Genetic ablation of caveolin-2 sensitizes mice to bleomycin-induced injury

Almeida, Cecília J. G. de; Jasmin, Jean François; Galdo, Francesco Del; Lisanti, Michael P.

doi:10.4161/cc.25335

Cited by 12 publications

(12 citation statements)

References 22 publications

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“…Its related family member CAV1 is reported to be a critical regulator of lung injury [ 35 ]. De Almeida et al find that genetic ablation of caveolin-2 sensitizes mice to bleomycin-induced injury [ 36 ]. We speculated that CAV2 might play a role in the pathogenesis of ALI.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Gene expression profiles analysis identifies key genes for acute lung injury in patients with sepsis

2014

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BackgroundTo identify critical genes and biological pathways in acute lung injury (ALI), a comparative analysis of gene expression profiles of patients with ALI + sepsis compared with patients with sepsis alone were performed with bioinformatic tools.MethodsGSE10474 was downloaded from Gene Expression Omnibus, including a collective of 13 whole blood samples with ALI + sepsis and 21 whole blood samples with sepsis alone. After pre-treatment with robust multichip averaging (RMA) method, differential analysis was conducted using simpleaffy package based upon t-test and fold change. Hierarchical clustering was also performed using function hclust from package stats. Beisides, functional enrichment analysis was conducted using iGepros. Moreover, the gene regulatory network was constructed with information from Kyoto Encyclopedia of Genes and Genomes (KEGG) and then visualized by Cytoscape.ResultsA total of 128 differentially expressed genes (DEGs) were identified, including 47 up- and 81 down-regulated genes. The significantly enriched functions included negative regulation of cell proliferation, regulation of response to stimulus and cellular component morphogenesis. A total of 27 DEGs were significantly enriched in 16 KEGG pathways, such as protein digestion and absorption, fatty acid metabolism, amoebiasis, etc. Furthermore, the regulatory network of these 27 DEGs was constructed, which involved several key genes, including protein tyrosine kinase 2 (PTK2), v-src avian sarcoma (SRC) and Caveolin 2 (CAV2).ConclusionPTK2, SRC and CAV2 may be potential markers for diagnosis and treatment of ALI.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/5865162912987143

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Gene expression profiles analysis identifies key genes for acute lung injury in patients with sepsis

2014

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“…These results allowed us to understand that pulmonary remodeling is specifically attributed to the loss of Cav-2 and not to a loss of Cav-1 or caveolae. Cav-2-deficient mice further showed more a sensitive phenotype to lung injury models by bleomycin or LPSinduced sepsis models in comparison with Cav-1-deficient mice (45,46). These observations are suggestive of not just the absence of Cav-2 being responsible for these effects, but that the balance between Cav-1 and Cav-2 is important.…”

Section: Caveolin-2-deficient Mouse Modelsupporting

confidence: 55%

Myocardial Tissue Caveolae

Sanon

Sawaki

Mjaatvedt

et al. 2015

Comprehensive Physiology

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Caveolae and their coat proteins, caveolins (Cav), are cave-like invaginations found in the plasma membrane of a variety of cells. These unique vesicles and their coat proteins, Cavs, have diverse effects on endothelial function, nitric oxide synthesis regulation, signal transduction, cholesterol metabolism, and apoptosis. Animal studies in Cav knockout mice demonstrate the vital role of these structural proteins on endothelial and vascular function. Genetic studies have proposed that beside neoplasia, Cavs may play a role in the development of atherosclerosis, cardiomyopathy, long QT syndrome, pulmonary fibrosis, and muscular dystrophy. The role of Cav expression in atherosclerotic disease is poorly understood and remains controversial. Interestingly, there is emerging evidence between low Cav-1 levels and the vulnerable plaque, which could potentially identify Cav-1 as a novel plaque biomarker. Cavs, through intricate biochemical pathways involving endothelial nitric oxide synthase and mitogen-activated protein kinase, are known to affect the cardiovascular system at multiple levels. In the present review, we aim to highlight the nature and types of caveolae, caveolar signaling mechanisms and regulation, and the pathophysiology of Cavs as it pertains to the cardiovascular system. Ongoing research is needed to clarify the diagnostic and prognostic role of these novel proteins and to determine how the effects of Cavs can translate into clinical medicine.

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“…TGF-␤ is the major cytokine that contributes to activation of fibroblasts and is elaborated in fibrotic lungs, including IPF lungs (33,34). Furthermore, TGF-␤ augments PAI-1 expression via increased synthesis and stabilization of PAI-1 mRNA (27).…”

Section: Differential Expression Of Pai-1 In Proliferating Hfl-fibrobmentioning

confidence: 99%

Plasminogen Activator Inhibitor-1 Suppresses Profibrotic Responses in Fibroblasts from Fibrotic Lungs

Marudamuthu

Shetty

Bhandary

et al. 2015

Journal of Biological Chemistry

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Background:The long term survival outcome of patients with IPF is bleak, with a paucity of effective treatments. Results: The changes in baseline PAI-1 expression regulate fibroblast activation and expansion in fibrotic lung diseases. Conclusion: Targeted restoration, rather than inhibition of PAI-1 in activated fibroblasts, mitigates fibrosis. Significance: This study defines a new role of PAI-1 in the pathogenesis of fibrosing lung diseases, including IPF.

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Genetic ablation of caveolin-2 sensitizes mice to bleomycin-induced injury

Cited by 12 publications

References 22 publications

RETRACTED ARTICLE: Gene expression profiles analysis identifies key genes for acute lung injury in patients with sepsis

RETRACTED ARTICLE: Gene expression profiles analysis identifies key genes for acute lung injury in patients with sepsis

Myocardial Tissue Caveolae

Plasminogen Activator Inhibitor-1 Suppresses Profibrotic Responses in Fibroblasts from Fibrotic Lungs

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