Neural regeneration research, 2015
    Co-Authors: Seongkweon Hong, Ji Yun Ahn, Geum-sil Cho, In Hye Kim, Jeong Hwi Cho, Ji Hyeon Ahn, Joon Ha Park, Moo-ho Won, Bai Hui Chen, Bich-na Shin
    Abstract:

    Monocarboxylate transporters (MCTs), which carry monocarboxylates such as lactate across biological membranes, have been associated with cerebral ischemia/reperfusion process. In this study, we studied the effect of ischemic preconditioning (IPC) on MCT4 immunoreactivity after 5 minutes of transient cerebral ischemia in the gerbil. Animals were randomly designated to four groups (sham-operated group, ischemia only group, IPC + sham-operated group and IPC + ischemia group). A serious loss of neuron was found in the Stratum Pyramidale of the hippocampal CA1 region (CA1), not CA2/3, of the ischemia-only group at 5 days post-ischemia; however, in the IPC + ischemia groups, neurons in the Stratum Pyramidale of the CA1 were well protected. Weak MCT4 immunoreactivity was found in the Stratum Pyramidale of the CA1 in the sham-operated group. MCT4 immunoreactivity in the Stratum Pyramidale began to decrease at 2 days post-ischemia and was hardly detected at 5 days post-ischemia; at this time point, MCT4 immunoreactivity was newly expressed in astrocytes. In the IPC + sham-operated group, MCT4 immunoreactivity in the Stratum Pyramidale of the CA1 was increased compared with the sham-operated group, and, in the IPC + ischemia group, MCT4 immunoreactivity was also increased in the Stratum Pyramidale compared with the ischemia only group. Briefly, present findings show that IPC apparently protected CA1 pyramidal neurons and increased or maintained MCT4 expression in the Stratum Pyramidale of the CA1 after transient cerebral ischemia. Our findings suggest that MCT4 appears to play a significant role in the neuroprotective mechanism of IPC in the gerbil with transient cerebral ischemia.

Moo-ho Won - One of the best experts on this subject based on the ideXlab platform.

  • Age‑dependent alterations in the immunoreactivity of macrophage inflammatory protein‑3α and its receptor CCR6 in the gerbil hippocampus.
    Molecular medicine reports, 2020
    Co-Authors: Ji Hyeon Ahn, Joon Ha Park, Moo-ho Won, Tae‑kyung Lee, Go Eun Yang, Myoung Cheol Shin, Jun Hwi Cho, Choong Hyun Lee
    Abstract:

    Neuroinflammation is a primary characteristic of the aging brain. During normal aging, macrophage inflammatory protein‑3α (MIP‑3α) and its receptor C‑C chemokine receptor type 6 (CCR6) serve pivotal roles in the neuroinflammatory process in the brain. The aim of the present study was to investigate age‑dependent alterations in the immunoreactivity of MIP‑3α and CCR6 in the gerbil hippocampus at postnatal month (PM) 1, 6, 12 and 24 via immunohistochemistry. In the PM 1 group, both MIP‑3α and CCR6 immunoreactivity were observed primarily in the Stratum Pyramidale in the hippocampus proper and in the granule cell layer in the dentate gyrus. In the PM 6 and PM 12 groups, MIP‑3α in the Stratum Pyramidale and granule cell layer was decreased compared with the PM 1 group, and CCR6 immunoreactivity in both layers was faint. In the PM 24 group, MIP‑3α expression in the Stratum Pyramidale and granule cell layer was higher than that in the PM 1 group, and CCR6 immunoreactivity in both layers was increased compared with the PM 12 group; however, it was decreased compared with the PM 1 group. In conclusion, MIP‑3α and CCR6 immunoreactivity were altered in the hippocampus during normal aging. The results of the current study suggested that age‑dependent alterations of MIP‑3α and CCR6 may be associated with age‑related neuroinflammation in the hippocampus.

