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Background

Caveolin-1 (Cav-1) is a multifunctional scaffolding protein serving as a platform for the cell's signal-transduction and playing an important role in inflammation. However, its role in inflammatory bowel disease is not clear. A recent study showed that Cav-1 is increased and mediates angiogenesis in dextran sodium sulphate-induced colitis, which are contradictory to our pilot findings in 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis. In the present study, we further clarified the role of Cav-1 in TNBS-induced colitis.

Methods

In BALB/c mice, acute colitis was induced by intra-rectal administration of one dose TNBS, while chronic colitis was induced by administration of TNBS once a week for 7 weeks. To assess the effects of complete loss of Cav-1, Cav-1 knockout (Cav-1-/-) and control wild-type C57 mice received one TNBS administration. Body weight and clinical scores were monitored. Colon Cav-1 and pro-inflammatory cytokine levels were quantified through ELISAs. Inflammation was evaluated through histological analysis.

Results

Colon Cav-1 levels were significantly decreased in TNBS-induced colitis mice when compared to normal mice and also inversely correlated with colon inflammation scores and proinflammatory cytokine levels (IL-17, IFN-γ and TNF) significantly. Furthermore, after administration of TNBS, Cav-1-/-mice showed significantly increased clinical and colon inflammatory scores and body weight loss when compared with control mice.

Conclusions and significance

Cav-1 may play a protective role in the development of TNBS-induced colitis. Our findings raise an important issue in the evaluation of specific molecules in animal models that different models may exhibit opposite results because of the different mechanisms involved."xsd:string
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http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/author"Ma Y."xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/author"Peng Z."xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/author"Guan Q."xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/author"Bernstein C.N."xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/author"Qing G."xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/author"Warrington R.J."xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/author"Weiss C.R."xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/pages"e0119004"xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/title"The potential protective role of caveolin-1 in intestinal inflammation in TNBS-induced murine colitis."xsd:string
http://purl.uniprot.org/citations/25756273http://purl.uniprot.org/core/volume"10"xsd:string
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