Interleukin-1β induces intercellular adhesion molecule-1 expression, thus enhancing the adhesion between mesenchymal stem cells and endothelial progenitor cells via the p38 MAPK signaling pathway

白细胞介素-1β诱导细胞间黏附分子-1的表达,从而通过p38 MAPK信号通路增强间充质干细胞和内皮祖细胞之间的黏附。

阅读:7
作者:Jun Guo ,Hongwei Zhang ,Jie Xia ,Jixue Hou ,Yixiao Wang ,Tao Yang ,Sibo Wang ,Xuyong Zhang ,Xuelin Chen ,Xiangwei Wu

Abstract

Endothelial progenitor cells (EPCs) are an important component of stem-cell niches, which are able to promote the self-renewal and pluripotency of mesenchymal stem cells (MSCs). The biological functions of these two cell types is dependent on adhesion, and the adhesion between MSCs and EPCs is important due to their critical role in neovascularization and bone regeneration in tissue engineering. Intercellular adhesion molecule-1 (ICAM-1, also known as cluster of differentiation 54), is a member of the immunoglobulin supergene family, which functions in cell-cell and cell-matrix adhesive interactions. Compared with other adhesion molecules, ICAM-1 is expressed in hematopoietic and nonhematopoietic cells, and can mediate adhesive interactions. The present study aimed to investigate the importance of ICAM-1 in the adhesion of MSCs and EPCs, and demonstrated that adhesion between these cells could be regulated by interleukin (IL)-1β via the p38 mitogen‑activated protein kinase pathway. In addition, the results confirmed that ICAM-1 served a critical role in regulation of adhesion between MSCs and EPCs. ELISA, cell immunofluorescence, western blot analysis and adhesion assay were used to confirm our theory from phenomenon to essence. The present study provided evidence to support and explain the adhesion between MSCs and EPCs. Furthermore, the present findings provide a theoretical basis for further stem‑cell niche transplantation to increase understanding of the function of MSCs and the crosstalk between MSCs and EPCs in the stem-cell niche.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。