  • Ischemia-related changes of fat-mass and obesity-associated protein expression in the gerbil hippocampus
    Metabolic brain disease, 2019
    Co-Authors: Woosuk Kim, Joon Ha Park, Moo-ho Won, Dae Young Yoo, Hyo Young Jung, Min Soo Kang, Tae Hyeong Kim, Jung Hoon Choi, In Koo Hwang
    Abstract:

    Fat-mass and obesity-associated protein (Fto) plays important roles in energy metabolism. It also acts as a demethylase and is most abundantly found in the brain. In the present study, we examined the spatial and temporal changes of Fto immunoreactivity after five minutes of transient forebrain ischemia in the hippocampus. In the control group, Fto immunoreactivity was mainly observed in the nucleus of pyramidal cells in the CA1 and CA3 regions as well as the polymorphic layer, granule cell layer, and subgranular zone of the dentate gyrus. Fto immunoreactivity was transiently, but not significantly, increased in the hippocampal CA3 region and the dentate gyrus two days after ischemia compared to mice without ischemia in the sham-operated group. Four days after ischemia, low Fto immunoreactivity was observed in the Stratum Pyramidale of the CA1 region because of neuronal death, but Fto immunoreactive cells were abundantly detected in the Stratum Pyramidale of the CA3 region, which is relatively resistant to ischemic damage. Thereafter, Fto immunoreactivity progressively decreased in the hippocampal CA1 and CA3 regions and the dentate gyrus until ten days after ischemia. At this time-point, Fto immunoreactivity was significantly lower in the hippocampal CA1 and CA3 regions and the dentate gyrus compared to that in the sham-operated group. The reduction of Fto immunoreactive structures in the hippocampus may be associated with impairments in Fto-related hippocampal function.

  • Monocarboxylate transporter 4 plays a significant role in the neuroprotective mechanism of ischemic preconditioning in transient cerebral ischemia
    Neural regeneration research, 2015
    Co-Authors: Seongkweon Hong, Ji Yun Ahn, Geum-sil Cho, In Hye Kim, Jeong Hwi Cho, Ji Hyeon Ahn, Joon Ha Park, Moo-ho Won, Bai Hui Chen, Bich-na Shin
    Abstract:

    Monocarboxylate transporters (MCTs), which carry monocarboxylates such as lactate across biological membranes, have been associated with cerebral ischemia/reperfusion process. In this study, we studied the effect of ischemic preconditioning (IPC) on MCT4 immunoreactivity after 5 minutes of transient cerebral ischemia in the gerbil. Animals were randomly designated to four groups (sham-operated group, ischemia only group, IPC + sham-operated group and IPC + ischemia group). A serious loss of neuron was found in the Stratum Pyramidale of the hippocampal CA1 region (CA1), not CA2/3, of the ischemia-only group at 5 days post-ischemia; however, in the IPC + ischemia groups, neurons in the Stratum Pyramidale of the CA1 were well protected. Weak MCT4 immunoreactivity was found in the Stratum Pyramidale of the CA1 in the sham-operated group. MCT4 immunoreactivity in the Stratum Pyramidale began to decrease at 2 days post-ischemia and was hardly detected at 5 days post-ischemia; at this time point, MCT4 immunoreactivity was newly expressed in astrocytes. In the IPC + sham-operated group, MCT4 immunoreactivity in the Stratum Pyramidale of the CA1 was increased compared with the sham-operated group, and, in the IPC + ischemia group, MCT4 immunoreactivity was also increased in the Stratum Pyramidale compared with the ischemia only group. Briefly, present findings show that IPC apparently protected CA1 pyramidal neurons and increased or maintained MCT4 expression in the Stratum Pyramidale of the CA1 after transient cerebral ischemia. Our findings suggest that MCT4 appears to play a significant role in the neuroprotective mechanism of IPC in the gerbil with transient cerebral ischemia.

