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Shimin Dong - One of the best experts on this subject based on the ideXlab platform.
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microrna 214 protects Cardiac Myocytes against h2o2 induced injury
Journal of Cellular Biochemistry, 2014Co-Authors: Suxia Shao, Hua Dong, Xiaohua Bian, Xingwei Yang, Shimin DongAbstract:Reactive oxygen species (ROS)-induced Cardiac myocyte injury resulting from changes in the expression levels of multiple genes plays a critical role in the pathogenesis of numerous heart diseases. The purpose of this study was to determine the potential roles of microRNA-214 (miR-214) in hydrogen peroxide (H2O2)-mediated gene regulation in Cardiac Myocytes. In this study, we used quantitative real-time RT-PCR (qRT-PCR) to demonstrate that miR-214 was upregulated in Cardiac Myocytes after treatment with H2O2. We transfected cells with pre-miR-214 to upregulate miR-214 expression and transfected cells with a miR-214 inhibitor (anti-miR-214) to downregulate miR-214 expression. H2O2-induced Cardiac cell apoptosis was detected by flow cytometry. The level of apoptosis was increased by the miR-214 inhibitor and decreased by pre-miR-214. Therefore, we believe that miR-214 plays a positive role in H2O2-induced Cardiac cell apoptosis. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is constitutively active and is considered to be the primary downregulator of the pro-oncogenic PI3K/Akt pathway. Western blot analysis revealed that the expression of the PTEN protein in Cardiac Myocytes decreased after H2O2 induction. Anti-miR-214 increased PTEN protein expression level, in contrast, pre-miR-214 decreased the PTEN protein expression level in cultured Cardiac Myocytes. These results indicate that PTEN is regulated by miR-214 and serves as an important target of miR-214 in Cardiac Myocytes. In conclusion, miR-214 is sensitive to H2O2 stimulation, and miR-214 protects Cardiac Myocytes against H2O2-induced injury via one of its targets, PTEN.
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MicroRNA‐214 Protects Cardiac Myocytes Against H2O2‐Induced Injury
Journal of cellular biochemistry, 2013Co-Authors: Suxia Shao, Hua Dong, Xiaohua Bian, Xingwei Yang, Shimin DongAbstract:Reactive oxygen species (ROS)-induced Cardiac myocyte injury resulting from changes in the expression levels of multiple genes plays a critical role in the pathogenesis of numerous heart diseases. The purpose of this study was to determine the potential roles of microRNA-214 (miR-214) in hydrogen peroxide (H2O2)-mediated gene regulation in Cardiac Myocytes. In this study, we used quantitative real-time RT-PCR (qRT-PCR) to demonstrate that miR-214 was upregulated in Cardiac Myocytes after treatment with H2O2. We transfected cells with pre-miR-214 to upregulate miR-214 expression and transfected cells with a miR-214 inhibitor (anti-miR-214) to downregulate miR-214 expression. H2O2-induced Cardiac cell apoptosis was detected by flow cytometry. The level of apoptosis was increased by the miR-214 inhibitor and decreased by pre-miR-214. Therefore, we believe that miR-214 plays a positive role in H2O2-induced Cardiac cell apoptosis. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is constitutively active and is considered to be the primary downregulator of the pro-oncogenic PI3K/Akt pathway. Western blot analysis revealed that the expression of the PTEN protein in Cardiac Myocytes decreased after H2O2 induction. Anti-miR-214 increased PTEN protein expression level, in contrast, pre-miR-214 decreased the PTEN protein expression level in cultured Cardiac Myocytes. These results indicate that PTEN is regulated by miR-214 and serves as an important target of miR-214 in Cardiac Myocytes. In conclusion, miR-214 is sensitive to H2O2 stimulation, and miR-214 protects Cardiac Myocytes against H2O2-induced injury via one of its targets, PTEN.
Suxia Shao - One of the best experts on this subject based on the ideXlab platform.
