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

  • CD74-immunoreactive activated M1 microglia are shown late in the gerbil Hippocampal CA1 Region following transient cerebral ischemia.
    Molecular medicine reports, 2017
    Co-Authors: In Koo Hwang, Ji Hyeon Ahn, Joon Ha Park, Tae‑kyeong Lee, Dae Won Kim, Ki Yeon Yoo, Yang Hee Kim, Jun Hwi Cho, Young Myeong Kim, Moo Ho Won
    Abstract:

    Activated M1 microglia secrete proinflammatory cytokines into damaged brain areas. The present study examined activated M1 microglial morphology and expression in the Hippocampal Cornu Ammonis (CA) 1 Region, which is vulnerable to transient ischemia. Transient cerebral ischemia was performed for 5 min in gerbils, and neuronal death in the CA1 Region following transient cerebral ischemia was confirmed using cresyl violet staining, neuronal nuclear antigen immunohistochemistry and Fluoro‑Jade B histofluorescent staining. In addition, CA1 Regions were stained for cluster of differentiation (CD) 74, a marker for activated M1 microglia and a ligand for macrophage migration inhibitory factor In sham‑operated animals, no CD74 immunoreactivity was observed in the Hippocampal CA1 Region. CD74 immunoreactivity was not observed in the Hippocampal CA1 Region until 3 days post‑ischemic insult; however, elevated CD74 immunoreactivity was detected in the CA1 Region from 5 days post‑ischemia. Double immunofluorescence staining for CD74 and ionized calcium‑binding adapter molecule 1, a marker for M1 microglial cells, confirmed the expression of CD74 on this microglial subtype. These results indicated that M1 microglia are activated late in the Hippocampal CA1 Region following ischemic stroke. Therefore, optimizing the timing of therapeutic intervention may reduce activated M1 microglial-induced neuronal damage.

  • Ischemia-Induced Changes of PRAS40 and p-PRAS40 Immunoreactivities in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia.
    Cellular and molecular neurobiology, 2015
    Co-Authors: Joon Ha Park, Jeong Hwi Cho, Ji Hyeon Ahn, Bich-na Shin, Moo Ho Won, Dae Won Kim, Jun Hwi Cho, In Hye Kim, Seongkweon Hong, Choong-hyun Lee
    Abstract:

    Proline-rich Akt substrate of 40-kDa (PRAS40) is one of the important interactive linkers between Akt and mTOR signaling pathways. The increase of PRAS40 is related with the reduction of brain damage induced by cerebral ischemia. In the present study, we investigated time-dependent changes in PRAS40 and phospho-PRAS40 (p-PRAS40) immunoreactivities in the Hippocampal CA1 Region of the gerbil after 5 min of transient cerebral ischemia. PRAS40 immunoreactivity in the CA1 Region was decreased in pyramidal neurons from 12 h after ischemic insult in a time-dependent manner, and, at 5 days post-ischemia, PRAS40 immunoreactivity was newly expressed in astrocytes. p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was hardly found 12 h and apparently detected again 1 and 2 days after ischemic insult. At 5 days post-ischemia, p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was not found. These results indicate that ischemia-induced changes in PRAS40 and p-PRAS40 immunoreactivities in CA1 pyramidal neurons and astrocytes may be closely associated with delayed neuronal death in the Hippocampal CA1 Region following transient cerebral ischemia.

  • Neurons in the Hippocampal CA1 Region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes.
    Neural regeneration research, 2015
    Co-Authors: Sang Gun Lee, Dae Young Yoo, Sung Min Nam, Jung Hoon Choi, Yeo Sung Yoon, Moo Ho Won, Hyo Young Jung, Jong Whi Kim, In Koo Hwang
    Abstract:

    In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxidant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin (75 mg/kg) was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental parameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7-21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the Hippocampal CA1 Region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the Hippocampal CA1 Region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment.

  • New expression of 5-HT1A receptor in astrocytes in the gerbil Hippocampal CA1 Region following transient global cerebral ischemia.
    Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2014
    Co-Authors: Choong-hyun Lee, Ji Hyeon Ahn, Moo Ho Won
    Abstract:

    5-Hydroxytryptamine (5-HT, serotonin) plays protective or detrimental roles in the development of ischemic damage. In the present study, we investigated the time-course changes in 5-HT1A receptor protein expression in the gerbil Hippocampal CA1 Region after transient global cerebral ischemia. 5-HT1A receptor immunoreactivity in the stratum pyramidale (SP) of the CA1 Region was decreased from 6 h and hardly observed 1 and 2 days after ischemic insult. Five and 10 days after ischemia/reperfusion, 5-HT1A receptor immunoreactivity was increased and detected in astrocyte of the ischemic CA1 Region. Furthermore, the pattern of changes in 5-HT1A receptor protein levels in the CA1 Region after ischemia–reperfusion was similar to that observed in the immunohistochemical data. These results indicate that 5-HT1A receptor protein expressions may be related with the ischemia-induced neuronal death and the function of astrocytes in the ischemic Hippocampal CA1 Region.

