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- W1977272735 abstract "This study was aimed to determine the role and regulation of progranulin (PGRN) in the pathogenesis of inflammatory bowel diseases (IBD). Dextran sulfate sodium (DSS)−, picrylsulfonic acid (TNBS)-induced, bone marrow chimera and CD4+CD45Rbhi T cell transfer colitis model were established and analyzed in wild-type and several genetically-modified mice, including PGRN, IL-10 and TNFR2 deficient mice. Elevated levels of PGRN were found in colitis samples from human IBD patients and mouse colitis models in comparison to the corresponding controls. PGRN-deficient mice became highly susceptible to DSS- and TNBS-induced colitis, whereas recombinant PGRN ameliorated the pathology and reduced the histological score in both DSS and TNBS colitis models. In addition, hematopoietic-derived PGRN was critical for protection against DSS-induced colitis and lack of PGRN signaling in CD4+ T cells also exacerbated experimental colitis. PGRN-mediated protective effect in colitis was compromised in the absence of IL-10 signaling. In addition, PGRN's effect was also largely lost in the TNFR2-deficient colitis model. Collectively, these findings not only provide the new insight into PGRN's anti-inflammatory action in vivo, but may also present PGRN and its derivatives as novel biological agent for treating IBD." @default.
- W1977272735 created "2016-06-24" @default.
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- W1977272735 date "2014-11-12" @default.
- W1977272735 modified "2023-10-12" @default.
- W1977272735 title "PGRN protects against colitis progression in mice in an IL-10 and TNFR2 dependent manner" @default.
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- W1977272735 doi "https://doi.org/10.1038/srep07023" @default.
- W1977272735 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4228332" @default.
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