Microtubule-associated deacetylase HDAC6 promotes angiogenesis by regulating cell migration in an EB1-dependent manner.
10.1007/s13238-011-1015-4
- Author:
Dengwen LI
1
;
Songbo XIE
;
Yuan REN
;
Lihong HUO
;
Jinmin GAO
;
Dandan CUI
;
Min LIU
;
Jun ZHOU
Author Information
1. Department of Genetics and Cell Biology, Tianjin Key Laboratory of Protein Science, College of Life Sciences, Nankai University, Tianjin 300071, China.
- Publication Type:Journal Article
- MeSH:
Anilides;
pharmacology;
Animals;
Cell Movement;
Cell Polarity;
Cells, Cultured;
Chick Embryo;
Chickens;
Endothelial Cells;
cytology;
Histone Deacetylase 6;
Histone Deacetylases;
metabolism;
physiology;
Humans;
Hydroxamic Acids;
pharmacology;
Mice;
Microtubule-Associated Proteins;
metabolism;
physiology;
Neovascularization, Physiologic
- From:
Protein & Cell
2011;2(2):150-160
- CountryChina
- Language:English
-
Abstract:
Angiogenesis, a process by which the preexisting blood vasculature gives rise to new capillary vessels, is associated with a variety of physiologic and pathologic conditions. However, the molecular mechanism underlying this important process remains poorly understood. Here we show that histone deacetylase 6 (HDAC6), a microtubule-associated enzyme critical for cell motility, contributes to angiogenesis by regulating the polarization and migration of vascular endothelial cells. Inhibition of HDAC6 activity impairs the formation of new blood vessels in chick embryos and in angioreactors implanted in mice. The requirement for HDAC6 in angiogenesis is corroborated in vitro by analysis of endothelial tube formation and capillary sprouting. Our data further show that HDAC6 stimulates membrane ruffling at the leading edge to promote cell polarization. In addition, microtubule end binding protein 1 (EB1) is important for HDAC6 to exert its activity towards the migration of endothelial cells and generation of capillary-like structures. These results thus identify HDAC6 as a novel player in the angiogenic process and offer novel insights into the molecular mechanism governing endothelial cell migration and angiogenesis.