  • Chronological changes and effects of AMP-activated kinase in the Hippocampal CA1 Region after transient forebrain ischemia in gerbils
    Neurological research, 2013
    Co-Authors: Han Ga Wi Nam, Dae Young Yoo, Woosuk Kim, Jung Hoon Choi, Moo Ho Won, In Koo Hwang, Je Hoon Jeong, Hyung Sik Hwang, Seung-myung Moon
    Abstract:

    Objectives: Adenosine monophosphate-activated kinase (AMPK) is an energy-specific sensor within the central nervous system. In this study, we observed AMPK and its phosphorylated form (pAMPK) in the Hippocampal CA1 Region after 5 minutes of transient forebrain ischemia. In addition, we also investigated the effects of Compound C, an AMPK inhibitor, against ischemic damage in gerbils. Methods: Adenosine monophosphate-activated kinase and pAMPK immunoreactivity was observed in the Hippocampal CA1 Region at various time points after ischemia and Compound C was intraperitoneally administered to gerbils immediately after reperfusion and the animals were sacrificed at 5 days after ischemia/reperfusion. Results: Adenosine monophosphate-activated kinase immunoreactivity was transiently increased in the Hippocampal CA1 Region 1–2 days after ischemia/reperfusion, while AMPK immunoreactivity was almost undetectable in the stratum pyramidale of the CA1 Region 4–7 days after ischemia/reperfusion. The administration of...

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

  • CD74-immunoreactive activated M1 microglia are shown late in the gerbil Hippocampal CA1 Region following transient cerebral ischemia.
    Molecular medicine reports, 2017
    Co-Authors: In Koo Hwang, Ji Hyeon Ahn, Joon Ha Park, Tae‑kyeong Lee, Dae Won Kim, Ki Yeon Yoo, Yang Hee Kim, Jun Hwi Cho, Young Myeong Kim, Moo Ho Won
    Abstract:

    Activated M1 microglia secrete proinflammatory cytokines into damaged brain areas. The present study examined activated M1 microglial morphology and expression in the Hippocampal Cornu Ammonis (CA) 1 Region, which is vulnerable to transient ischemia. Transient cerebral ischemia was performed for 5 min in gerbils, and neuronal death in the CA1 Region following transient cerebral ischemia was confirmed using cresyl violet staining, neuronal nuclear antigen immunohistochemistry and Fluoro‑Jade B histofluorescent staining. In addition, CA1 Regions were stained for cluster of differentiation (CD) 74, a marker for activated M1 microglia and a ligand for macrophage migration inhibitory factor In sham‑operated animals, no CD74 immunoreactivity was observed in the Hippocampal CA1 Region. CD74 immunoreactivity was not observed in the Hippocampal CA1 Region until 3 days post‑ischemic insult; however, elevated CD74 immunoreactivity was detected in the CA1 Region from 5 days post‑ischemia. Double immunofluorescence staining for CD74 and ionized calcium‑binding adapter molecule 1, a marker for M1 microglial cells, confirmed the expression of CD74 on this microglial subtype. These results indicated that M1 microglia are activated late in the Hippocampal CA1 Region following ischemic stroke. Therefore, optimizing the timing of therapeutic intervention may reduce activated M1 microglial-induced neuronal damage.

  • Differential Effects of Pioglitazone in the Hippocampal CA1 Region Following Transient Forebrain Ischemia in Low- and High-Fat Diet-Fed Gerbils
    Neurochemical research, 2015
    Co-Authors: Seung-myung Moon, Dae Young Yoo, In Koo Hwang, Dae Won Kim, Hyo Young Jung, Goang-min Choi, Hee Sun Yim, Byung Moon Cho, In Bok Chang, Sung-min Cho
    Abstract:

