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Role of MCPIP1 in High Insulin‐Related Endothelial Cell Dysfunction
Author(s) -
Chen Renee,
Chang Yingzi
Publication year - 2017
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.31.1_supplement.lb559
Subject(s) - downregulation and upregulation , cell , proinflammatory cytokine , cell migration , cell growth , microbiology and biotechnology , insulin , hyperinsulinemia , medicine , chemistry , insulin resistance , inflammation , biology , biochemistry , gene
Vascular complications are one of the major adverse outcomes for diabetic individuals. Elevated inflammatory cytokines are thought to contribute to impaired vascular function. MCP‐1‐induced protein 1 (MCPIP1) is a negative regulator in inflammatory response. Previous research has shown that the proinflammatory cytokine MCP‐1 induces endothelial cell migration and proliferation that is mediated by the induction of MCPIP1. The goal of this project is to better understand the role of MCPIP1 in hyperinsulinemia‐associated endothelial dysfunction. Previous data from our lab showed that pre‐treatment of vascular smooth muscle cells suppresses MCPIP1 expression, suggesting that downregulation of MCPIP1 in diabetic patients may contribute to the development of endothelial dysfunction and subsequent vascular complications. A scratch migration assay and BrdU cell proliferation assay were conducted to determine whether or not a hyperinsulinemic state can suppress MCPIP1 mediated cell migration and proliferation. Our preliminary data revealed that morphology of Human Umbilical Vascular Endothelial Cells (HUVEC) were changed from a cobblestone morphology into an elongated fusiform morphology following transfection with adenovirus expressing GFP‐tagged MCPIP1, overexpression of MCPIP1 increased HUVEC cell migration, and pretreatment with insulin suppressed MCPIP1‐induced HUVEC cell migration. These results suggest that MCPIP1 not only affects cell morphology, but also cell function and that insulin inhibits upregulation of MCPIP1‐induced cell movement. Experiments observing the effect of MCPIP1 on HUVEC cell proliferation and the possible impact of insulin are still being conducted.