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通过内皮细胞中纤维连接蛋白的表达来抵消 Tenascin-C 的抗黏附作用。

Counterbalancing anti-adhesive effects of Tenascin-C through fibronectin expression in endothelial cells.

机构信息

Université Côte d'Azur, CNRS, INSERM, iBV, France.

Centre Antoine Lacassagne, Nice, 06189, France.

出版信息

Sci Rep. 2017 Oct 6;7(1):12762. doi: 10.1038/s41598-017-13008-9.

Abstract

Cellular fibronectin (FN) and tenascin-C (TNC) are prominent development- and disease-associated matrix components with pro- and anti-adhesive activity, respectively. Whereas both are present in the tumour vasculature, their functional interplay on vascular endothelial cells remains unclear. We have previously shown that basally-oriented deposition of a FN matrix restricts motility and promotes junctional stability in cultured endothelial cells and that this effect is tightly coupled to expression of FN. Here we report that TNC induces FN expression in endothelial cells. This effect counteracts the potent anti-adhesive activity of TNC and leads to the assembly of a dense highly-branched subendothelial matrix that enhances tubulogenic activity. These findings suggest that pro-angiogenic remodelling of the perivascular matrix may involve TNC-induced upregulation of FN in endothelial cells.

摘要

细胞纤维连接蛋白 (FN) 和 tenascin-C (TNC) 是与发育和疾病相关的主要基质成分,分别具有促进和抑制黏附的活性。尽管两者都存在于肿瘤血管中,但它们在血管内皮细胞上的功能相互作用尚不清楚。我们之前的研究表明,FN 基质的基底定向沉积限制了培养的内皮细胞的迁移并促进了细胞连接的稳定性,并且这种效应与 FN 的表达紧密相关。在这里,我们报告 TNC 可诱导内皮细胞中 FN 的表达。这种作用抵消了 TNC 的强烈抗黏附活性,并导致密集的高度分支的基底膜的组装,从而增强了管状形成活性。这些发现表明,血管周围基质的促血管生成重塑可能涉及内皮细胞中 TNC 诱导的 FN 上调。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1093/5630602/89a4b1a106d0/41598_2017_13008_Fig1_HTML.jpg

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