    In the present study, we investigated the effects of pioglitazone (PGZ) in the Hippocampal CA1 Region of low- or high-fat diet (LFD or HFD) fed gerbils after transient forebrain ischemia. After 8 weeks of LFD or HFD feeding, PGZ (30 mg/kg) was intraperitoneally administered to the gerbils, following which ischemia was induced by occlusion of the bilateral common carotid arteries for 5 min. Administration of PGZ significantly reduced the ischemia-induced hyperactivity 1 day after ischemia/reperfusion in both LFD- and HFD-fed gerbils. At 4 days after ischemia/reperfusion, the neurons were significantly reduced and microglial activation was observed in the Hippocampal CA1 Region in LFD- and HFD-fed gerbils. The microglial activation was more prominent in the HFD-fed gerbils compared to the LFD-fed gerbils. Administration of PGZ ameliorated ischemia-induced neuronal death and microglial activation in the Hippocampal CA1 Region 4 days after ischemia/reperfusion in the LFD-fed gerbils, but not in the HFD-gerbils. At 6 h after ischemia/reperfusion, tumor necrosis factor-α (TNF-α) and interlukin-1β (IL-1β) levels were significantly increased in the Hippocampal homogenates of LFD-fed group compared to control group, and HFD feeding further increased TNF-α and IL-1β levels. PGZ treatment significantly ameliorated the increase of TNF-α and IL-1β levels in LFD-fed gerbils, not in the HFD-fed gerbils. At 12 h after ischemia/reperfusion, superoxide dismutase (SOD) and malondialdehyde (MDA) levels in Hippocampal homogenates were significantly increased in the LFD-fed group compared to the control group, and HFD feeding significantly showed relatively reduction in SOD activity and increase in MDA level. PGZ administration significantly reduced the increase in MDA levels 12 h after ischemia/reperfusion in the LFD-fed gerbils, but not in the HFD-fed gerbils. These results suggest that PGZ ameliorates the neuronal damage induced by ischemia by maintaining the TNF-α, IL-1β, SOD and MDA levels in LFD-fed gerbils. In addition, HFD feeding affects the modulation of these parameters in the hippocampus after transient forebrain ischemia.

  • Neurons in the Hippocampal CA1 Region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes.
    Neural regeneration research, 2015
    Co-Authors: Sang Gun Lee, Dae Young Yoo, Sung Min Nam, Jung Hoon Choi, Yeo Sung Yoon, Moo Ho Won, Hyo Young Jung, Jong Whi Kim, In Koo Hwang
    Abstract:

    In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxidant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin (75 mg/kg) was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental parameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7-21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the Hippocampal CA1 Region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the Hippocampal CA1 Region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment.

  • Chronological changes and effects of AMP-activated kinase in the Hippocampal CA1 Region after transient forebrain ischemia in gerbils
    Neurological research, 2013
    Co-Authors: Han Ga Wi Nam, Dae Young Yoo, Woosuk Kim, Jung Hoon Choi, Moo Ho Won, In Koo Hwang, Je Hoon Jeong, Hyung Sik Hwang, Seung-myung Moon
    Abstract:

    Objectives: Adenosine monophosphate-activated kinase (AMPK) is an energy-specific sensor within the central nervous system. In this study, we observed AMPK and its phosphorylated form (pAMPK) in the Hippocampal CA1 Region after 5 minutes of transient forebrain ischemia. In addition, we also investigated the effects of Compound C, an AMPK inhibitor, against ischemic damage in gerbils. Methods: Adenosine monophosphate-activated kinase and pAMPK immunoreactivity was observed in the Hippocampal CA1 Region at various time points after ischemia and Compound C was intraperitoneally administered to gerbils immediately after reperfusion and the animals were sacrificed at 5 days after ischemia/reperfusion. Results: Adenosine monophosphate-activated kinase immunoreactivity was transiently increased in the Hippocampal CA1 Region 1–2 days after ischemia/reperfusion, while AMPK immunoreactivity was almost undetectable in the stratum pyramidale of the CA1 Region 4–7 days after ischemia/reperfusion. The administration of...

  • Chronic effects of pyridoxine in the gerbil Hippocampal CA1 Region after transient forebrain ischemia.
    Neurochemical research, 2012
    Co-Authors: Dae Young Yoo, Woosuk Kim, Sung Min Nam, Jin Young Chung, Jung Hoon Choi, Yeo Sung Yoon, Moo Ho Won, In Koo Hwang
    Abstract:

    In a previous study, we reported that the administration of pyridoxine (vitamin B6) to mice for 3 weeks significantly increased cell proliferation and neuroblast differentiation in the dentate gyrus without any neuronal damage. In the present study, we investigated the restorative potentials of pyridoxine on ischemic damage in the Hippocampal CA1 Region of Mongolian gerbils. Gerbils were subjected to 5 min of transient ischemia, and surgical operation success was assessed by ophthalmoscope during occlusion of common carotid arteries and spontaneous motor activity at 1 day after ischemia/reperfusion. Pyridoxine (350 mg/kg) or its vehicle (physiological saline) was intraperineally administered to ischemic gerbils twice a day starting 4 days after ischemia/reperfusion for 30 or 60 days. The repeated administration of pyridoxine for 30 and 60 days significantly increased doublecortin-immunoreactive neuroblasts in the dentate gyrus and increased NeuN-immunoreactive mature neurons and βIII-tubulin-immunoreactive dendrites in the Hippocampal CA1 Region. Furthermore, brain-derived neurotrophic factor (BDNF) protein levels were significantly increased in pyridoxine-treated groups compared to those in the vehicle-treated groups. These results suggest that chronic administration of pyridoxine enhances neuroblast differentiation in the dentate gyrus and induces new mature neurons in the Hippocampal CA1 Region by up-regulating BDNF expression in Hippocampal homogenates.

