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High Glucose Induced Monocyte‐to‐Macrophage Differentiation: Role of AMPk
Author(s) -
VASAMSETTI SATHISH BABU,
Rao Padmapriya,
Kotamraju Srigiridhar
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.870.7
Subject(s) - proinflammatory cytokine , monocyte , ampk , macrophage , endocrinology , inflammation , metformin , diabetes mellitus , medicine , immunology , chemistry , microbiology and biotechnology , biology , phosphorylation , protein kinase a , biochemistry , in vitro
Diabetes‐induced vascular dysfunctions are on the upsurge and earlier studies have correlated increased inflammatory events as a result of hyperglycemia, plays a major role in the development of diabetes‐associated vascular dysfunctions including atherosclerosis. Monocyte‐to‐Macrophage differentiation has been implicated as a key event during the progression of atherosclerosis. This process induces an inflammatory environment by generating proinflammatory cytokines. In this study, we tested the hypothesis that high glucose levels which mimic diabetic conditions can augment monocyte to macrophage differentiation and also promote the release of inflammatory mediators. It was found that glucose dose‐dependently increased PMA‐induced THP‐1 monocyte differentiation which is coincided by the production of proinflammatory cytokines like IL‐1â, MCP‐1 and MMP‐9. Interestingly, High glucose–induced monocyte differentiation as well as proinflammatory cytokine production was attenuated by AMPk activators like metformin. In conclusion, our results show that high glucose levels cause increased monocyte activation via altered regulation of AMPk signaling cascade and thereby may promote a proatherogenic setting.