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The roles of integrin β 4 in Vascular Endothelial Cells
Author(s) -
Wang Li,
Dong ZhiWu,
Zhang Yun,
Miao JunYing
Publication year - 2012
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22769
Subject(s) - integrin , microbiology and biotechnology , biology , angiogenesis , cell adhesion , signal transduction , endothelial stem cell , cancer cell , cd49c , integrin, beta 6 , cancer research , cell , cancer , genetics , in vitro
Integrin heterodimers play diverse and important roles in physiological and pathological processes, such as cell adhesion, migration, proliferation, differentiation, angiogenesis, and tumor progression, via the outside‐in and/or inside‐out signaling pathways. Aberrant functions of integrins have been implicated in the causation and intervention of multiple diseases. Integrin β 4 , a laminin‐5 (LN5) receptor, mainly locates in the adhesion structure of hemidesmosome (HD). Most of the previous researches concentrated on the role of integrin β 4 in cancer and cancer therapy, and a few focused on the physiological roles of normal mammalian cells. Recently, accumulating data reveal that integrin β 4 participates in cell death, macroautophagy (hereafter autophagy), senescence, and differentiation regulations in various cell types including human umbilical vein endothelial cells (HUVECs), mesenchymal stem cells, and mouse neural cells, implying the key roles of integrin β 4 in the physiological alteration of mammalian cells. Thus, the elucidation of integrin β 4 ‐mediated signaling may undoubtedly contribute to novel therapeutic strategies for various human diseases, such as vascular and neural disorders. We have reviewed the roles of integrin β 4 in neural cells. In the present review we will discuss the recent research progress in the inherent functions and pharmacological modulation of integrin β 4 in vascular endothelial cells. J. Cell. Physiol. 227: 474–478, 2012. © 2011 Wiley Periodicals, Inc.