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

  • CD74-immunoreactive activated M1 microglia are shown late in the gerbil Hippocampal CA1 Region following transient cerebral ischemia.
    Molecular medicine reports, 2017
    Co-Authors: In Koo Hwang, Ji Hyeon Ahn, Joon Ha Park, Tae‑kyeong Lee, Dae Won Kim, Ki Yeon Yoo, Yang Hee Kim, Jun Hwi Cho, Young Myeong Kim, Moo Ho Won
    Abstract:

    Activated M1 microglia secrete proinflammatory cytokines into damaged brain areas. The present study examined activated M1 microglial morphology and expression in the Hippocampal Cornu Ammonis (CA) 1 Region, which is vulnerable to transient ischemia. Transient cerebral ischemia was performed for 5 min in gerbils, and neuronal death in the CA1 Region following transient cerebral ischemia was confirmed using cresyl violet staining, neuronal nuclear antigen immunohistochemistry and Fluoro‑Jade B histofluorescent staining. In addition, CA1 Regions were stained for cluster of differentiation (CD) 74, a marker for activated M1 microglia and a ligand for macrophage migration inhibitory factor In sham‑operated animals, no CD74 immunoreactivity was observed in the Hippocampal CA1 Region. CD74 immunoreactivity was not observed in the Hippocampal CA1 Region until 3 days post‑ischemic insult; however, elevated CD74 immunoreactivity was detected in the CA1 Region from 5 days post‑ischemia. Double immunofluorescence staining for CD74 and ionized calcium‑binding adapter molecule 1, a marker for M1 microglial cells, confirmed the expression of CD74 on this microglial subtype. These results indicated that M1 microglia are activated late in the Hippocampal CA1 Region following ischemic stroke. Therefore, optimizing the timing of therapeutic intervention may reduce activated M1 microglial-induced neuronal damage.

  • Comparison of glial activation in the Hippocampal CA1 Region between the young and adult gerbils after transient cerebral ischemia.
    Cellular and molecular neurobiology, 2012
    Co-Authors: Bing Chun Yan, Ji Hyeon Ahn, Joon Ha Park, Choong-hyun Lee, Jung Hoon Choi, Ki Yeon Yoo, Jun Hwi Cho, Sung Koo Kim, Yun Lyul Lee, Hyung-cheul Shin
    Abstract:

    It has been reported that young animals are less vulnerable to brain ischemia. In the present study, we compared gliosis in the Hippocampal CA1 Region of the young gerbil with those in the adult gerbil induced by 5 min of transient cerebral ischemia by immunohistochemistry and western blot for glial cells. We used male gerbils of postnatal month 1 (PM 1) as the young and PM 6 as the adult. Neuronal death in CA1 pyramidal neurons in the adult gerbil occurred at 4 days posti-schemia; the neuronal death in the young gerbil occurred at 7 days post-ischemia. The findings of glial changes in the young gerbil after ischemic damage were distinctively different from those in the adult gerbil. Glial fibrillary acidic protein-immunoreactive astrocytes, ionized calcium-binding adapter molecule (Iba-1), and isolectin B4-immunoreactive microglia in the ischemic CA1 Region were activated much later in the young gerbil than in the adult gerbil. In brief, very less gliosis occurred in the Hippocampal CA1 Region of the young gerbil than in the adult gerbil after transient cerebral ischemia.

  • Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress
    Neurochemical Research, 2011
    Co-Authors: Ki Yeon Yoo, Choong-hyun Lee, Jung Hoon Choi, In Koo Hwang, Jun Hwi Cho, Young Myeong Kim, Youdong Sohn, Moo Ho Won
    Abstract:

    Restraint stress produces physiological changes including suppression of long-term potentiation in the brain. We observed the effects of repeated stress on ischemic damage associated with corticosteroid hormone receptors in gerbils. Animals were placed into restrainers for 5 h (between 09:30 h and 14:30 h) for 21 consecutive days prior to induction of transient cerebral ischemia. The animals were divided into 4 groups; (1) sham-operated-control-group (sham-group), (2) ischemia-operated-control-group (ischemia-group), (3) sham-operated-stress-group (stressed-sham-group), and (4) ischemia-operated-stress-group (stressed-ischemia-group). We found that serum corticosterone level in the ischemia-group was highest (374% of the sham-group) 12 h after ischemia/reperfusion and its level in the stressed-ischemia-group was significantly lower than the ischemia-group. Locomotor activity in the ischemia-group was significantly increased (295% of the sham-group) at 1 day post-ischemia; however, the locomotor activity in the stressed-ischemia-group was less increased compared to the ischemia-group. Cresyl violet positive (CV^+) cells were significantly decreased in the stratum pyramidale (SP) of the Hippocampal CA1 Region (CA1) of the 4 days post-ischemia-group, while 79.4% of CV^+ cells were detected in the CA1 of the stressed-ischemia-group. Also, a few NeuN (neuron-specific soluble nuclear antigen)^+ cells were detected in the SP of the 4 days post-ischemia-group; however, in the 4 days stressed-post-ischemia-group, 77.2% of NeuN^+ neurons were found in the SP. Glial fibrillary acidic protein^+ astrocytes in the CA1 in the stressed-ischemia-groups were similar to those in the ischemia-groups; however, ionized calcium-binding adapter molecule 1^+ microglia in the stressed-ischemia-groups were less activated compared to the ischemia-groups. Mineralocorticoid receptor (MCR) and glucocorticoid receptor (GR) immunoreactivity in the SP of the stressed-ischemia-group were higher than the ischemia-group; at 4 days post-ischemia, MCR and GR immunoreactivity were expressed in non-pyramidal cells. In brief, our results indicate that repeated restraint stress significantly increase levels of corticosteroid hormone receptors and attenuates neuronal damage in the ischemic Hippocampal CA1 Region.