  • ischemia induced ribosomal protein s3 expressional changes and the neuroprotective effect against experimental cerebral ischemic damage
    Journal of Neuroscience Research, 2008
    Co-Authors: In Koo Hwang, Ki-yeon Yoo, Dae Won Kim, So Young Kim, Jun Hong Park, Zae Young Ryoo, Joon Kim, Soo Young Choi, Moo-ho Won
    Abstract:

    Some ribosomal proteins are important regulators of development and DNA repair. However, few studies have been conducted on ribosomal protein S3 (rpS3) in the ischemic hippocampus. In the present study, we investigated ischemia-induced changes in rpS3 immunoreactivity, rpS3 mRNA, and protein levels in the hippocampal CA1 region of Mongolian gerbil after 5 min of transient forebrain ischemia. RpS3 immunoreactivity and its protein level were found to be significantly elevated at 6 hr after ischemia/reperfusion and then continuously decreased with time. RT-PCR analysis also showed that rpS3 mRNA levels were significantly elevated in CA1 at 6 hr after transient ischemia. In addition, during the course of this study, we developed a delivery vector (Pep-1) and its rpS3 fusion protein (Pep-1-rpS3) to elucidate the role of rpS3 in ischemia-induced damage. Pep-1-rpS3 administration to ischemic animals significantly and dose dependently increased neuronal survival in the Stratum Pyramidale of CA1. Moreover, Pep-1-rpS3 treatment reduced terminal deoxynucleotidyl dUTP nick-end labeling-positive CA1 pyramidal cell numbers in the Stratum Pyramidale. To elucidate how Pep-1-rpS3 ameliorates ischemic damage, changes in 4-hydroxy-2-nonnenal (HNE; an indicator of lipid peroxidation) immunoreactivity and protein levels were investigated. HNE levels and immunoreactivities in Pep-1-rpS3-treated ischemic animals were lower than in corresponding Pep-1-treated ischemic animals. These results indicate that rpS3 has a neuroprotective effect in the brain exposed to ischemia.

  • Berberry extract reduces neuronal damage and N-Methyl-D-aspartate receptor 1 immunoreactivity in the gerbil hippocampus after transient forebrain ischemia.
    Biological & pharmaceutical bulletin, 2006
    Co-Authors: Ki-yeon Yoo, In Koo Hwang, Beong Ou Lim, Tae-cheon Kang, Dong-woo Kim, Sang Moo Kim, Hyeon Yong Lee, Jong Dai Kim, Moo-ho Won
    Abstract:

    In the present study, we studied the neuroprotective effects of berberry extract (BE) against ischemic damage and the temporal and spatial alterations of N-methyl-D-aspartate receptor type 1 (NR1) and NR2A/2B immunoreactivities in the gerbil hippocampal CA1 region after transient ischemia to examine anti-ischemic effects and its role in transient forebrain ischemia. In the vehicle-treated group, the percentage of cresyl violet positive pyramidal cells in the CA1 region was about 11.4% compared to the sham-operated group 4 d after ischemic insult. BE showed neuroprotective effects against ischemic damage after ischemia-reperfusion. In the BE-treated groups, about 60-75% of CA1 pyramidal cells were stained with cresyl violet 4 d after ischemic insult. We observed the percentage of berberine (7.45+0.85 mg/g in BE) by HPLC, which is active ingredient of BE. NR1 immunoreactivity in the Stratum Pyramidale of the CA1 region in the vehicle-treated group was significantly increased at 30 min after transient forebrain ischemia, while at this time the NR1 immunoreactivity in the BE-treated groups was significantly low compared to the vehicle-treated group. The pattern of NR2A/B immunoreactivity in the Stratum Pyramidale of the BE-treated group and its protein levels were similar to that in the vehicle-treated group after ischemic insult. These results suggest that BE has potent neuroprotective effects against ischemic damage via the reduction of NR1 activity.

Bing Chun Yan - One of the best experts on this subject based on the ideXlab platform.

