Important role of apoptosis signal-regulating kinase 1 in ischemia-induced angiogenesis - PubMed (original) (raw)

. 2005 Sep;25(9):1877-83.

doi: 10.1161/01.ATV.0000174801.76234.bd. Epub 2005 Jun 23.

Shokei Kim-Mitsuyama, Minoru Yoshiyama, Takashi Omura, Masayuki Shiota, Atsushi Matsuzawa, Tokihito Yukimura, Toyoaki Murohara, Motohiro Takeya, Hidenori Ichijo, Junichi Yoshikawa, Hiroshi Iwao

Affiliations

• PMID: 15976330
• DOI: 10.1161/01.ATV.0000174801.76234.bd

Important role of apoptosis signal-regulating kinase 1 in ischemia-induced angiogenesis

Yasukatsu Izumi et al. Arterioscler Thromb Vasc Biol. 2005 Sep.

Abstract

Objective: We first examined the role of apoptosis signal-regulating kinase 1 (ASK1), one of mitogen-activated protein kinase kinase kinases, in ischemia-induced angiogenesis.

Methods and results: Unilateral hindlimb ischemia was induced surgically in C57BL/6J wild-type (WT) mice or mice deficient in ASK1 (ASK1(-/-)). ASK1 activity in WT mouse hindlimb was increased dramatically after ischemia. By laser Doppler analysis, well-developed collateral vessels and angiogenesis were observed in WT mice in response to hindlimb ischemia, whereas these responses were reduced in ASK1(-/-) mice. Immunostaining revealed that infiltration of macrophages and T lymphocytes was suppressed in the ischemic tissues of ASK1(-/-) mice compared with WT mice. The expression of vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1) proteins in ischemic tissues was weaker in ASK1(-/-) mice compared with WT mice. In vitro study on endothelial cells indicated that dominant-negative ASK1 significantly attenuated hydrogen peroxide-induced VEGF and MCP-1 production. Furthermore, in vivo blockade of MCP-1 by its neutralizing antibody suppressed the recovery of the blood flow and capillary formation after ischemia.

Conclusions: ASK1 pathway promotes early angiogenesis by inducing inflammatory cell infiltration and VEGF and MCP-1 expression. ASK1 may provide the basis for the development of new therapeutic strategy for angiogenesis.

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