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microrna 214 protects Cardiac Myocytes against h2o2 induced injury
Journal of Cellular Biochemistry, 2014Co-Authors: Suxia Shao, Hua Dong, Xiaohua Bian, Xingwei Yang, Shimin DongAbstract:Reactive oxygen species (ROS)-induced Cardiac myocyte injury resulting from changes in the expression levels of multiple genes plays a critical role in the pathogenesis of numerous heart diseases. The purpose of this study was to determine the potential roles of microRNA-214 (miR-214) in hydrogen peroxide (H2O2)-mediated gene regulation in Cardiac Myocytes. In this study, we used quantitative real-time RT-PCR (qRT-PCR) to demonstrate that miR-214 was upregulated in Cardiac Myocytes after treatment with H2O2. We transfected cells with pre-miR-214 to upregulate miR-214 expression and transfected cells with a miR-214 inhibitor (anti-miR-214) to downregulate miR-214 expression. H2O2-induced Cardiac cell apoptosis was detected by flow cytometry. The level of apoptosis was increased by the miR-214 inhibitor and decreased by pre-miR-214. Therefore, we believe that miR-214 plays a positive role in H2O2-induced Cardiac cell apoptosis. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is constitutively active and is considered to be the primary downregulator of the pro-oncogenic PI3K/Akt pathway. Western blot analysis revealed that the expression of the PTEN protein in Cardiac Myocytes decreased after H2O2 induction. Anti-miR-214 increased PTEN protein expression level, in contrast, pre-miR-214 decreased the PTEN protein expression level in cultured Cardiac Myocytes. These results indicate that PTEN is regulated by miR-214 and serves as an important target of miR-214 in Cardiac Myocytes. In conclusion, miR-214 is sensitive to H2O2 stimulation, and miR-214 protects Cardiac Myocytes against H2O2-induced injury via one of its targets, PTEN.
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MicroRNA‐214 Protects Cardiac Myocytes Against H2O2‐Induced Injury
Journal of cellular biochemistry, 2013Co-Authors: Suxia Shao, Hua Dong, Xiaohua Bian, Xingwei Yang, Shimin DongAbstract:Reactive oxygen species (ROS)-induced Cardiac myocyte injury resulting from changes in the expression levels of multiple genes plays a critical role in the pathogenesis of numerous heart diseases. The purpose of this study was to determine the potential roles of microRNA-214 (miR-214) in hydrogen peroxide (H2O2)-mediated gene regulation in Cardiac Myocytes. In this study, we used quantitative real-time RT-PCR (qRT-PCR) to demonstrate that miR-214 was upregulated in Cardiac Myocytes after treatment with H2O2. We transfected cells with pre-miR-214 to upregulate miR-214 expression and transfected cells with a miR-214 inhibitor (anti-miR-214) to downregulate miR-214 expression. H2O2-induced Cardiac cell apoptosis was detected by flow cytometry. The level of apoptosis was increased by the miR-214 inhibitor and decreased by pre-miR-214. Therefore, we believe that miR-214 plays a positive role in H2O2-induced Cardiac cell apoptosis. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is constitutively active and is considered to be the primary downregulator of the pro-oncogenic PI3K/Akt pathway. Western blot analysis revealed that the expression of the PTEN protein in Cardiac Myocytes decreased after H2O2 induction. Anti-miR-214 increased PTEN protein expression level, in contrast, pre-miR-214 decreased the PTEN protein expression level in cultured Cardiac Myocytes. These results indicate that PTEN is regulated by miR-214 and serves as an important target of miR-214 in Cardiac Myocytes. In conclusion, miR-214 is sensitive to H2O2 stimulation, and miR-214 protects Cardiac Myocytes against H2O2-induced injury via one of its targets, PTEN.
Kazuyuki Shimada - One of the best experts on this subject based on the ideXlab platform.
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Carvedilol stimulates nitric oxide synthesis in rat Cardiac Myocytes.