  • Differences in neuronal damage and gliosis in the hippocampus between young and adult gerbils induced by long duration of transient cerebral ischemia.
    Journal of the neurological sciences, 2013
    Co-Authors: Bing Chun Yan, Ji Hyeon Ahn, Joon Ha Park, Bai Hui Chen, Jae-chul Lee, Myoung Cheol Shin, Choong Hyun Lee, In Koo Hwang, Taek Geun Ohk, Seung Myung Moon
    Abstract:

    Response to cerebral ischemia in young animals was very different from that in the adult. The aim of this study was to investigate differences in neuronal death and gliosis in the hippocampal CA1 region (CA1) between adult and young gerbils following 5 and 15 min of transient cerebral ischemia. Delayed neuronal death (DND) of pyramidal cells occurred in the CA1 was similar in all the adult gerbils after 5 and 15 min of ischemia: the DND occurred 4 days after ischemia. In the young groups, DND of pyramidal cells in the CA1 region occurred 7 and 3 days after 5 and 15 min of ischemia, respectively. On the other hand, the activation of GFAP-immunoreactive ((+)) astrocytes and Iba-1(+) microglia was different in the young groups from the adult groups after ischemia. The change pattern of GFAP immunoreactivity in the adult groups was similar in both the adult groups after ischemia; in the young groups, the activation of GFAP(+) astrocytes after 5 min of ischemia was much delayed than that after 15 min of ischemia. Activated Iba-1(+) microglia were aggregated in the Stratum Pyramidale 4 days after ischemia in all the adult ischemia-operated groups; in the young groups, activated Iba-1(+) microglia were aggregated in the Stratum Pyramidale 7 days after 5 min of ischemia and 3 days after 15 min of ischemia. These observations indicate that DND in young animals is very different from the adult according to different duration of transient cerebral ischemia and glial activation is very different in young animals after different duration of transient ischemia.

  • Effects of transient cerebral ischemia on the expression of DNA methyltransferase 1 in the gerbil hippocampal CA1 region.
    Neurochemical research, 2012
    Co-Authors: Jae-chul Lee, In Hye Kim, Joon Ha Park, Bing Chun Yan, G. Cho, Dooil Jeoung, Young Geun Kwon, Young Myeong Kim, Yun Lyul Lee, Hyung Cheul Shin
    Abstract:

    DNA methylation is a key epigenetic modification of DNA that is catalyzed by DNA methyltransferases (Dnmt). Increasing evidences suggest that DNA methylation in neurons regulates synaptic plasticity as well as neuronal network activity. In the present study, we investigated the changes in DNA methyltransferases 1 (Dnmt1) immunoreactivity and its protein levels in the gerbil hippocampal CA1 region after 5 min of transient global cerebral ischemia. CA1 pyramidal neurons were well stained with NeuN (a neuron-specific soluble nuclear antigen) antibody in the sham-group, Four days after ischemia–reperfusion (I–R), NeuN-positive (+) cells were significantly decreased in the Stratum Pyramidale (SP) of the CA1 region, and many Fluro-Jade B (a marker for neuronal degeneration)+ cells were observed in the SP. Dnmt1 immunoreactivity was well detected in all the layers of the sham-group. Dnmt1 immunoreactivity was hardly detected only in the Stratum Pyramidale of the CA1 region from 4 days post-ischemia; however, at these times, Dnmt1 immunoreactivity was newly expressed in GABAergic interneurons or astrocytes in the ischemic CA1 region. In addition, the level of Dnmt1 was lowest at 4 days post-ischemia. In brief, both the Dnmt1 immunoreactivity and protein levels were distinctively decreased in the ischemic CA1 region 4 days after transient cerebral ischemia. These results indicate that the decrease of Dnmt1 expression at 4 days post-ischemia may be related to ischemia-induced delayed neuronal death.

