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Changes of c-fos and c-jun mRNA Expression in Angiotensin Ⅱ-induced Cardiomyocyte Hypertrophy and Effects of Sodium Tanshinone ⅡA Sulfonate 被引量:9
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作者 周代星 梁黔生 +1 位作者 何雪心 占成业 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2008年第5期531-534,共4页
The changes of proto-oncogene c-fos and c-jun mRNA expression in angiotensin Ⅱ (AngⅡ)-induced hypertrophy and effects of sodium tanshinone ⅡA sulfonate (STS) in the primary culture of neonatal rat cardiomyocyte... The changes of proto-oncogene c-fos and c-jun mRNA expression in angiotensin Ⅱ (AngⅡ)-induced hypertrophy and effects of sodium tanshinone ⅡA sulfonate (STS) in the primary culture of neonatal rat cardiomyocytes were investigated. Twelve neonatal clean grade Wistar rats were selected. The cardiomyocytes were isolated, cultured and divided according to different treatments in the medium. The cardiomyocyte size was determined by phase contrast microscope, and the rate of protein synthesis was measured by [3H]-Leucine incorporation. The c-fos and c-jun mRNA expression in cardiomyocytes was detected by reverse transcription polymerase chain reaction (RT-PCR). It was found after cardiomyocytes were treated with AngⅡ for 30 min, the c-fos and c-jun mRNA expression in cardiomyocytes was increased significantly (P〈0.01). After treatment with AngⅡ for 24 h, the rate of protein synthesis in AngⅡ group was significantly increased as compared with control group (P〈0.01). After treatment with AngⅡ for 7 days, the size of cardiomyocytes in AngⅡ group was increased obviously as compared with control group (P〈0.05). After pretreatment with STS or Valsartan before AngⅡ treatment, both of them could inhibit the above effects of AngⅡ (P〈0.05 or P〈0.01). It was suggested that STS could ameliorate AngⅡ-induced cardiomyocyte hy- pertrophy by inhibiting c-fos and c-jun mRNA expression and reducing protein synthesis rate of cardiomyocytes. 展开更多
关键词 sodium tanshinone A sulfonate angiotensin cardiomyocyte hypertrophy C-LOS C-JUN
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Effects of Cyclosporine A on Angiotensin Ⅱ-induced Cardiomyocyte Hypertrophy in Neonatal Rats
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作者 韩召敏 杨运海 +1 位作者 张凯伦 向继洲 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2005年第5期558-560,共3页
Summary: The effects of cyclosporine A (CsA) on Angiontensin Ⅱ (Ang Ⅱ )-induced protein contents, c los protein levels and cytosolic Ca^2+ level ([Ca^2+]i) in cultured eardiomyocytes of neonatal rats were o... Summary: The effects of cyclosporine A (CsA) on Angiontensin Ⅱ (Ang Ⅱ )-induced protein contents, c los protein levels and cytosolic Ca^2+ level ([Ca^2+]i) in cultured eardiomyocytes of neonatal rats were observed. Total protein contents were determined by Bradford method. The expression of c-fos protein was detected by Western blot. ([Ca^2+]i) labeled with fluorescent probe Fluo-3/AM was measured under a laser scanning confoeal microscope. The results revealed that as compared with control, the total protein contents were increased in cardiomyocytes treated with Ang Ⅱ (10-1 mol/ L), which could be inhibited by CsA in a dose-dependent manner. It was found that Ang Ⅱ could increase the c-los protein expression, which could be inhibited by CsA in a dose-dependent manner. Ang Ⅱ induced the [Ca^2+]i elevation in cardiomyocytes. CsA did not influence the resting intracellular Ca^2+ , but inhibited significantly the Ang Ⅱ-induced [Ca^2+]i elevation. It was concluded that CsA can suppress the Ang Ⅱ-induced c-fos protein expression and [Ca^2+]i elevation in single cardiomyocyte, which might play a role in the prevention of Ang Ⅱ-induced cardiomyocyte hypertrophy by CsA. 展开更多
关键词 cardiomyocyte hypertrophy angiotensin cyclosporine A C-FOS Ca2+
