Cavin1; a regulator of lung function and macrophage phenotype.

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 struct...

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Autores principales: Praveen Govender, Freddy Romero, Dilip Shah, Jesus Paez, Shi-Ying Ding, Libin Liu, Adam Gower, Elizabeth Baez, Sherif Shawky Aly, Paul Pilch, Ross Summer
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Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/5f2091cbea0f4c5fbea72946b2cfdcef
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spelling oai:doaj.org-article:5f2091cbea0f4c5fbea72946b2cfdcef2021-11-18T07:47:52ZCavin1; a regulator of lung function and macrophage phenotype.1932-620310.1371/journal.pone.0062045https://doaj.org/article/5f2091cbea0f4c5fbea72946b2cfdcef2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23634221/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Caveolae 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 Cavin1-/- mice suggesting a possible mechanism by which these cells accumulate. In addition, lung macrophages from Cavin1-/- 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 Cavin1-/- mice, and similar tissue specificity for macrophage accumulation was observed in lungs and adipose tissue from Caveolin1-/- 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.Praveen GovenderFreddy RomeroDilip ShahJesus PaezShi-Ying DingLibin LiuAdam GowerElizabeth BaezSherif Shawky AlyPaul PilchRoss SummerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 4, p e62045 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Praveen Govender
Freddy Romero
Dilip Shah
Jesus Paez
Shi-Ying Ding
Libin Liu
Adam Gower
Elizabeth Baez
Sherif Shawky Aly
Paul Pilch
Ross Summer
Cavin1; a regulator of lung function and macrophage phenotype.
description 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 Cavin1-/- mice suggesting a possible mechanism by which these cells accumulate. In addition, lung macrophages from Cavin1-/- 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 Cavin1-/- mice, and similar tissue specificity for macrophage accumulation was observed in lungs and adipose tissue from Caveolin1-/- 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.
format article
author Praveen Govender
Freddy Romero
Dilip Shah
Jesus Paez
Shi-Ying Ding
Libin Liu
Adam Gower
Elizabeth Baez
Sherif Shawky Aly
Paul Pilch
Ross Summer
author_facet Praveen Govender
Freddy Romero
Dilip Shah
Jesus Paez
Shi-Ying Ding
Libin Liu
Adam Gower
Elizabeth Baez
Sherif Shawky Aly
Paul Pilch
Ross Summer
author_sort Praveen Govender
title Cavin1; a regulator of lung function and macrophage phenotype.
title_short Cavin1; a regulator of lung function and macrophage phenotype.
title_full Cavin1; a regulator of lung function and macrophage phenotype.
title_fullStr Cavin1; a regulator of lung function and macrophage phenotype.
title_full_unstemmed Cavin1; a regulator of lung function and macrophage phenotype.
title_sort cavin1; a regulator of lung function and macrophage phenotype.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/5f2091cbea0f4c5fbea72946b2cfdcef
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