  • Comparison of the Immunoreactivity of Trx2/Prx3 Redox System in the Hippocampal CA1 Region Between the Young and Adult Gerbil Induced by Transient Cerebral Ischemia
    Neurochemical research, 2012
    Co-Authors: Bing Chun Yan, Ji Hyeon Ahn, Joon Ha Park, Jun Hwi Cho, Choong Hyun Lee, Young Joo Lee, Tae Hun Lee, Myong Jo Kim, Taeyoung Kim, Il-jun Kang
    Abstract:

    In the present study, we compared the immunoreactivities and levels of Trx/prx redox system, thioredoxin 2 (Trx2), thioredoxin reductase 2 (TrxR2) and peroxiredoxin 3 (Prx3), as well as neuronal death in the hippocampal CA1 region between the adult and young gerbil after 5 min of transient cerebral ischemia. At 4 days post-ischemia, pyramidal neurons (about 90%) in the adult Stratum Pyramidale of the CA1 region showed “delayed neuronal death (DND)”; however, at this time point, few pyramidal neurons showed DND in the young Stratum Pyramidale. At 7 days post-ischemia, about 56% of pyramidal neurons showed DND in the young Stratum Pyramidale. The immunoreactivities of all the antioxidants in the young sham-group were similar to those in the adult sham-group. At 4 days post-ischemia, the immunoreactivity of TrxR2, not Trx2 and Prx3 in the adult ischemia-group was dramatically decreased in CA1 pyramidal neurons. At this time point, the immunoreactivities of all the antioxidants in the young ischemia-group were apparently increased compared to the adult ischemia-group. From 7 days pots-ischemia, non-pyramidal cells showed the immunoreactivities of all the antioxidants in the ischemic CA1 region; however, in the young ischemia-groups, the immunoreactivities were much lower than those in the adult ischemia-groups. In brief, our results showed that the immunoreactivities of Trx2, TrxR2 and Prx3 were dramatically increased in CA1 pyramidal neurons of the young ischemia-groups at 4 days post-ischemia compared to those in the adult ischemia-groups induced by transient cerebral ischemia.

Ki-yeon Yoo - One of the best experts on this subject based on the ideXlab platform.

  • Time- and cell-type specific changes in iron, ferritin, and transferrin in the gerbil hippocampal CA1 region after transient forebrain ischemia.
    Neural regeneration research, 2016
    Co-Authors: Dae Young Yoo, Joon Ha Park, Ki-yeon Yoo, Hyun Jung Kwon, Hyo Young Jung, Jong Whi Kim, Goang-min Choi, Seung Myung Moon, Dae Won Kim, Yeo Sung Yoon
    Abstract:

    In the present study, we used immunohistochemistry and western blot analysis to examine changes in the levels and cellular localization of iron, heavy chain ferritin (ferritin-H), and transferrin in the gerbil hippocampal CA1 region from 30 minutes to 7 days following transient forebrain ischemia. Relative to sham controls, iron reactivity increased significantly in the Stratum Pyramidale and Stratum oriens at 12 hours following ischemic insult, transiently decreased at 1-2 days and then increased once again within the CA1 region at 4-7 days after ischemia. One day after ischemia, ferritin-H immunoreactivity increased significantly in the Stratum Pyramidale and decreased at 2 days. At 4-7 days after ischemia, ferritin-H immunoreactivity in the glial components in the CA1 region was significantly increased. Transferrin immunoreactivity was increased significantly in the Stratum Pyramidale at 12 hours, peaked at 1 day, and then decreased significantly at 2 days after ischemia. Seven days after ischemia, Transferrin immunoreactivity in the glial cells of the Stratum oriens and radiatum was significantly increased. Western blot analyses supported these results, demonstrating that compared to sham controls, ferritin H and transferrin protein levels in hippocampal homogenates significantly increased at 1 day after ischemia, peaked at 4 days and then decreased. These results suggest that iron overload-induced oxidative stress is most prominent at 12 hours after ischemia in the Stratum Pyramidale, suggesting that this time window may be the optimal period for therapeutic intervention to protect neurons from ischemia-induced death.