  • Expression of tissue-type transglutaminase (tTG) and the effect of tTG inhibitor on the Hippocampal CA1 Region after transient ischemia in gerbils
    Brain research, 2009
    Co-Authors: In Koo Hwang, Yeo Sung Yoon, Ki Yeon Yoo, In Se Lee, Il Yong Kim, Hye Sook Hwang, Kyung-yul Lee, Sun Mi Choi, Soo Youl Kim
    Abstract:

    Chronological changes of tissue-type transglutaminase (tTG) were observed in the Hippocampal CA1 Region after transient forebrain ischemia in gerbils. In the sham-operated group, tTG immunoreactivity was weakly detected in blood vessels which were immunostained with platelet endothelial cell adhesion molecule-1 (PECAM-1), and tTG immunoreactivity in blood vessels was highest 5 days after ischemia/reperfusion. In addition, tTG immunoreaction was expressed in microglia which were immunostained with Iba-1 at 4 days post-ischemia, and tTG immunoreactivity in the microglia was also highest at 5 days post-ischemia. In Western blot analysis, tTG protein levels in the CA1 Region after ischemia/reperfusion began to increase 3 days after ischemia/reperfusion and peaked 5 days after ischemia/reperfusion. The expression of tTG in PECAM-1-immunoreactive blood vessels may be associated with integrin regulation or transendothelial migration of leukocytes in the ischemic CA1 Region. In this study, we also observed the effect of cystamine, a tTG inhibitor, against ischemic damage. Administration of cystamine protected in certain degree neuronal damage from ischemic damage in the CA1 Region. These results suggest that tTG may be associated with neuronal death in the Hippocampal CA1 Region induced by ischemia/reperfusion.

  • late expression of na h exchanger 1 nhe1 and neuroprotective effects of nhe inhibitor in the gerbil Hippocampal CA1 Region induced by transient ischemia
    Experimental Neurology, 2008
    Co-Authors: In Koo Hwang, Choong-hyun Lee, Jung Hoon Choi, Ki Yeon Yoo, Young Myeong Kim, Youngguen Kwon, Bonghee Lee, Jaeyong Lee, Moo Ho Won
    Abstract:

    Although acidosis may be involved in neuronal death, the participation of Na(+)/H(+) exchanger (NHE) in delayed neuronal death in the Hippocampal CA1 Region induced by transient forebrain ischemia has not been well established. In the present study, we investigated the chronological alterations of NHE1 in the Hippocampal CA1 Region using a gerbil model after ischemia/reperfusion. In the sham-operated group, NHE1 immunoreactivity was weakly detected in the CA1 Region. Two and 3 days after ischemia/reperfusion, NHE1 immunoreactivity was observed in glial components, not in neurons, in the CA1 Region. Four days after ischemia/reperfusion, NHE1 immunoreactivity was markedly increased in CA1 pyramidal neurons as well as glial cells. These glial cells were identified as astrocytes based on double immunofluorescence staining. Western blot analysis also showed that NHE protein level in the CA1 Region began to increase 2 days after ischemia/reperfusion. The treatment of 10 mg/kg 5-(N-ethyl-N-isopropyl) amiloride, a NHE inhibitor, significantly reduced the ischemia-induced hyperactivity 1 day after ischemia/reperfusion. In addition, NHE inhibitor potently protected CA1 pyramidal neurons from ischemic damage, and NHE inhibitor attenuated the activation of astrocytes and microglia in the ischemic CA1 Region. In addition, NHE inhibitor treatment blocked Na(+)/Ca(2+) exchanger 1 immunoreactivity in the CA1 Region after transient forebrain ischemia. These results suggest that NHE1 may play a role in the delayed death, and the treatment with NHE inhibitor protects neurons from ischemic damage.

Choong-hyun Lee - One of the best experts on this subject based on the ideXlab platform.

