p42/p44 mitogen-activated protein kinases inhibit atrial natriuretic peptide mRNA transcription in gp130-mediated hypertrophic ventricular myocytes.
p42/p44 mitogen-activated protein kinases inhibit atrial natriuretic peptide mRNA transcription in gp130-mediated hypertrophic ventricular myocytes.
复制标题
p42/p44 丝裂原激活蛋白激酶抑制 gp130 介导的肥厚心室肌细胞中心房钠尿肽 mRNA 转录。
DOI：
10.1016/s1995-7645(14)60024-9
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发表时间：
2014
影响因子：
3.1
通讯作者：
S. Fu
中科院分区：
文献类型：
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作者：
Zhan;Yang Wang;Tian;S. Zheng;Yueqiong Kong;Youling Lan;Jun;S. Fu
目的了解anpmrna转录调控在gp130介导的心肌细胞肥大中的作用，以及所涉及的丝裂原活化蛋白激酶(MEK)-细胞外信号调节激酶（ERK，又称p42/p44 MAPK）信号通路。方法用不同浓度的CT-1（10−9、10−8和10−7mol/L）处理新生儿心室肌细胞。MTT法检测心肌细胞活力，RT-PCR法检测心肌细胞tanpmrna水平。为了抑制肥厚性心肌细胞中p42/p44 MAPK的活性，用一种特异性的MEK1抑制剂对细胞进行预处理。结果sct -1显著诱导心肌细胞anpmrna表达，并呈剂量依赖性和时间依赖性。此外，通过特殊的MEK1抑制剂阻断p42/p44 MAPK活性可上调anpmrna。结论在gp130介导的肥厚性心室肌细胞中，sp42/p44 MAPK在抑制anpmrna转录和细胞活性中起重要作用。
ObjectiveTo understand the role ofANPmRNA transcription regulation in gp130-mediated cardiomyocyte hypertrophy, and the involved mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK, also called p42/p44 MAPK) signaling pathway.MethodsIsolated neonatal ventricular myocytes were treated with different concentrations of CT-1 (10−9, 10−8and 10−7mol/L). MTT was used to analyze the viability and RT-PCR was used to detectANPmRNA levels in cardiomyocyte. To inhibit p42/p44 MAPK activity in hypertrophic cardiomyocytes, the cells were pretreated with a specific MEK1 inhibitor.ResultsCT-1 significantly inducedANPmRNA expression and the viability of cardiomyocytes in a dose- and time-dependent manner. Furthermore, blocking p42/p44 MAPK activity by the special MEK1 inhibitor upregulated theANPmRNA.Conclusionsp42/p44 MAPK have an important role in suppressingANPmRNA transcription and cell activity in gp130-mediated hypertrophic ventricular myocytes.
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作者：
Biochemistr;Biochemistr And Biochemistry;Athanassios Vassilopoulos;C. Gaitanaki;P. Papazafiri;I. Beis
通讯作者：
Biochemistr;Biochemistr And Biochemistry;Athanassios Vassilopoulos;C. Gaitanaki;P. Papazafiri;I. Beis
G.Takemura 等人：“心房钠尿肽的心室表达及其与扩张的人心脏中的血流动力学和组织学的关系：心内膜心肌活检标本的免疫组织化学研究”循环。
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