Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 297, Issue 3, Pages L432-L438Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.90599.2008
Keywords
adipose tissue; inflammation; obesity
Categories
Funding
- National Institutes of Health [K08-HL077138, AG-15052, HL-59215]
- Gilead Sciences Research Scholars Program in Pulmonary Arterial Hypertension
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K08HL077138, R01HL059215] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG015052, R37AG015052] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Summer R, Fiack CA, Ikeda Y, Sato K, Dwyer D, Ouchi N, Fine A, Farber HW, Walsh K. Adiponectin deficiency: a model of pulmonary hypertension associated with pulmonary vascular disease. Am J Physiol Lung Cell Mol Physiol 297: L432-L438, 2009. First published June 26, 2009; doi: 10.1152/ajplung.90599.2008.-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-alpha-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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available