  • ischemia induced ribosomal protein s3 expressional changes and the neuroprotective effect against experimental cerebral ischemic damage
    Journal of Neuroscience Research, 2008
    Co-Authors: In Koo Hwang, Ki-yeon Yoo, Dae Won Kim, So Young Kim, Jun Hong Park, Zae Young Ryoo, Joon Kim, Soo Young Choi, Moo-ho Won
    Abstract:

    Some ribosomal proteins are important regulators of development and DNA repair. However, few studies have been conducted on ribosomal protein S3 (rpS3) in the ischemic hippocampus. In the present study, we investigated ischemia-induced changes in rpS3 immunoreactivity, rpS3 mRNA, and protein levels in the hippocampal CA1 region of Mongolian gerbil after 5 min of transient forebrain ischemia. RpS3 immunoreactivity and its protein level were found to be significantly elevated at 6 hr after ischemia/reperfusion and then continuously decreased with time. RT-PCR analysis also showed that rpS3 mRNA levels were significantly elevated in CA1 at 6 hr after transient ischemia. In addition, during the course of this study, we developed a delivery vector (Pep-1) and its rpS3 fusion protein (Pep-1-rpS3) to elucidate the role of rpS3 in ischemia-induced damage. Pep-1-rpS3 administration to ischemic animals significantly and dose dependently increased neuronal survival in the Stratum Pyramidale of CA1. Moreover, Pep-1-rpS3 treatment reduced terminal deoxynucleotidyl dUTP nick-end labeling-positive CA1 pyramidal cell numbers in the Stratum Pyramidale. To elucidate how Pep-1-rpS3 ameliorates ischemic damage, changes in 4-hydroxy-2-nonnenal (HNE; an indicator of lipid peroxidation) immunoreactivity and protein levels were investigated. HNE levels and immunoreactivities in Pep-1-rpS3-treated ischemic animals were lower than in corresponding Pep-1-treated ischemic animals. These results indicate that rpS3 has a neuroprotective effect in the brain exposed to ischemia.

  • Berberry extract reduces neuronal damage and N-Methyl-D-aspartate receptor 1 immunoreactivity in the gerbil hippocampus after transient forebrain ischemia.
    Biological & pharmaceutical bulletin, 2006
    Co-Authors: Ki-yeon Yoo, In Koo Hwang, Beong Ou Lim, Tae-cheon Kang, Dong-woo Kim, Sang Moo Kim, Hyeon Yong Lee, Jong Dai Kim, Moo-ho Won
    Abstract:

    In the present study, we studied the neuroprotective effects of berberry extract (BE) against ischemic damage and the temporal and spatial alterations of N-methyl-D-aspartate receptor type 1 (NR1) and NR2A/2B immunoreactivities in the gerbil hippocampal CA1 region after transient ischemia to examine anti-ischemic effects and its role in transient forebrain ischemia. In the vehicle-treated group, the percentage of cresyl violet positive pyramidal cells in the CA1 region was about 11.4% compared to the sham-operated group 4 d after ischemic insult. BE showed neuroprotective effects against ischemic damage after ischemia-reperfusion. In the BE-treated groups, about 60-75% of CA1 pyramidal cells were stained with cresyl violet 4 d after ischemic insult. We observed the percentage of berberine (7.45+0.85 mg/g in BE) by HPLC, which is active ingredient of BE. NR1 immunoreactivity in the Stratum Pyramidale of the CA1 region in the vehicle-treated group was significantly increased at 30 min after transient forebrain ischemia, while at this time the NR1 immunoreactivity in the BE-treated groups was significantly low compared to the vehicle-treated group. The pattern of NR2A/B immunoreactivity in the Stratum Pyramidale of the BE-treated group and its protein levels were similar to that in the vehicle-treated group after ischemic insult. These results suggest that BE has potent neuroprotective effects against ischemic damage via the reduction of NR1 activity.

