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首页> 外文期刊>American Journal of Physiology >Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, avp3-integrin, and TGF-beta1 in response to ANG II and high glucose
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Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, avp3-integrin, and TGF-beta1 in response to ANG II and high glucose

机译:微血管维管平滑肌细胞通过ERK1 / 2 MAP激酶,avp3-整联蛋白和TGF-beta1响应ANG II和高血糖而促进I型胶原沉积

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摘要

This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta_3-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from Type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. Isolated MRA were subjected to a pressure-passive-diameter relationship. To delineate cell types and mechanisms, cultured VSMC were prepared from MRA and stimulated with ANG II (100 nM) and high glucose (HG, 22 mM).
机译:这项研究确定血管平滑肌细胞(VSMC)通过细胞外信号调节激酶(ERK)1 / 2-促丝裂原激活蛋白(MAP)激酶,αvbeta_3-整联蛋白和转化生长因子(TGF)-beta1的信号决定了胶原类型我在1型糖尿病(链脲佐菌素)或高血压(HT; ANG II)小鼠的肠系膜阻力动脉(MRA)中进行网络诱导。隔离的MRA处于压力-被动-直径关系。为了描述细胞类型和机制,从MRA制备培养的VSMC,并用ANG II(100 nM)和高葡萄糖(HG,22 mM)刺激。

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