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This Article Full Text Full Text (PDF) Supplemental Figures and Tables All Versions of this Article: 297/3/L432    most recent 90599.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Summer, R. Articles by Walsh, K. PubMed PubMed Citation Articles by Summer, R. Articles by Walsh, K.

Adiponectin deficiency: a model of pulmonary hypertension associated with pulmonary vascular disease

¹The Pulmonary Center and ²Whitaker Cardiovascular Institute/Molecular Cardiology, Boston University School of Medicine, Boston, Massachusetts

Submitted 4 December 2008 ; accepted in final form 20 June 2009

Adiponectin (APN) is an adipocyte-derived factor that exists at high concentrations in serum and has anti-inflammatory and systemic vascular-protective properties. In this study, we investigated the role of APN in pulmonary vascular homeostasis. We found that APN localizes to the luminal side of blood vessels in lung and acts in vitro to block TNF--induced E-selectin upregulation in pulmonary artery endothelial cells. Targeted deletion of the APN gene in mice leads to a vascular phenotype in lung characterized by E-selectin upregulation and age-dependent increases in perivascular inflammatory cell infiltration and pulmonary arterial pressures. Taken together, these findings demonstrate an important role for APN in lung vascular homeostasis and suggest that APN-deficient states may contribute to the pathogenesis of inflammatory pulmonary vascular disease and to the development of pulmonary hypertension.

adipose tissue; inflammation; obesity