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Regulation of the EGFR pathway by visfatin and its effect on cardiac hypertrophy
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作者 Liang Chang Lu Xu +2 位作者 Yan Jia Su-Yun Liu Yong-Jun Li 《Journal of Hainan Medical University》 2021年第3期7-11,共5页
Objective:To investigate the regulation of the epidermal growth factor receptor(EGFR)pathway by visfatin and its effect on cardiac hypertrophy.Methods:60 Wistar male rats were randomly divided into control group,visfa... Objective:To investigate the regulation of the epidermal growth factor receptor(EGFR)pathway by visfatin and its effect on cardiac hypertrophy.Methods:60 Wistar male rats were randomly divided into control group,visfatin group and visfatin+AG1478 group,with 20 rats in each group.The cardiac mass index,left ventricular mass index and cardiomyocyte volume of rats in each group were calculated.The total protein content of each group of cardiomyocytes was detected by coomassie bright blue staining,and the protein expression was detected by Western blotting.Results:Compared with the control group,the cardiac mass index,left ventricular mass index,cardiomyocyte volume,protein content,and relative expressions of ANP and BNP were significantly increased in the visfatin group(P<0.05).The relative expression levels of EGFR,p-AKT,p-ERK1/2,p-STAT3,ANP and BNP in cardiac myocytes in the visfatin group were significantly higher than those in the control group and the visfatin+AG1478 group(P<0.05).Conclusion:Visfatin induces hypertrophy in cardiomyocytes by activating the EGFR signaling pathway. 展开更多
关键词 VISFATIN Epidermal growth factor receptor signaling pathway Cardiomyocyte hypertrophy Extracellular signaling kinase Signal transduction and transcription activator 3 Serine threonine kinase
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Effects of Angiotensin II on Expression of the Gap Junction Channel Protein Connexin 43 in Neonatal Rat Ventricular Myocytes
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作者 Jun Yang Wei Wu 《South China Journal of Cardiology》 CAS 2007年第4期206-211,共6页
Objectives To study the effects of angiotensin Ⅱ, as a mediator of cardiac hypertrophy, on expression of connexin 43 (Cx43) in cultured neonatal rat ventricular myocytes and correlation of expression of Cx43 and ca... Objectives To study the effects of angiotensin Ⅱ, as a mediator of cardiac hypertrophy, on expression of connexin 43 (Cx43) in cultured neonatal rat ventricular myocytes and correlation of expression of Cx43 and cardiomyocyte hypertrophy. Methods Cardiomyocytes were isolated from newborn SD rats. Angiotensin Ⅱwas added into the media to induce myocyte hypertrophy. Cultures were exposed to 10 ~ 6 mol/L angiotensin Ⅱ for 72 h, Cx43 expression was characterized by RT-PCR and Immunofluorescence methods. Results Immunofluorescence analysis revealed decreased Cx43 immunoreactivity in cells treated for 72 h with angiotensin Ⅱ. RT-PCR analysis demonstrated there was an obvious decrease of Cx43 mRNA level in cells exposed to angiotensin U for 72 h. The changes of expression of connexin 43 were related to its entrance into S phase of the cell cycle. Cultured neonatal rat cardiomyocytes were exposed for 72 h to increase concentrations of angiotensin II ( 1.0 × 10^ -9 ~ 1.0 × 10^ -6mol/L), resulting in significantly decreased Cx43 expression. Conclusions Angiotensin/I leads to a concentration-dependent decrease in Cx43 protein in cultured neonatal rat ventricular myocytes by decreasing Cx43 mRNA synthesis. Signal transduction pathways activated by angiotensin II under pathophysiologic conditions of cardiac hypertrophy could initiate remodeling of gap junctions. 展开更多
关键词 angiotensin cardiomyocyte hypertrophy connexin 43 gap junction
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