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Am J Physiol Lung Cell Mol Physiol 283: L815-L829, 2002. First published May 24, 2002; doi:10.1152/ajplung.00485.2001
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Vol. 283, Issue 4, L815-L829, October 2002

Mitogen-activated protein kinases regulate HO-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 Medicine, Yale University School of Medicine, New Haven, Connecticut 06520; 2 Department of Surgery, University of Western Ontario, London Ontario, Canada N6A 5A5; 3 Department of Molecular Genetics, Alton Ochsner Medical Foundation and Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, New Orleans, Louisiana 70121; and 4 Division of Pulmonary, Allergy, and Critical Care, University of Pittsburgh, Pittsburgh, Pennsylvania 15213

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 with 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. Together, our data show that I-R not only induces HO-1 gene expression in mouse lungs and vascular cells but that gene transcription occurs via the promoter and E1 enhancer and involves upstream MAPK pathways.

oxidant injury; gene regulation; heme oxygenase; mitogen-activated protein kinases


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