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首页> 外文期刊>American Journal of Physiology >Role of AT1 and AT2 receptors in regulation of MAPKs and MKP-1 by ANG II in adult cardiac myocytes.
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Role of AT1 and AT2 receptors in regulation of MAPKs and MKP-1 by ANG II in adult cardiac myocytes.

机译：AT1和AT2受体在成年心肌细胞中ANG II调控MAPK和MKP-1中的作用。

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摘要

ANG II has been implicated in the hypertrophic response in ventricular myocytes by acting at the angiotensin type 1 (AT1) receptor. However, the role of the angiotensin type 2 (AT2) receptor in the adult heart is not as clearly understood. In adult rat ventricular myocytes (ARVM) and cardiac microvascular endothelial cells (CMEC), we examined the role of ANG II signaling, via AT1 and AT2 receptors, on the activation of the extracellular signal-regulated protein kinases (ERKs) and on the expression of the mitogen-activated protein kinase (MAPK) phosphatase MKP-1. ANG II caused no detectable increase in ERK activity or in c-fos mRNA abundance in ARVM but increased ERK activity within 5 min in CMEC and increased c-fos mRNA levels. However, in the presence of the selective phosphoprotein phosphatase (PP-2A/PP-1) inhibitor okadaic acid (OA), a sustained increase in ERK activity, as well as in c-jun NH2-terminal protein kinase activity, in ARVM was observed. ANG II increased MKP-1 mRNA levels within 15 min in ARVM and CMEC. In contrast to the response in endothelial cells, however, ANG II activation of MKP-1 in ARVM was mediated by AT2-receptor activation. Thus there is constitutive as well as inducible suppression of ERKs and c-jun NH2-terminal protein kinases by MKP and PP-2A/PP-1 in the adult cardiac myocyte phenotype.
机译：ANG II通过作用于1型血管紧张素（AT1）受体而参与了心室肌细胞的肥大反应。然而，尚不清楚血管紧张素2型（AT2）受体在成年心脏中的作用。在成年大鼠心室肌细胞（ARVM）和心脏微血管内皮细胞（CMEC）中，我们研究了ANG II信号通过AT1和AT2受体在细胞外信号调节蛋白激酶（ERKs）激活和表达上的作用丝裂原活化蛋白激酶（MAPK）磷酸酶MKP-1的表达。 ANG II在ARVM中未导致ERK活性或c-fos mRNA丰度的可检测增加，但在CMEC中在5分钟内增加了ERK活性，并增加了c-fos mRNA的水平。但是，在存在选择性磷蛋白磷酸酶（PP-2A / PP-1）抑制剂冈田酸（OA）的情况下，ARVM中ERK活性以及c-jun NH2末端蛋白激酶活性的持续增加是观测到的。 ANG II在15分钟内在ARVM和CMEC中增加了MKP-1 mRNA水平。然而，与内皮细胞的应答相反，ARVM中MKP-1的ANG II激活是由AT2-受体激活介导的。因此，在成年心肌细胞表型中，MKP和PP-2A / PP-1对ERK和c-jun NH2末端蛋白激酶具有组成性和诱导性抑制作用。

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