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Targeted expression of heme oxygenase-1 prevents the pulmonary inflammatory and vascular responses to hypoxia.

Abstract：

:Chronic hypoxia causes pulmonary hypertension with smooth muscle cell proliferation and matrix deposition in the wall of the pulmonary arterioles. We demonstrate here that hypoxia also induces a pronounced inflammation in the lung before the structural changes of the vessel wall. The proinflammatory action of hypoxia is mediated by the induction of distinct cytokines and chemokines and is independent of tumor necrosis factor-alpha signaling. We have previously proposed a crucial role for heme oxygenase-1 (HO-1) in protecting cardiomyocytes from hypoxic stress, and potent anti-inflammatory properties of HO-1 have been reported in models of tissue injury. We thus established transgenic mice that constitutively express HO-1 in the lung and exposed them to chronic hypoxia. HO-1 transgenic mice were protected from the development of both pulmonary inflammation as well as hypertension and vessel wall hypertrophy induced by hypoxia. Significantly, the hypoxic induction of proinflammatory cytokines and chemokines was suppressed in HO-1 transgenic mice. Our findings suggest an important protective function of enzymatic products of HO-1 activity as inhibitors of hypoxia-induced vasoconstrictive and proinflammatory pathways.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Minamino T,Christou H,Hsieh CM,Liu Y,Dhawan V,Abraham NG,Perrella MA,Mitsialis SA,Kourembanas S

doi

10.1073/pnas.161272598

keywords:

subject

Has Abstract

pub_date

2001-07-17 00:00:00

pages

8798-803

issue

15

eissn

0027-8424

issn

1091-6490

pii

161272598

journal_volume

98

pub_type

杂志文章

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