Role and impact of the extracellular matrix on integrin-mediated pancreatic β-cell functions

被引:37
作者
Arous, Caroline [1 ]
Wehrle-Haller, Bernhard [1 ]
机构
[1] Univ Geneva, Med Ctr, Dept Cell Physiol & Metab, Geneva, Switzerland
关键词
Actin; Cell adhesion; Extracellular matrix; Peptide hormones/insulin; Secretion; STIMULATED INSULIN-SECRETION; TYPE-2; DIABETES-MELLITUS; ISLET BASEMENT-MEMBRANE; GROWTH-FACTOR-BETA; FOCAL-ADHESION; GENE-EXPRESSION; MOUSE ISLETS; HIGH GLUCOSE; IN-VITRO; SIGNALING PATHWAYS;
D O I
10.1111/boc.201600076
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Understanding the organisation and role of the extracellular matrix (ECM) in islets of Langerhans is critical for maintaining pancreatic beta-cells, and to recognise and revert the physiopathology of diabetes. Indeed, integrin-mediated adhesion signalling in response to the pancreatic ECM plays crucial roles in beta-cell survival and insulin secretion, two major functions, which are affected in diabetes. Here, we would like to present an update on the major components of the pancreatic ECM, their role during integrin-mediated cell-matrix adhesions and how they are affected during diabetes. To treat diabetes, a promising approach consists in replacing beta-cells by transplantation. However, efficiency is low, because beta-cells suffer of anoikis, due to enzymatic digestion of the pancreatic ECM, which affects the survival of insulin-secreting beta-cells. The strategy of adding ECM components during transplantation, to reproduce the pancreatic microenvironment, is a challenging task, as many of the regulatory mechanisms that control ECM deposition and turnover are not sufficiently understood. A better comprehension of the impact of the ECM on the adhesion and integrin-dependent signalling in beta-cells is primordial to improve the healthy state of islets to prevent the onset of diabetes as well as for enhancing the efficiency of the islet transplantation therapy.
引用
收藏
页码:223 / 237
页数:15
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