PMID- 27261611 OWN - NLM STAT- MEDLINE DCOM- 20170131 LR - 20180412 IS - 1950-6007 (Electronic) IS - 0753-3322 (Linking) VI - 81 DP - 2016 Jul TI - Protection of rats spinal cord ischemia-reperfusion injury by inhibition of MiR-497 on inflammation and apoptosis: Possible role in pediatrics. PG - 337-344 LID - S0753-3322(16)30077-4 [pii] LID - 10.1016/j.biopha.2016.04.028 [doi] AB - MicroRNAs are extensively included in the pathogenesis and progression of many diseases by inhibiting target gene expression. Recently, studies have demonstrated that microRNA-497 (miR-497) may be implicated in human breast cancer that miR-497 predicts the prognosis of breast cancer patients from the posttranscriptional level. However, the specific function of miR-497 in spinal cord ischemia-reperfusion (IR) injury is far from clear nowadays. The present study was designed to determine the role of miR-497 in spinal cord IR injury and investigate the underlying spinal cord protective mechanism. The rat spinal cord IR injury model was performed by occluding the left anterior descending coronary artery for 30 min, which is then followed by 12h reperfusion. As predicted, miR-497 over-expression markedly decreased the expression of IL-1 receptor associated kinase (IRAK1) and Cyclic AMP response element binding protein (CREB). Moreover, Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-kappaB) and Caspase-3, as miR-497 potential targets were significantly suppressed after miR-497 transfection, then preventing inflammatory cytokines and factors regulating apoptosis. We also found that tumor necrosis factor-a (TNF-alpha) and interleukin-1beta (IL-1beta) activity, pro-apoptotic related genes, such as extracellular regulated protein kinases (ERK), Bcl-2 Associated X Protein (Bax), Bcl-2, Bcl-xL levels were all decreased associated with the down-regulation of IRAK1 and CREB. In conclusion, our data demonstrate that miR-497 could inhibit inflammation and apoptosis of spinal cord IR through its targets, IRAK1 of TLR4 and CREB signaling pathway. Thus, miR-497 may constitute a new therapeutic target for the prevention of spinal cord IR injury. CI - Copyright (c) 2016 Elsevier Masson SAS. All rights reserved. FAU - Xu, Meng AU - Xu M AD - Department of Pediatric Surgery, Yishui Central Hospital, Linyi, Shandong 276400, China. FAU - Wang, Hai-Feng AU - Wang HF AD - Department of Pediatric Surgery, Yishui Central Hospital, Linyi, Shandong 276400, China. FAU - Zhang, Ying-Ying AU - Zhang YY AD - Department of Hand and Foot Surgery, Yishui Central Hospital, Linyi, Shandong 276400, China. FAU - Zhuang, Hui-Wen AU - Zhuang HW AD - Department of Pediatric Surgery, Yishui Central Hospital, Linyi, Shandong 276400, China. LA - eng PT - Journal Article PT - Retracted Publication DEP - 20160425 PL - France TA - Biomed Pharmacother JT - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JID - 8213295 RN - 0 (Cyclic AMP Response Element-Binding Protein) RN - 0 (Cytokines) RN - 0 (Inflammation Mediators) RN - 0 (MIRN497 microRNA, rat) RN - 0 (MicroRNAs) RN - 0 (NF-kappa B) RN - 0 (Neuroprotective Agents) RN - 0 (Toll-Like Receptor 4) RN - EC 2.7.11.1 (IRAK1 protein, rat) RN - EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases) SB - IM RIN - Biomed Pharmacother. 2018 Feb;98 :927. PMID: 29421863 MH - Animals MH - *Apoptosis MH - Base Sequence MH - Cell Line, Tumor MH - Cyclic AMP Response Element-Binding Protein/metabolism MH - Cytokines/metabolism MH - Humans MH - Inflammation/*pathology MH - Inflammation Mediators/metabolism MH - Injections, Spinal MH - Interleukin-1 Receptor-Associated Kinases/metabolism MH - Male MH - MicroRNAs/genetics/metabolism MH - NF-kappa B/metabolism MH - Neuroprotective Agents/*metabolism MH - *Pediatrics MH - Rats, Sprague-Dawley MH - Reperfusion Injury/*genetics/*pathology MH - Spinal Cord/*blood supply/*pathology MH - Toll-Like Receptor 4/metabolism OTO - NOTNLM OT - CREB OT - IRAK1 OT - Spinal cord ischemia-reperfusion OT - TLR4 OT - miR-497 EDAT- 2016/06/05 06:00 MHDA- 2017/02/01 06:00 CRDT- 2016/06/05 06:00 PHST- 2016/01/20 00:00 [received] PHST- 2016/04/08 00:00 [revised] PHST- 2016/04/11 00:00 [accepted] PHST- 2016/06/05 06:00 [entrez] PHST- 2016/06/05 06:00 [pubmed] PHST- 2017/02/01 06:00 [medline] AID - S0753-3322(16)30077-4 [pii] AID - 10.1016/j.biopha.2016.04.028 [doi] PST - ppublish SO - Biomed Pharmacother. 2016 Jul;81:337-344. doi: 10.1016/j.biopha.2016.04.028. Epub 2016 Apr 25.