Journal of molecular and cellular cardiology, 2000Co-Authors: Kenji Kurosaki, Uichi Ikeda, Yoshikazu Maeda, Kazuyuki ShimadaAbstract:Abstract The purpose of this study was to investigate the effects of the β-adrenergic blocker carvedilol on nitric oxide (NO) synthesis in Cardiac Myocytes. We measured the accumulation of nitrite, a stable oxidation product of NO, and the expression of inducible NO synthase (iNOS) protein in cultured neonatal rat Cardiac Myocytes. Incubation of the cultures with interleukin 1 β (IL-1 β; 10 ng/ml) caused a marked increase in nitrite production. Although carvedilol alone showed no effect on nitrite accumulation, it significantly enhanced IL-1 β-induced nitrite production by Cardiac Myocytes. The effect of carvedilol was completely abolished in the presence of aminoguanidine or actinomycin D. The nitrite production enhanced by carvedilol was accompanied by increased iNOS protein expression. Unlike carvedilol, other β-blockers, namely propranolol, atenolol and arotinolol, did not enhance IL-1 β-induced nitrite production. Addition of isoproterenol significantly increased nitrite production by IL-1 β-stimulated Cardiac Myocytes. Atenolol suppressed this isoproterenol-induced nitrite accumulation, while carvedilol further increased the nitrite accumulation. These findings indicate that carvedilol increases NO synthesis in IL-1 β-stimulated rat Cardiac Myocytes by a β-adrenoceptor-independent mechanism.
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alpha adrenergic stimulation enhances inducible nitric oxide synthase expression in rat Cardiac Myocytes
Journal of Molecular and Cellular Cardiology, 1996Co-Authors: Uichi Ikeda, Yoshiaki Murakami, Toshiko Kanbe, Kazuyuki ShimadaAbstract:Abstract We investigated the effects of α 1 -adrenergic stimulation on nitric oxide (NO) production by Cardiac Myocytes. Incubation of cultured neonatal rat Cardiac Myocytes with interleukin-1 β (IL-1 β ) caused a significant increase in the production of nitrite, a stable metabolite of NO. Addition of phenylephrine significantly augmented nitrite production by IL-1 β -stimulated but not by unstimulated Myocytes in a dose-dependent manner. The effect of phenylephrine was completely abolished in the presence of N G -monomethyl-L-arginine (L-NMMA) or actinomycin D. Northern blotting revealed increased inducible NO synthase mRNA accumulation in Cardiac Myocytes treated with IL-1 β and phenylephrine compared with those treated with IL-1 β alone. After protein kinase C activity was functionally depleted by treating cells with phorbol 12-myristate 13-acetate for 24 h, phenylephrine did not augment IL-1 β -induced NO production. The effect of phenylephrine was also abolished in the presence of protein kinase C inhibitor calphostin C. These observations suggest that α 1 -adrenergic stimulation causes an upregulation of cytokine-induced NO production by Cardiac Myocytes, which is mediated at least partially via activation of protein kinase C.
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Nitric oxide synthesis in Cardiac Myocytes and fibroblasts by inflammatory cytokines
Cardiovascular research, 1995Co-Authors: Takayuki Shindo, Uichi Ikeda, Fujio Ohkawa, Yasuhiro Kawahara, Mitsuhiro Yokoyama, Kazuyuki ShimadaAbstract:Objective: The aim was to investigate nitric oxide (NO) synthase activity in cultured neonatal rat Cardiac Myocytes and fibroblasts upon treatment with inflammatory cytokines interleukin 1β (IL-1β), tumour necrosis factor a (TNF-α), IL-2, IL-6, IL-8, transforming growth factor β (TGF-β) and gram negative bacterial lipopolysaccharide (LPS). Methods : NO and guanosine 3′,5′-cyclic monophosphate (cGMP) synthesis was measured in cultured neonatal rat Cardiac Myocytes and fibroblasts, using Griess reagent and an enzyme immunoassay kit, respectively. The expression of inducible NO synthase (iNOS) mRNA and protein was assayed by northern and western blotting, respectively. Results : Incubation of Cardiac Myocytes for 24 h with IL-1β (10 ng·ml−1) or LPS (1 μg·ml−1) caused significant increases in NO and cGMP production. TNF-α, IL-2, IL-6, IL-8, and TGF-β showed no significant effect on their production. IL-1β induced NO and cGMP production in a time and dose dependent manner. IL-β also increased iNOS mRNA and protein accumulation in Cardiac Myocytes. Simultaneous incubation of IL-1β with NG-monomethyl- L -arginine, genistein, calphostin C, cycloheximide, or actinomycin D completely inhibited the IL-1β induced NO production by Cardiac Myocytes. TGF-β, dexamethasone, or cyclosporin A also dose dependently inhibited the IL-1β induced NO production. Exposure to IL-1β for 12–24 h decreased the beating rate of Cardiac Myocytes, but addition of dexamethasone completely overcame this inhibition. In contrast to Cardiac Myocytes, incubation of Cardiac fibroblasts for 24 h with IL-1β or LPS showed no significant effect on NO or cGMP production. Conclusions : These observations suggest that IL-1β/LPS responsive iNOS, which is an important regulator of contractile function of the heart, is present in Cardiac Myocytes but not in Cardiac fibroblasts.
