Dr. Summer's Lab Publishes New Findings

Abstract

Caveolae are cell membrane invaginations that are highly abundant in adipose tissue, endothelial cells and the lung. The formation of caveolae is dependent on the expression of various structural proteins that serve as scaffolding for these membrane invaginations. Cavin1 is a newly identified structural protein whose deficiency in mice leads to loss of caveolae formation and to development of a lipodystrophic phenotype. In this study, we sought to investigate the functional role of Cavin1 in the lung. Cavin1 deficient mice possessed dramatically altered distal lung morphology and exhibited significant physiological alterations, notably, increased lung elastance. The changes in distal lung architecture were associated with hypercellularity and the accumulation of lung macrophages. The increases in lung macrophages occurred without changes to circulating numbers of mononuclear cells and without evidence for increased proliferation. However, the increases in lung macrophages were associated with higher levels of macrophage chemotactic factors CXCL2 and CCL2 in BAL fluid from Cavin -/- mice suggesting a possible mechanism by which these cells accumulate. In addition, lung macrophages from Cavin -/- mice were larger and displayed measurable differences in gene expression when compared to macrophages from wild-type mice. Interestingly, macrophages were also increased in adipose tissue but not in liver, kidney or skeletal muscle from Cavin -/- mice, and similar tissue specificity for macrophage accumulation was observed in lungs and adipose tissue from Caveolin -/- mice. In conclusion, this study demonstrates an important role for Cavin1 in lung homeostasis and suggests that caveolae structural proteins are necessary for regulating macrophage number and phenotype in the lung.

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Citation: Govender P, Romero F, Shah D, Paez J, Ding S-Y, et al. (2013) Cavin1; a Regulator of Lung Function and Macrophage Phenotype. PLoS ONE 8(4): e62045.doi:10.1371/journal.pone.0062045

Editor: Stephania Ann Cormier, Louisiana State University Health Sciences Center, United States of America

Received November 16, 2012; Accepted March 16, 2013; Published April 25, 2013

Copyright:  2013 Govender et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work was supported by the National Institutes of Health (NIH) R01HL105490. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interests: The authors have declared that no competing interests exist.

* E-mail: Ross.summer@jefferson.edu

Published: 05-06-2013

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