  • Copper chaperone for Cu,Zn-SOD supplement potentiates the Cu,Zn-SOD function of neuroprotective effects against ischemic neuronal damage in the gerbil hippocampus
    Free radical biology & medicine, 2005
    Co-Authors: In Koo Hwang, Ki-yeon Yoo, Dae Won Kim, Jun Hwi Cho, Tae-cheon Kang, J.h Kang, Won Sik Eum, Soo Hyun Choi, Oh-shin Kwon, Soo Young Choi
    Abstract:

    In the present study, we investigated the chronological alterations in SOD1 and its copper chaperone (chaperone for superoxide dismutase, CCS) immunoreactivities and their neuroprotective effects against neuronal damage in the gerbil hippocampus after 5 min of transient forebrain ischemia. SOD1 and CCS immunoreactivities were significantly increased in the Stratum Pyramidale of the CA1 region at 24 and 12 h after ischemic insult, respectively. At 24 h after ischemic insult, the SOD1 and CCS immunoreactivities were colocalized in the CA1 pyramidal cells of the Stratum Pyramidale. Thereafter, their immunoreactivities were significantly decreased in the CA1 region. To elucidate the effects of CCS or CCS/SOD1, we constructed the expression vectors PEP-1-SOD and PEP-1-CCS. In the CCS-treated group and the CCS/SOD1-treated group, 43.9 and 78.9% pyramidal cells, respectively, compared to the sham-operated group, were stained with cresyl violet 5 or 7 days after ischemic insult. The distribution pattern of active astrocytes and microglia in the PEP-CCS/SOD1-treated group 5 days after ischemic insult was similar to that of the sham-operated group. In addition, the SOD activity in the PEP-CCS- or PEP-CCS/SOD1-treated group was maintained by 10 days after ischemic insult. The SOD activity was higher in the PEP-CCS/SOD1-treated group vs the CCS-treated group. These results suggest that the enhanced expression of SOD1 and CCS may be related to compensatory mechanisms against ischemic damage and that cotreatment with CCS and SOD1 has a greater neuroprotective effect than treatment with CCS or SOD1 in isolation.

  • Ischemia-related changes of adrenocorticotropic hormone immunoreactivity and its protective effect in the gerbil hippocampus after transient forebrain ischemia
    Neuroscience, 2004
    Co-Authors: In Koo Hwang, Ki-yeon Yoo, Soo Young Choi, Tae-cheon Kang, J.-k Park, Young Sam Nam, I. S. Lee, J.h Kang, Jae-yong Lee, Moo-ho Won
    Abstract:

    In the present study, the temporal and spatial alterations of adrenocorticotropic hormone (ACTH) immunoreactivity in the gerbil hippocampus after 5 min transient forebrain ischemia were investigated as followed up 7 days after ischemic insult, and the effects of ACTH after ischemic insult were also investigated 4 days after ischemic insult. The ectopic expression of ACTH (1-24 fragments) immunoreactive neurons in the cornus ammonis 1 (CA1) region of hippocampus and hilar region of the dentate gyrus 1 day after the ischemic insult was observed. Judging from the double immunofluorescence study, these neurons contain GABA. Four days after ischemic insult, the ACTH immunoreactivity was localized in CA1 pyramidal cells and glia near the Stratum Pyramidale, which normally do not express ACTH. In addition, in the saline-treated groups, the percentage of the detected Cresyl Violet positive neurons was 11.2% compared with the sham-operated group 4 and 7 days after ischemic insult. In these groups, the OX-42 immunoreactive microglia were detected in the strata Pyramidale, oriens and radiatum. However, in the Org2766 (analog of ACTH)-treated group, 57.8% neurons compared with the sham-operated group were stained with Cresyl Violet 4 and 7 days after ischemic insult. In these groups, the OX-42 immunoreactive microglia were significantly reduced in the Stratum Pyramidale. These results suggest that transient forebrain ischemia may provoke selective ectopic and enhanced expression of ACTH in the hippocampus, and further suggest that ACTH plays an important role in reducing the ischemic damage.