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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Cardiomyocyte hypertrophy and degradation of connexin43 through spatially restricted autocrine/paracrine heparin-binding EGf
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Cardiomyocyte hypertrophy and degradation of connexin43 through spatially restricted autocrine/paracrine heparin-binding EGf

机译：心肌细胞肥大和连接蛋白43通过空间受限的自分泌/旁分泌肝素结合EGf的降解

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摘要

Growth factor signaling can affect tissue remodeling through autocrine/paracrine mechanisms. Recent evidence indicates that EGF receptor transactivation by heparin-binding EGF (HB-EGF) contributes to hypertrophic signaling in cardiomyocytes. Here, we show that HB-EGF operates in a spatially restricted circuit in the extracellular space within the myocardium, revealing the critical nature of the local microenvironment in intercellular signaling. This highly localized microenvironment of HB-EGF signaling was demonstrated with 3D morphology, consistent with predictions from a computational model of EGF signaling. HB-EGF secretion by a given cardiomyocyte in mouse left ventricles led to cellular hypertrophy and reduced expression of connexin43 in the overexpressing cell and in immediately adjacent cells but not in cells farther away. Thus, HB-EGF acts as an autocrine and local paracrine cardiac growth factor that leads to loss of gap junction proteins within a spatially confined microenvironment. These findings demonstrate how cells can coordinate remodeling with their immediate neighboring cells with highly localized extracellular EGF signaling.
机译：生长因子信号传导可通过自分泌/旁分泌机制影响组织重塑。最近的证据表明，肝素结合型EGF（HB-EGF）的EGF受体反式激活有助于心肌细胞中的肥大信号传导。在这里，我们显示HB-EGF在心肌细胞外空间的空间受限回路中运作，揭示了细胞间信号传导中局部微环境的关键性质。 HB-EGF信号这种高度局部化的微环境已通过3D形态学证明，与EGF信号计算模型的预测相符。给定心肌细胞在小鼠左心室中的HB-EGF分泌导致细胞肥大，并降低了过表达细胞和紧邻细胞中而非邻近细胞中connexin43的表达。因此，HB-EGF充当自分泌和局部旁分泌心脏生长因子，导致空间受限的微环境中间隙连接蛋白的丢失。这些发现证明细胞如何通过高度定位的细胞外EGF信号传导与其附近的细胞进行重塑。

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