Facilitated angiogenesis induced by heme oxygenase-1 gene transfer in a rat model of hindlimb ischemia

被引：84

作者：

Suzuki, M

Iso-o, N

Takeshita, S

Tsukamoto, K

Mori, I

Sato, T

Ohno, M

Nagai, R

Ishizaka, N

机构：

[1] Univ Tokyo, Grad Sch Med, Dept Cardiovasc Med, Bunkyo Ku, Tokyo 1138655, Japan

[2] Univ Tokyo, Grad Sch Med, Dept Diabet & Metab Dis, Bunkyo Ku, Tokyo 1138655, Japan

[3] Teikyo Univ, Sch Med, Dept Med, Itabashi Ku, Tokyo 1738606, Japan

[4] Wakayama Med Univ, Dept Pathol, Wakayama 6418509, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2003年 / 302卷 / 01期

关键词：

angiogenesis; ischemia; carbon monoxide; ferritin; adenovirus; gene transfer;

D O I：

10.1016/S0006-291X(03)00114-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Heme oxygenase-1 (HO-1) is an inducible form of heme oxygenase that catabolizes heme to carbon monoxide, biliverdin, and ferrous iron. We have investigated whether HO-1 can induce angiogenic effects in vivo. Rats were subjected to a bolus injection of either wild type adenovirus (ad-wt) or adenovirus encoding HO-1 (ad-HO-1) through the right femoral artery, which was then removed immediately. HO-1 gene transfer resulted in about a sixfold increase in HO-1 protein levels as compared to the non-treated animals. The increase in both blood flow and capillary density was significantly greater in the ischemic hindlimbs that had been injected with ad-HO-1 than in those injected with ad-wt. These angiogenic effects of ad-HO-1 infection could be completely abolished by treating the animals with the HO inhibitor, zinc protoporphyrin, indicating that they were specifically due to the expression of HO-1. Thus, HO-1 gene transfer improves the blood flow in ischemic hindlimb, at least in part, via angiogenesis facilitated by the induction of this molecule. (C) 2003 Elsevier Science (USA). All rights reserved.

引用

页码：138 / 143

页数：6

共 32 条

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