  • Time-Course Change of Redd1 Expressions in the Hippocampal CA1 Region Following Chronic Cerebral Hypoperfusion
    Cellular and Molecular Neurobiology, 2017
    Co-Authors: Jin-a Park, Choong-hyun Lee
    Abstract:

    Redd1, also known as RTP801/Dig2/DDIT4, is a stress-induced protein and marked changes of Redd1 expression occurs in response to hypoxia or cerebral ischemia. In the present study, we examined the time-course changes in Redd1 protein expressions in the rat Hippocampal CA1 Region following chronic cerebral hypoperfusion (CCH) induced by permanent bilateral common carotid arteries occlusion (2VO). Redd1 immunoreactivity in the pyramidal neurons of the Hippocampal CA1 Region was increased at 7 days after 2VO surgery, and then the immunoreactivity was decreased with time. Especially, very weak Redd1 immunoreactivity was observed in the Hippocampal CA1 Region at 28 days after 2VO surgery. Western blot analysis showed that Redd1 level in the Hippocampal CA1 Region was significantly increased at 7 days following CCH and significantly decreased at 28 days after 2VO surgery, compared with that of the sham-operated group. These results indicate that Redd1 expressions is markedly changed in the Hippocampal CA1 Region following CCH and that change of Redd1 expression may be associated with the CCH-induced neuronal damage in the Hippocampal CA1 Region.

  • Temporal changes in mammalian target of rapamycin (mTOR) and phosphorylated-mTOR expressions in the Hippocampal CA1 Region of rat with vascular dementia
    Journal of veterinary science, 2017
    Co-Authors: Jin-a Park, Choong-hyun Lee
    Abstract:

    Abstract The mammalian target of rapamycin (mTOR) has an important role in diverse biological processes in cell. In the present study, we investigated the time-course changes of mTOR and phosphorylated-mTOR (p-mTOR) expressions in the rat Hippocampal CA1 Region following chronic cerebral hypoperfusion (CCH) induced by permanent bilateral common carotid arteries occlusion (2VO). mTOR immunoreactivity in the pyramidal neurons and mTOR protein level in the Hippocampal CA1 Region were markedly decreased at 21 and 28 days after 2VO surgery. However, p-mTOR protein expression was significantly increased at 7 days following CCH, and then decreased with time. These results indicate that mTOR and p-mTOR expressions are apparently changed in the Hippocampal CA1 Region after 2VO surgery, and that reduced expressions of mTOR and p-mTOR may be closely related to the CCH-induced neuronal damage in the Hippocampal CA1 Region.

  • Ischemia-Induced Changes of PRAS40 and p-PRAS40 Immunoreactivities in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia.
    Cellular and molecular neurobiology, 2015
    Co-Authors: Joon Ha Park, Jeong Hwi Cho, Ji Hyeon Ahn, Bich-na Shin, Moo Ho Won, Dae Won Kim, Jun Hwi Cho, In Hye Kim, Seongkweon Hong, Choong-hyun Lee
    Abstract:

    Proline-rich Akt substrate of 40-kDa (PRAS40) is one of the important interactive linkers between Akt and mTOR signaling pathways. The increase of PRAS40 is related with the reduction of brain damage induced by cerebral ischemia. In the present study, we investigated time-dependent changes in PRAS40 and phospho-PRAS40 (p-PRAS40) immunoreactivities in the Hippocampal CA1 Region of the gerbil after 5 min of transient cerebral ischemia. PRAS40 immunoreactivity in the CA1 Region was decreased in pyramidal neurons from 12 h after ischemic insult in a time-dependent manner, and, at 5 days post-ischemia, PRAS40 immunoreactivity was newly expressed in astrocytes. p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was hardly found 12 h and apparently detected again 1 and 2 days after ischemic insult. At 5 days post-ischemia, p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was not found. These results indicate that ischemia-induced changes in PRAS40 and p-PRAS40 immunoreactivities in CA1 pyramidal neurons and astrocytes may be closely associated with delayed neuronal death in the Hippocampal CA1 Region following transient cerebral ischemia.

  • New expression of 5-HT1A receptor in astrocytes in the gerbil Hippocampal CA1 Region following transient global cerebral ischemia.
    Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2014
    Co-Authors: Choong-hyun Lee, Ji Hyeon Ahn, Moo Ho Won
    Abstract:

    5-Hydroxytryptamine (5-HT, serotonin) plays protective or detrimental roles in the development of ischemic damage. In the present study, we investigated the time-course changes in 5-HT1A receptor protein expression in the gerbil Hippocampal CA1 Region after transient global cerebral ischemia. 5-HT1A receptor immunoreactivity in the stratum pyramidale (SP) of the CA1 Region was decreased from 6 h and hardly observed 1 and 2 days after ischemic insult. Five and 10 days after ischemia/reperfusion, 5-HT1A receptor immunoreactivity was increased and detected in astrocyte of the ischemic CA1 Region. Furthermore, the pattern of changes in 5-HT1A receptor protein levels in the CA1 Region after ischemia–reperfusion was similar to that observed in the immunohistochemical data. These results indicate that 5-HT1A receptor protein expressions may be related with the ischemia-induced neuronal death and the function of astrocytes in the ischemic Hippocampal CA1 Region.