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Nitric oxide synthesis in rat Cardiac Myocytes and fibroblasts.
Life sciences, 1994Co-Authors: Takayuki Shindo, Uichi Ikeda, Fujio Ohkawa, Masafumi Takahashi, Hiroshi Funayama, Masanori Nishinaga, Yasuhiro Kawahara, Mitsuhiro Yokoyama, Tadashi Kasahara, Kazuyuki ShimadaAbstract:Abstract We investigated nitric oxide (NO) synthase activity in cultured neonatal rat Cardiac Myocytes and fibroblasts upon treatment with interleukin 1β (IL-1β) and lipopolysaccharide (LPS). Incubation of Cardiac Myocytes for 24 h with IL-1β or LPS caused a significant increase in NO and cGMP production. Simultaneous incubation of IL-1β with N G -monomethyl-L-arginine or transforming growth factor β (TGF-β) completely inhibited the IL-1β-induced NO and cGMP production in Cardiac Myocytes. In contrast, incubation of Cardiac fibroblasts for 24 h with Il-1β or LPS showed no significant effect on NO or cGMP production. Addition of IL-1gb decreased the beating rate of Cardiac Myocytes, but TGF-β overcame that inhibition. These observations suggest the presence of iNOS in Cardiac Myocytes, which is an important regulator of contractile function of the heart.
Jane Lise Samuel - One of the best experts on this subject based on the ideXlab platform.
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Self-Protection by Cardiac Myocytes Against Hypoxia and Hyperoxia
Circulation research, 1999Co-Authors: Saul Winegrad, Daniel Henrion, Lydie Rappaport, Jane Lise SamuelAbstract:Abstract —Cardiac muscle must maintain a continuous balance between its energy supply and work performed. An important mechanism involved in achievement of this balance is cross talk via chemical signals between Cardiac Myocytes and the Cardiac muscle vascular system . This has been demonstrated by incubating isolated Cardiac Myocytes in different concentrations of oxygen and then assaying the conditioned media for vasoactive substances on isolated aortic rings and small-resistance arteries. With increasing oxygen concentrations above 6%, Cardiac Myocytes produce increasing amounts of angiotensin I, which is converted to angiotensin II by the blood vessel. The angiotensin II stimulates vascular endothelial cells to secrete endothelin and increase vascular tone. Below 6% oxygen, Cardiac Myocytes secrete adenosine, which acts directly on vascular smooth muscle to block the effect of α-adrenergic agonists and reduce vascular tone. In an intact heart, the net effect of these 2 regulatory systems would be the maintenance of oxygen concentration within a narrow range at the Cardiac Myocytes. By acting as oxygen sensors, Cardiac Myocytes modulate vascular tone according to the needs of the Myocytes and reduce potential problems of hypoxia and extensive formation of reactive oxygen species.
Jens R Nyengaard - One of the best experts on this subject based on the ideXlab platform.
