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Role of caveolin-1 in asthma and chronic inflammatory respiratory diseases

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Pages 339-347 | Published online: 18 Apr 2014
 

Abstract

Caveolin-1 (Cav-1) is the major protein present in invaginations of the plasma membrane of cells known as caveolae. Cav-1 is expressed in numerous resident and inflammatory cells implicated in the pathogenesis of asthma and chronic inflammatory respiratory diseases including chronic obstructive pulmonary disease. A remarkable repertoire of functions has been identified for Cav-1 and these extend to, and have relevance to, asthma and chronic inflammatory respiratory diseases. Important processes influenced by Cav-1 include inflammation, fibrosis, smooth muscle contractility, regulation of apoptosis and cell senescence as well as epithelial barrier function and homeostasis. A better understanding of Cav-1 may be useful in developing new therapies for chronic inflammatory respiratory diseases.

Acknowledgement

The authors would like to thank Dr Sherry Werner (UTHSCSA Pathology) and Cheresa Calhoun for help in the preparation of Figure 1.

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

  • Important lung phenotype for caveolin-1 (Cav-1) was detected in Cav-1-deficient mice.

  • Decreased expression in human disease (reduced in peripheral blood mononuclear cells) and airway epithelia in asthma, and lung parenchyma in chronic obstructive pulmonary disease.

  • Cav-1-deficient mice have worse fibrosis and airway hyperresponsiveness in mouse asthma and chronic obstructive pulmonary disease models (ovalbumin and bleomycin).

  • Cav-1 is expressed in resident structural as well as inflammatory cells.

  • May regulate TGF-β axis and fibrosis as well as smooth muscle contraction and hence airway hyperresponsiveness as well as apoptosis and cell senescence although these areas still needs further experiments for clarification.

Notes

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