Journal
ONCOTARGET
Volume 7, Issue 21, Pages 30575-30584Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.8872
Keywords
colitis; inflammation; blimp-1; NLRP12; TLR4
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Funding
- National Natural Science Foundation of China [31402164]
- National Key Basic Research Program (973 Program) of China [2015CB150300]
- Zhejiang Provincial Natural Science Foundation of China [LQ14C180001]
- Fundamental Research Funds for the Central Universities [2014QNA6026]
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NLRP12 is a member of the Nod-like receptor (NLR). Previous studies have reported enhanced colitis-associated inflammatory responses in NLRP12-deficient mice. In this study, we sought to investigate the role of NLRP12 in DSS-stimulated proinflammatory response in dendritic cells and mice colitis, and the molecular mechanisms involved in the development of the inflammation. Our results showed that down-regulation of NLRP12 is required for DSS-induced release of proinflammatory cytokines IL-1 beta and TNF-alpha; that PR domain zinc finger protein 1 (also known as Blimp-1) induces NLRP12 down-regulation during DSS-induced proinflammatory response and colitis; and that TLR4 is implicated in the up-regulation of Blimp-1 that led to the down-regulation of NLRP12 expression in DSS-induced colitis. Taken together, the results suggest that the TLR4-Blimp-1 axis promotes DSS induced experimental colitis through the down-regulation of NLRP12.
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