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10.1038/srep36207 http://scihub22266oqcxt.onion/10.1038/srep36207 C5101812!5101812 !27827458     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27827458 &cmd=llinks): Failed to open stream: HTTP request failed! 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MicroRNA-126 overexpression rescues diabetes-induced impairment in efferocytosis of apoptotic cardiomyocytes |pdf=|usr=}}{{27827458 }} gab.com Text MicroRNA-126 overexpression rescues diabetes-induced impairment in efferocytosis of apoptotic cardiomyocytes JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27827458 #FOAvip Efferocytosis, a process of clearance of apoptotic cells by phagocytes, is essential for successful resolution of inflammation and maintenance of tissue homeostasis. Diabetes compromises the function of macrophages leading to adverse inflammatory response during wound healing, myocardial injury, atherosclerosis and autoimmune disorders. However, the effect of diabetes on macrophage-mediated efferocytosis of apoptotic cardiomyocytes (ACM) and the molecular mechanisms involved are not understood so far. In the present study we found that invitro efferocytosis of ACM was impaired in macrophages from db/db (diabetic) mice. Macrophages exposed to high glucose (HG) decreases microRNA-126 (miR-126) expression with a corresponding increase in ADAM9 expression. Dual-luciferase reporter assay confirms that ADAM9 3'UTR contains miR-126 target site. ADAM9 inhibition reduces HG-induced proteolytic cleavage of Mer tyrosine receptor kinase (MerTK, a proto-oncogene that plays a critical role in phagocytosis), resulting in shedding of soluble-Mer (sMER) and loss of MERTK function. Over-expression of miR-126 attenuates HG-induced impairment of efferocytosis. Furthermore, human diabetic hearts show lower miR-126 expression with a corresponding increase in ADAM9 expression vs. normal counterparts. These data suggests that diabetes impairs efferocytosis of ACM and that strategies to enhance efferocytosis might attenuate diabetes-induced impairment in inflammation resolution and cardiac repair after injury. Twit Text FOAVip MicroRNA-126 overexpression rescues diabetes-induced impairment in efferocytosis of apoptotic cardiomyocytes ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27827458 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27827458 #FOAvip English Wikipedia <ref>{{Cite pmid|27827458 }}</ref> MicroRNA-126 overexpression rescues diabetes-induced impairment in efferocytosis of apoptotic cardiomyocytes #MMPMID27827458 Suresh Babu S ; Thandavarayan RA ; Joladarashi D ; Jeyabal P ; Krishnamurthy S ; Bhimaraj A ; Youker KA ; Krishnamurthy P Sci Rep 2016[Nov]; 6 (ä): 36207 PMID27827458 show ga Efferocytosis, a process of clearance of apoptotic cells by phagocytes, is essential for successful resolution of inflammation and maintenance of tissue homeostasis. Diabetes compromises the function of macrophages leading to adverse inflammatory response during wound healing, myocardial injury, atherosclerosis and autoimmune disorders. However, the effect of diabetes on macrophage-mediated efferocytosis of apoptotic cardiomyocytes (ACM) and the molecular mechanisms involved are not understood so far. In the present study we found that invitro efferocytosis of ACM was impaired in macrophages from db/db (diabetic) mice. Macrophages exposed to high glucose (HG) decreases microRNA-126 (miR-126) expression with a corresponding increase in ADAM9 expression. Dual-luciferase reporter assay confirms that ADAM9 3'UTR contains miR-126 target site. ADAM9 inhibition reduces HG-induced proteolytic cleavage of Mer tyrosine receptor kinase (MerTK, a proto-oncogene that plays a critical role in phagocytosis), resulting in shedding of soluble-Mer (sMER) and loss of MERTK function. Over-expression of miR-126 attenuates HG-induced impairment of efferocytosis. Furthermore, human diabetic hearts show lower miR-126 expression with a corresponding increase in ADAM9 expression vs. normal counterparts. These data suggests that diabetes impairs efferocytosis of ACM and that strategies to enhance efferocytosis might attenuate diabetes-induced impairment in inflammation resolution and cardiac repair after injury. |3' Untranslated Regions [MESH] |ADAM Proteins/*genetics [MESH] |Animals [MESH] |Apoptosis [MESH] |Diabetes Mellitus, Experimental/*genetics [MESH] |Gene Expression Regulation/drug effects [MESH] |Glucose/pharmacology [MESH] |Humans [MESH] |Macrophages/*cytology/drug effects [MESH] |Membrane Proteins/*genetics [MESH] |Mice [MESH] |MicroRNAs/*genetics [MESH] |Myocytes, Cardiac/*cytology [MESH] |Phagocytosis [MESH] |Proto-Oncogene Mas [MESH] |RAW 264.7 Cells [MESH] |THP-1 Cells [MESH]MicroRNA-126 overexpression rescues diabetes-induced impairment in eff(epmc).pdf DeepDyve Pubget Overpricing