细胞黏附分子调控干细胞衰老机制的概述

Regulation and mechanism of cell adhesion molecules in stem cell senescence

作为具有自我更新和多向分化潜能的细胞,干细胞具有组织修复能力,对于维持组织稳态至关重要。然而,与体细胞一样,干细胞也会发生细胞衰老和死亡,干细胞的衰老会影响机体整体的衰老。因此,深入研究干细胞衰老的分子机制有助于实现对衰老干细胞乃至衰老机体的有效干预。影响干细胞衰老的因素有很多,如miRNAs、DNA损伤、细胞极性丧失、端粒缩短以及表观遗传调控等。胞间通讯与干细胞衰老密切相关。存在于干细胞生态位中的细胞黏附分子可以介导干细胞与其他细胞或者基质蛋白之间的相互作用,对于维持干细胞生态位及调节干细胞衰老有重要作用。本文综述了不同的细胞黏附分子家族:整合素家族、免疫球蛋白超家族、选择素家族以及钙黏蛋白家族对各类成体干细胞衰老的影响,总结了干细胞衰老过程中细胞外基质的改变与功能,并对黏附分子调控干细胞衰老机制的研究及应用进行了展望。本文旨在从胞间通讯角度为进一步探究干细胞衰老新机制及开发抗干细胞衰老策略提供新的方向。

Stem cells have the ability of self-renewal and multi-directional differentiation potential,which play a vital role in tissue repair and homeostasis.Whereas,similar to somatic cells,stem cells suffer from cell senescence and death over time.The senescence of stem cells will further affect the overall aging of the whole body.Therefore,in-depth study of the molecular mechanism of stem cell senescence is helpful to develop effective therapeutic intervention in senescent stem cells and even the aging body.A plenty of factors have been demonstrated to affect stem cell senescence,such as miRNAs,DNA damage,loss of cell polarity,telomere shortening,and epigenetic regulation.Recently,increasing evidences show that intercellular communication is related to stem cell senescence.Cell adhesion molecules in the stem cell niche can mediate the interaction between stem cells and other cells or matrix proteins,which play an important role in maintaining stem cell niche and regulating stem cell senescence.In this paper,we have reviewed the effects of different cell adhesion molecule families(including integrin,immunoglobulin superfamily,selectin and cadherin)on the senescence of various adult stem cells,and summarized the changes and functions of extracellular matrix during stem cell senescence.We further prospect the research on the mechanism of adhesion molecules in regulating stem cell senescence and its future application.This review sheds light on exploring the new mechanism of stem cell senescence and developing anti-stem cell senescence strategies from the perspective of intercellular communication.