Endothelial injury induces vascular smooth muscle cell proliferation in highly localized regions of a direct contact co-culture system.

Endothelial injury induces vascular smooth muscle cell proliferation in highly localized regions of a direct contact co-culture system.
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DOI:
10.1007/s12013-008-9023-6
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发表时间:
2008
影响因子:
2.6
通讯作者:
Wong, Joyce Y.
Wong, Joyce Y.
中科院分区:
生物学4区
文献类型:
--
作者:
Jacot, Jeffrey G.;Wong, Joyce Y.

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虽然先前的研究表明,在共培养中内皮细胞和血管平滑肌细胞(VSMCs)的增殖之间存在关系,但结果是相互矛盾的,信号机制也鲜为人知。在这项跨膜共培养研究中,血管平滑肌细胞和内皮细胞在微孔膜的两侧融合生长,以模拟血管的内膜/中膜边界。损伤内皮层,培养3天,部分再内皮化。损伤/部分恢复内皮区的VSMC增殖明显高于去内皮化区(增加7倍)和未损伤区(增加3倍)。ELISA法显示,在未损伤的共培养细胞和同型对照中未检测到的PDGF在损伤后增加,加入哌嗪基喹唑啉羧胺PDGF受体抑制剂可阻断损伤/部分恢复区域的VSMC增殖。结论:内皮细胞损伤引起的共培养信号局部刺激VSMC增殖,此信号转导可能由PDGF-BB介导。
Though previous studies have indicated a relationship between the proliferation of endothelial cells and vascular smooth muscle cells (VSMCs) in co-culture, the results have been contradictory and the signaling mechanism poorly understood. In this transmembrane co-culture study, VSMCs and endothelial cells were grown to confluence on opposite sides of a microporous membrane to mimic the intima/media border of vessels. The endothelial layer was injured, and then cultured for three days, resulting in partial re-endothelialization. VSMC proliferation across from the injured/partially recovered endothelial region was significantly higher than across from the de-endothelialized region (a 7-fold increase) and the uninjured region (a 3-fold increase). ELISA indicated that PDGF, which was undetectable in uninjured co-culture and homotypic controls, increased after injury and the addition of a piperazinylquinazoline carboxamide PDGF receptor inhibitor blocked VSMC proliferation across from the injured/partially recovered region. We conclude that co-culture signaling initiated by endothelial cell injury locally stimulates VSMC proliferation and that this signaling could be mediated by PDGF-BB.
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