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间隙连接通讯介导转化生长因子-β激活及内皮细胞诱导的壁细胞分化。

Gap junction communication mediates transforming growth factor-beta activation and endothelial-induced mural cell differentiation.

作者信息

Hirschi Karen K, Burt Janis M, Hirschi Kendal D, Dai Cuiping

机构信息

Department of Pediatrics, Children's Nutrition Research Center, Baylor College of Medicine, Houston, TX 77030, USA.

出版信息

Circ Res. 2003 Sep 5;93(5):429-37. doi: 10.1161/01.RES.0000091259.84556.D5. Epub 2003 Aug 14.

DOI:10.1161/01.RES.0000091259.84556.D5
PMID:12919949
Abstract

During blood vessel assembly, endothelial cells recruit mesenchymal progenitors and induce their differentiation into mural cells via contact-dependent transforming growth factor-beta (TGF-beta) activation. We investigated whether gap junction channels are formed between endothelial cells and recruited mesenchymal progenitors and whether intercellular communication is necessary for endothelial-induced mural cell differentiation. Mesenchymal progenitors from Cx43-/- murine embryos and Cx43+/+ littermates were cocultured with prelabeled endothelial cells. Intracellular dye injection and dual whole-cell voltage clamp revealed that endothelial cells formed gap junction channels with Cx43+/+ but not Cx43-/- progenitors. In coculture with endothelial cells, Cx43-/- progenitors did not undergo mural cell differentiation as did Cx43+/+ cells. Stable reexpression of Cx43 in Cx43-/- cells (reCx43) restored their ability to form gap junctions with endothelial cells and undergo endothelial-induced mural cell differentiation. Cocultures of endothelial cells and either Cx43+/+ or reCx43 mesenchymal cells produced activated TGF-beta; endothelial-Cx43-/- cocultures did not. However, Cx43-/- cells did produce latent TGF-beta and undergo mural cell differentiation in response to exogenous TGF-beta1. These studies indicate that gap junction communication between endothelial and mesenchymal cells mediates TGF-beta activation and subsequent mural cell differentiation.

摘要

在血管组装过程中，内皮细胞招募间充质祖细胞，并通过接触依赖性转化生长因子-β（TGF-β）激活诱导它们分化为壁细胞。我们研究了内皮细胞与招募的间充质祖细胞之间是否形成间隙连接通道，以及细胞间通讯对于内皮诱导的壁细胞分化是否必要。将来自Cx43-/-小鼠胚胎和Cx43+/+同窝小鼠的间充质祖细胞与预先标记的内皮细胞共培养。细胞内染料注射和双全细胞膜片钳显示，内皮细胞与Cx43+/+祖细胞形成间隙连接通道，但不与Cx43-/-祖细胞形成。与内皮细胞共培养时，Cx43-/-祖细胞不像Cx43+/+细胞那样经历壁细胞分化。Cx43-/-细胞中Cx43的稳定重新表达（reCx43）恢复了它们与内皮细胞形成间隙连接以及经历内皮诱导的壁细胞分化的能力。内皮细胞与Cx43+/+或reCx43间充质细胞的共培养产生了活化的TGF-β；内皮细胞与Cx43-/-细胞的共培养则没有。然而，Cx43-/-细胞确实产生了潜伏性TGF-β，并在外源性TGF-β1作用下经历壁细胞分化。这些研究表明，内皮细胞与间充质细胞之间的间隙连接通讯介导了TGF-β激活及随后的壁细胞分化。

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