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[关于培养的内皮细胞和平滑肌细胞之间缝隙连接形成及连接通讯的研究]

[Studies on gap junction formation and junctional communication between cultured endothelial cells and smooth muscle cells].

作者信息

Zhang R, Lou D A

机构信息

Department of Pathology, Zhejiang Medical University.

出版信息

Shi Yan Sheng Wu Xue Bao. 1993 Jun;26(2):119-25.

PMID:8237221
Abstract

Gap junction (GJ) between two contacted cells is the structural basis of intercellular communication. Gap junction transfer plays an important role in regulation of cell proliferation. Cultured endothelial cells (EC) and smooth muscle cells (SMC) were injected with fluorescein Lucifer Yellow by iontophoretic injection, and examined under fluorescein microscope. We have demonstrated that there existed homologous and heterologous GJ and contact mediated dye transfer between cultured EC and SMC. LDL and insulin which promote SMC proliferation may inhibit the junctional communication between SMC and EC. Tumor promoter TPA induced almost complete inhibition of junctional communication between EC and SMC. The results indicate that normally regulative signals of metabolism and growth are transferred between EC and SMC via junctional communication to maintain the vessel wall homeostasis. High dosage LDL and insulin may keep SMC away from normal growth control and induce their proliferation by means of inhibiting junctional communication. It may be one of important mechanisms of atherogenesis.

摘要

两个相邻细胞间的间隙连接(GJ)是细胞间通讯的结构基础。间隙连接传递在细胞增殖调控中起重要作用。通过离子电渗注射法将荧光素异硫氰酸荧光素注入培养的内皮细胞(EC)和平滑肌细胞(SMC),并在荧光显微镜下观察。我们已经证明,培养的EC和SMC之间存在同源和异源GJ以及接触介导的染料传递。促进SMC增殖的低密度脂蛋白(LDL)和胰岛素可能会抑制SMC与EC之间的连接通讯。肿瘤启动子佛波酯(TPA)几乎完全抑制了EC和SMC之间的连接通讯。结果表明,正常情况下,代谢和生长的调节信号通过连接通讯在EC和SMC之间传递,以维持血管壁的稳态。高剂量的LDL和胰岛素可能使SMC脱离正常生长控制,并通过抑制连接通讯诱导其增殖。这可能是动脉粥样硬化发生的重要机制之一。

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