Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 58, Issue -, Pages 145-153Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2018.03.019
Keywords
Bruton's tyrosine kinases; Diabetic nephropathy; NF-kappa B; Inflammation
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Funding
- Natural Science Foundation of China [81470965, 81374034]
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Accumulating evidence has shown that macrophages play a vital role in development and pathogenesis of diabetic nephropathy (DN) by secreting inflammatory cytokines. Although Bruton's tyrosine kinases (Btk) is a biologically important molecule implicated in immune regulation, the role of Btk in high glucose (HG)-stimulated inflammatory response in macrophages and the mechanism involved need further investigation. In our study, we used bone marrow-derived macrophages (BMMs) to investigate the involvement of Btk on HG-induced inflammatory cytokines expression and to explore the underlying mechanisms. We found that high glucose induced phosphorylation of Btk, MAPKs and NF-kappa B, and the expression of downstream inflammation cytokines monocyte chemo-attractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha) and interleukin-lbeta (IL-1 beta). Btk inhibitor (PCI-32765) not only down-regulated EFtK1/2 phosphorylation and NF-kappa B activation, but also decreased the secretion of MCP-1, TNF-alpha and IL-1 beta in HG-treated BMMs. These results indicate that Btk plays an important role in HG-induced inflammatory cytokines expression and that PCI-32765 may be used as an immunoregulatory agent against hyperglycemia-induced inflammatory response in DN.
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