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Am J Physiol Lung Cell Mol Physiol (May 24, 2002). doi:10.1152/ajplung.00485.2001
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Articles in PresS, published online ahead of print May 24, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00485.2001
Submitted on December 17, 2001
Accepted on May 17, 2002

Mitogen activated protein kinases regulate heme oxygenase-1 gene transcription after ischemia-reperfusion lung injury

Xuchen Zhang1, Eric L. Bedard2, Richard Potter2, Robert Zhong2, Jawed Alam3, Augustine M.K. Choi4, and Patty J. Lee1*

1 Section of Pulmonary and Critical Care, Yale University School of Medicine, New Haven, CT, USA
2 Department of Surgery, University of Western Ontario, London, Ontario, Canada
3 Department of Molecular Genetics, Biochemistry, and Molecular Biology, Alton Ochsner Medical Foundation and Louisiana State University Medical Center, New Orleans, LA, USA
4 Division of Pulmonary, Allergy, and Critical Care, University of Pittsburgh, Pittsburgh, PA, USA

* To whom correspondence should be addressed. E-mail: patty.lee{at}yale.edu.

Lung ischemia-reperfusion (I-R) is an important model of oxidant-mediated acute lung and vascular injury. Heme oxygenase-1 (HO-1) is a cytoprotective gene that is markedly induced by lung I-R injury. HO-1 mRNA is increased in mouse lung after 30 min of lung hilar clamping (ischemia) followed by 2-6 h of unclamping (reperfusion) compared to control mice. In a variety of vascular cell types, HO-1 mRNA is induced after 24 h of anoxia followed by 30 min-1 h of reoxygenation (A-R). Transfection studies reveal that the promoter and 5' distal enhancer E1 are necessary and sufficient for increased HO-1 gene transcription after A-R. Immunoblotting studies show all three subfamilies of MAPKs (ERK, JNK, and p38) are activated by 15 min of reperfusion. We also demonstrate that HO-1 gene transcription after A-R involves ERK, JNK, and p38 MAPK pathways. Taken together, our data show that I-R not only induces HO-1 gene expression in mouse lungs and vascular cells but gene transcription occurs via the promoter and E1 enhancer and involves upstream MAPK pathways.




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