  • Comparison of glial activation in the Hippocampal CA1 Region between the young and adult gerbils after transient cerebral ischemia.
    Cellular and molecular neurobiology, 2012
    Co-Authors: Bing Chun Yan, Ji Hyeon Ahn, Joon Ha Park, Choong-hyun Lee, Jung Hoon Choi, Ki Yeon Yoo, Jun Hwi Cho, Sung Koo Kim, Yun Lyul Lee, Hyung-cheul Shin
    Abstract:

    It has been reported that young animals are less vulnerable to brain ischemia. In the present study, we compared gliosis in the Hippocampal CA1 Region of the young gerbil with those in the adult gerbil induced by 5 min of transient cerebral ischemia by immunohistochemistry and western blot for glial cells. We used male gerbils of postnatal month 1 (PM 1) as the young and PM 6 as the adult. Neuronal death in CA1 pyramidal neurons in the adult gerbil occurred at 4 days posti-schemia; the neuronal death in the young gerbil occurred at 7 days post-ischemia. The findings of glial changes in the young gerbil after ischemic damage were distinctively different from those in the adult gerbil. Glial fibrillary acidic protein-immunoreactive astrocytes, ionized calcium-binding adapter molecule (Iba-1), and isolectin B4-immunoreactive microglia in the ischemic CA1 Region were activated much later in the young gerbil than in the adult gerbil. In brief, very less gliosis occurred in the Hippocampal CA1 Region of the young gerbil than in the adult gerbil after transient cerebral ischemia.

Jung Hoon Choi - One of the best experts on this subject based on the ideXlab platform.

  • Neurons in the Hippocampal CA1 Region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes.
    Neural regeneration research, 2015
    Co-Authors: Sang Gun Lee, Dae Young Yoo, Sung Min Nam, Jung Hoon Choi, Yeo Sung Yoon, Moo Ho Won, Hyo Young Jung, Jong Whi Kim, In Koo Hwang
    Abstract:

    In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxidant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin (75 mg/kg) was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental parameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7-21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the Hippocampal CA1 Region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the Hippocampal CA1 Region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment.

  • Chronological changes and effects of AMP-activated kinase in the Hippocampal CA1 Region after transient forebrain ischemia in gerbils
    Neurological research, 2013
    Co-Authors: Han Ga Wi Nam, Dae Young Yoo, Woosuk Kim, Jung Hoon Choi, Moo Ho Won, In Koo Hwang, Je Hoon Jeong, Hyung Sik Hwang, Seung-myung Moon
    Abstract:

    Objectives: Adenosine monophosphate-activated kinase (AMPK) is an energy-specific sensor within the central nervous system. In this study, we observed AMPK and its phosphorylated form (pAMPK) in the Hippocampal CA1 Region after 5 minutes of transient forebrain ischemia. In addition, we also investigated the effects of Compound C, an AMPK inhibitor, against ischemic damage in gerbils. Methods: Adenosine monophosphate-activated kinase and pAMPK immunoreactivity was observed in the Hippocampal CA1 Region at various time points after ischemia and Compound C was intraperitoneally administered to gerbils immediately after reperfusion and the animals were sacrificed at 5 days after ischemia/reperfusion. Results: Adenosine monophosphate-activated kinase immunoreactivity was transiently increased in the Hippocampal CA1 Region 1–2 days after ischemia/reperfusion, while AMPK immunoreactivity was almost undetectable in the stratum pyramidale of the CA1 Region 4–7 days after ischemia/reperfusion. The administration of...

  • Comparison of glial activation in the Hippocampal CA1 Region between the young and adult gerbils after transient cerebral ischemia.
    Cellular and molecular neurobiology, 2012
    Co-Authors: Bing Chun Yan, Ji Hyeon Ahn, Joon Ha Park, Choong-hyun Lee, Jung Hoon Choi, Ki Yeon Yoo, Jun Hwi Cho, Sung Koo Kim, Yun Lyul Lee, Hyung-cheul Shin
    Abstract:

    It has been reported that young animals are less vulnerable to brain ischemia. In the present study, we compared gliosis in the Hippocampal CA1 Region of the young gerbil with those in the adult gerbil induced by 5 min of transient cerebral ischemia by immunohistochemistry and western blot for glial cells. We used male gerbils of postnatal month 1 (PM 1) as the young and PM 6 as the adult. Neuronal death in CA1 pyramidal neurons in the adult gerbil occurred at 4 days posti-schemia; the neuronal death in the young gerbil occurred at 7 days post-ischemia. The findings of glial changes in the young gerbil after ischemic damage were distinctively different from those in the adult gerbil. Glial fibrillary acidic protein-immunoreactive astrocytes, ionized calcium-binding adapter molecule (Iba-1), and isolectin B4-immunoreactive microglia in the ischemic CA1 Region were activated much later in the young gerbil than in the adult gerbil. In brief, very less gliosis occurred in the Hippocampal CA1 Region of the young gerbil than in the adult gerbil after transient cerebral ischemia.

