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10.1038/srep27945 http://scihub22266oqcxt.onion/10.1038/srep27945 C4906401!4906401 !27297958     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27297958 &cmd=llinks): Failed to open stream: HTTP request failed! 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Urinary miR-16 transactivated by C/EBP? reduces kidney function after ischemia/reperfusion-induced injury |pdf=|usr=}}{{27297958 }} gab.com Text Urinary miR-16 transactivated by C/EBP reduces kidney function after ischemia/reperfusion-induced injury JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27297958 #FOAvip Ischemia-reperfusion (I/R) induced acute kidney injury (AKI) is regulated by transcriptional factors and microRNAs (miRs). However, modulation of miRs by transcriptional factors has not been characterized in AKI. Here, we found that urinary miR-16 was 100-fold higher in AKI patients. MiR-16 was detected earlier than creatinine in mouse after I/R. Using TargetScan, the 3'UTR of B-cell lymphoma 2 (BCL-2) was found complementary to miR-16 to decrease the fluorescent reporter activity. Overexpression of miR-16 in mice significantly attenuated renal function and increased TUNEL activity in epithelium tubule cells. The CCAAT enhancer binding protein beta (C/EBP-?) increased the expression of miR-16 after I/R injury. The ChIP and luciferase promoter assay indicated that about -1.0?kb to -0.5?kb upstream of miR-16 genome promoter region containing C/EBP-? binding motif transcriptionally regulated miR-16 expression. Meanwhile, the level of pri-miR-16 was higher in mice infected with lentivirus containing C/EBP-? compared with wild-type (WT) mice and overexpression of C/EBP-? in the kidney of WT mice reduced kidney function, increased kidney apoptosis, and elevated urinary miR-16 level. Our results indicated that miR-16 was transactivated by C/EBP-? resulting in aggravated I/R induced AKI and that urinary miR-16 may serve as a potential biomarker for AKI. Twit Text FOAVip Urinary miR-16 transactivated by C/EBP reduces kidney function after ischemia/reperfusion-induced injury ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27297958 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27297958 #FOAvip English Wikipedia <ref>{{Cite pmid|27297958 }}</ref> Urinary miR-16 transactivated by C/EBP? reduces kidney function after ischemia/reperfusion-induced injury #MMPMID27297958 Chen HH ; Lan YF ; Li HF ; Cheng CF ; Lai PF ; Li WH ; Lin H Sci Rep 2016[Jun]; 6 (ä): 27945 PMID27297958 show ga Ischemia-reperfusion (I/R) induced acute kidney injury (AKI) is regulated by transcriptional factors and microRNAs (miRs). However, modulation of miRs by transcriptional factors has not been characterized in AKI. Here, we found that urinary miR-16 was 100-fold higher in AKI patients. MiR-16 was detected earlier than creatinine in mouse after I/R. Using TargetScan, the 3'UTR of B-cell lymphoma 2 (BCL-2) was found complementary to miR-16 to decrease the fluorescent reporter activity. Overexpression of miR-16 in mice significantly attenuated renal function and increased TUNEL activity in epithelium tubule cells. The CCAAT enhancer binding protein beta (C/EBP-?) increased the expression of miR-16 after I/R injury. The ChIP and luciferase promoter assay indicated that about -1.0?kb to -0.5?kb upstream of miR-16 genome promoter region containing C/EBP-? binding motif transcriptionally regulated miR-16 expression. Meanwhile, the level of pri-miR-16 was higher in mice infected with lentivirus containing C/EBP-? compared with wild-type (WT) mice and overexpression of C/EBP-? in the kidney of WT mice reduced kidney function, increased kidney apoptosis, and elevated urinary miR-16 level. Our results indicated that miR-16 was transactivated by C/EBP-? resulting in aggravated I/R induced AKI and that urinary miR-16 may serve as a potential biomarker for AKI. |Acute Kidney Injury/*genetics/pathology [MESH] |Animals [MESH] |Apoptosis/genetics/physiology [MESH] |CCAAT-Enhancer-Binding Protein-beta/*metabolism [MESH] |Creatinine/urine [MESH] |Epithelium/physiology [MESH] |Genetic Markers/genetics [MESH] |Humans [MESH] |Kidney/immunology/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |MicroRNAs/biosynthesis/*genetics/urine [MESH] |Promoter Regions, Genetic/genetics [MESH] |Proto-Oncogene Proteins c-bcl-2/genetics [MESH] |Reperfusion Injury/*genetics [MESH]Urinary miR-16 transactivated by C/EBP? reduces kidney function after (epmc).pdf DeepDyve Pubget Overpricing