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Articles in PresS, published online ahead of print December 3, 2002
Physiol Genomics, 10.1152/physiolgenomics.00081.2001
Submitted on September 13, 2001
Accepted on November 27, 2002
1 Department of Medicine, University of Colorado Health Sciences Center,Pulmonary Hypertension Center, Denver, CO, USA; Department of Medicine, University of Colorado Health Sciences Center, Division of Pulmonary Sciences and Critical Care Medicine, Denver, CO, USA; Department of Thoracic Surgery, Institute of Development, Aging, and Cancer Tohoku University, Sendai, Japan
2 Department of Medicine, University of Colorado Health Sciences Center, Division of Pulmonary Sciences and Critical Care Medicine, Denver, CO, USA
3 Department of Pharmacology, University of Colorado Health Sciences Center, Denver, CO, USA
4 Department of Medicine, University of Colorado Health Sciences Center, Cardiovascular Pulmonary Research Laboratory, Denver, CO, USA
5 Department of Thoracic Surgery, Institute of Development, Aging, and Cancer Tohoku University, Sendai, Japan
6 Department of Medicine, University of Colorado Health Sciences Center,Pulmonary Hypertension Center, Denver, CO, USA; Department of Pathology, University of Colorado Health Sciences Center, Denver, CO, USA
7 Department of Medicine, University of Colorado Health Sciences Center,Pulmonary Hypertension Center, Denver, CO, USA; Department of Medicine, University of Colorado Health Sciences Center, Division of Pulmonary Sciences and Critical Care Medicine, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: mark.geraci{at}uchsc.edu.
Different animal species have a varying response to hypoxia. Mice develop less pulmonary artery thickening after chronic hypoxia exposure than rats. We hypothesized that the lung tissue gene expression pattern displayed in hypoxic rats would differ from that of hypoxic mice. We exposed Sprague-Dawley rats and C57BL/6 mice to both one and three weeks of hypobaric hypoxia. While both species developed pulmonary hypertension, mice showed less pulmonary vascular remodeling than rats. Microarray gene analysis demonstrated a distinct pattern of gene expression between mice and rats when exposed to hypoxic conditions. In addition, some genes appeared to be more responsive at an earlier time point of 1 week of hypoxia. Hypoxic conditions in the rat induce genes involved in endothelial cell proliferation, repression of apoptosis, and vasodilation. Mice exposed to hypoxic conditions decrease the expression of genes involved in vasodilation and in endothelial cell proliferation. Although we cannot determine whether the differential expression of genes during chronic hypoxia is cause or consequence of the differential pulmonary vascular remodeling, we propose that a balance between over and under expression of a selective group of genes may be responsible for lung vascular remodeling and vascular tone control.
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