  • Chronic effects of pyridoxine in the gerbil Hippocampal CA1 Region after transient forebrain ischemia.
    Neurochemical research, 2012
    Co-Authors: Dae Young Yoo, Woosuk Kim, Sung Min Nam, Jin Young Chung, Jung Hoon Choi, Yeo Sung Yoon, Moo Ho Won, In Koo Hwang
    Abstract:

    In a previous study, we reported that the administration of pyridoxine (vitamin B6) to mice for 3 weeks significantly increased cell proliferation and neuroblast differentiation in the dentate gyrus without any neuronal damage. In the present study, we investigated the restorative potentials of pyridoxine on ischemic damage in the Hippocampal CA1 Region of Mongolian gerbils. Gerbils were subjected to 5 min of transient ischemia, and surgical operation success was assessed by ophthalmoscope during occlusion of common carotid arteries and spontaneous motor activity at 1 day after ischemia/reperfusion. Pyridoxine (350 mg/kg) or its vehicle (physiological saline) was intraperineally administered to ischemic gerbils twice a day starting 4 days after ischemia/reperfusion for 30 or 60 days. The repeated administration of pyridoxine for 30 and 60 days significantly increased doublecortin-immunoreactive neuroblasts in the dentate gyrus and increased NeuN-immunoreactive mature neurons and βIII-tubulin-immunoreactive dendrites in the Hippocampal CA1 Region. Furthermore, brain-derived neurotrophic factor (BDNF) protein levels were significantly increased in pyridoxine-treated groups compared to those in the vehicle-treated groups. These results suggest that chronic administration of pyridoxine enhances neuroblast differentiation in the dentate gyrus and induces new mature neurons in the Hippocampal CA1 Region by up-regulating BDNF expression in Hippocampal homogenates.

  • Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress
    Neurochemical Research, 2011
    Co-Authors: Ki Yeon Yoo, Choong-hyun Lee, Jung Hoon Choi, In Koo Hwang, Jun Hwi Cho, Young Myeong Kim, Youdong Sohn, Moo Ho Won
    Abstract:

    Restraint stress produces physiological changes including suppression of long-term potentiation in the brain. We observed the effects of repeated stress on ischemic damage associated with corticosteroid hormone receptors in gerbils. Animals were placed into restrainers for 5 h (between 09:30 h and 14:30 h) for 21 consecutive days prior to induction of transient cerebral ischemia. The animals were divided into 4 groups; (1) sham-operated-control-group (sham-group), (2) ischemia-operated-control-group (ischemia-group), (3) sham-operated-stress-group (stressed-sham-group), and (4) ischemia-operated-stress-group (stressed-ischemia-group). We found that serum corticosterone level in the ischemia-group was highest (374% of the sham-group) 12 h after ischemia/reperfusion and its level in the stressed-ischemia-group was significantly lower than the ischemia-group. Locomotor activity in the ischemia-group was significantly increased (295% of the sham-group) at 1 day post-ischemia; however, the locomotor activity in the stressed-ischemia-group was less increased compared to the ischemia-group. Cresyl violet positive (CV^+) cells were significantly decreased in the stratum pyramidale (SP) of the Hippocampal CA1 Region (CA1) of the 4 days post-ischemia-group, while 79.4% of CV^+ cells were detected in the CA1 of the stressed-ischemia-group. Also, a few NeuN (neuron-specific soluble nuclear antigen)^+ cells were detected in the SP of the 4 days post-ischemia-group; however, in the 4 days stressed-post-ischemia-group, 77.2% of NeuN^+ neurons were found in the SP. Glial fibrillary acidic protein^+ astrocytes in the CA1 in the stressed-ischemia-groups were similar to those in the ischemia-groups; however, ionized calcium-binding adapter molecule 1^+ microglia in the stressed-ischemia-groups were less activated compared to the ischemia-groups. Mineralocorticoid receptor (MCR) and glucocorticoid receptor (GR) immunoreactivity in the SP of the stressed-ischemia-group were higher than the ischemia-group; at 4 days post-ischemia, MCR and GR immunoreactivity were expressed in non-pyramidal cells. In brief, our results indicate that repeated restraint stress significantly increase levels of corticosteroid hormone receptors and attenuates neuronal damage in the ischemic Hippocampal CA1 Region.