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Growth hormone increases the proliferation of existing Cardiac Myocytes and the total number of Cardiac Myocytes in the rat heart
Cardiovascular Research, 2007Co-Authors: Annemarie Brüel, Tue E. H. Christoffersen, Jens R NyengaardAbstract:Objective: Growth hormone (GH) is known to induce growth of the normal rat heart. Whether this growth is due solely to hypertrophy of the Cardiac Myocytes or whether a concomitant hyperplasia of the Cardiac Myocytes also takes place is currently not known. Therefore, the aim of the present study was to investigate whether GH induces hyperplasia in the left ventricle (LV) of sexually mature rats. Methods: Three-month-old female Wistar rats were injected with GH (5 mg/kg/d) for 80 days, whereas a control group was injected with saline. Before perfusion–fixation, haemodynamic measurements were obtained. Isotropic, uniformly random sections were cut from the isolated LV, and the total number of myocyte nuclei and the average number of nuclei per myocyte were estimated using unbiased stereology. Immunohistochemistry was performed in order to detect proliferation (Ki-67), apoptosis (activated caspase-3), and stem cells (c-kit). Results: GH increased the total number of Cardiac Myocytes by 33% [GH: 25.7×10 6 (0.09), controls: 19.3×10 6 (0.14), Pb0.01, (mean (CV)], and this was accompanied by an increase in the percentage of Ki-67 positive Myocytes by 216% [GH: 0.0179% (0.65), controls: 0.0057% (1.43), Pb0.05]. No significant differences were found for caspase-3 positive or c-kit positive Myocytes. GH increased insulin-like growthfactorI(IGF-I)contentofthemyocardialtissueby754%[GH:247ng/gwetweight(0.75),controls:29ng/gwetweight(0.58),Pb0.01] and the LV wet weight by 50% [GH: 849 mg (0.15), controls: 567 mg (0.07), Pb0.001], but did not influence the haemodynamic parameters. Conclusion: These results strongly suggest that GH is able to stimulate Cardiac Myocytes to re-enter the cell cycle, divide, and thereby increase the number of Cardiac Myocytes in sexually mature rats.
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Growth hormone increases the proliferation of existing Cardiac Myocytes and the total number of Cardiac Myocytes in the rat heart
Cardiovascular research, 2007Co-Authors: Annemarie Brüel, Tue E. H. Christoffersen, Jens R NyengaardAbstract:Growth hormone (GH) is known to induce growth of the normal rat heart. Whether this growth is due solely to hypertrophy of the Cardiac Myocytes or whether a concomitant hyperplasia of the Cardiac Myocytes also takes place is currently not known. Therefore, the aim of the present study was to investigate whether GH induces hyperplasia in the left ventricle (LV) of sexually mature rats. Three-month-old female Wistar rats were injected with GH (5 mg/kg/d) for 80 days, whereas a control group was injected with saline. Before perfusion-fixation, haemodynamic measurements were obtained. Isotropic, uniformly random sections were cut from the isolated LV, and the total number of myocyte nuclei and the average number of nuclei per myocyte were estimated using unbiased stereology. Immunohistochemistry was performed in order to detect proliferation (Ki-67), apoptosis (activated caspase-3), and stem cells (c-kit). GH increased the total number of Cardiac Myocytes by 33% [GH: 25.7 x 10(6) (0.09), controls: 19.3 x 10(6) (0.14), P<0.01, (mean (CV)], and this was accompanied by an increase in the percentage of Ki-67 positive Myocytes by 216% [GH: 0.0179% (0.65), controls: 0.0057% (1.43), P<0.05]. No significant differences were found for caspase-3 positive or c-kit positive Myocytes. GH increased insulin-like growth factor I (IGF-I) content of the myocardial tissue by 754% [GH: 247 ng/g wet weight (0.75), controls: 29 ng/g wet weight (0.58), P<0.01] and the LV wet weight by 50% [GH: 849 mg (0.15), controls: 567 mg (0.07), P<0.001], but did not influence the haemodynamic parameters. These results strongly suggest that GH is able to stimulate Cardiac Myocytes to re-enter the cell cycle, divide, and thereby increase the number of Cardiac Myocytes in sexually mature rats.