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内皮祖细胞(EPC)与内皮细胞的间隙连接相互作用可在体外诱导血管生成网络形成。

Gap Junctional Interaction of Endothelial Progenitor Cells (EPC) with Endothelial Cells Induces Angiogenic Network Formation In Vitro.

作者信息

Buchberger Christina, Kameritsch Petra, Mannell Hanna, Beck Heike, Pohl Ulrich, Pogoda Kristin

机构信息

Physiology, Institute of Theoretical Medicine, Faculty of Medicine, University of Augsburg, 86159 Augsburg, Germany.

Walter Brendel Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-University, 81377 Munich, Germany.

出版信息

Int J Mol Sci. 2025 May 18;26(10):4827. doi: 10.3390/ijms26104827.

Abstract

Endothelial progenitor cells (EPC) are considered to support neovascularization and endothelial repair by being incorporated into newly formed or injured vessels and by improving vascularization in a paracrine manner by secreting proangiogenic factors. Here, we studied the role of gap junctional communication between EPC and endothelial cells in long-term co-cultures in vitro. The cultivation of endothelial cells together with mouse embryonic EPC (E 7.5) induced the spontaneous formation of angiogenic networks after 3-6 days consisting of both cell types, but not in the respective monocultures, whereas their respective cultivation on a basement matrix induced the formation of tube-like structures, as expected. The angiogenic network formation could not be mimicked by the incubation of endothelial cells with supernatants of EPC only. We therefore hypothesized that direct interaction and cell-cell communication is required to induce the angiogenic network formation in co-cultures with endothelial cells. Expression analysis demonstrated expression of the gap junctional protein connexin 43 (Cx43) in EPC. Moreover, dye injection studies as well as FACS analysis identified gap junctional communication between endothelial cells and EPC. The inhibition of gap junctions by pharmacological blockers significantly reduced the angiogenic network formation, confirming that gap junctional communication between both cell types is required for this process.

摘要

内皮祖细胞(EPC)被认为可通过整合到新形成或受损的血管中,并通过分泌促血管生成因子以旁分泌方式改善血管生成,从而支持新血管形成和内皮修复。在此,我们研究了体外长期共培养中EPC与内皮细胞之间缝隙连接通讯的作用。内皮细胞与小鼠胚胎EPC(E 7.5)共同培养3 - 6天后,诱导了由两种细胞类型组成的血管生成网络的自发形成,但在各自的单培养中未出现,而它们在基底基质上各自培养时,如预期那样诱导了管状结构的形成。仅用EPC的上清液孵育内皮细胞无法模拟血管生成网络的形成。因此,我们推测在与内皮细胞的共培养中,诱导血管生成网络形成需要直接相互作用和细胞间通讯。表达分析表明EPC中存在缝隙连接蛋白连接蛋白43(Cx43)的表达。此外,染料注射研究以及流式细胞术分析确定了内皮细胞与EPC之间存在缝隙连接通讯。用药物阻滞剂抑制缝隙连接显著减少了血管生成网络的形成,证实了这一过程需要两种细胞类型之间的缝隙连接通讯。

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