title: MicroRNA-210 knockdown contributes to apoptosis caused by oxygen glucose deprivation in PC12 cells.
abstract: It was previously demonstrated that microRNA-210 (miR-210) exhibited neuroprotective effects in a murine model of hypoxic-ischemic encephalopathy via inhibition of apoptosis. The aim of the present study was to further elucidate the effect of miR-210 on apoptosis in PC12 cells following transfection with miR-210 inhibitors and exposure to oxygen glucose deprivation (OGD). The expression levels of miR-210 were identified using reverse transcription-quantitative polymerase chain reaction analysis. Apoptosis was investigated using Annexin V-fluorescein isothiocyanate assays. Apoptosis-related protein expression levels were studied with western blot analysis. The results showed that the expression levels of miR-210 were upregulated in PC12 cells following a 4-h exposure to OGD, relative to those in normoxic control cells. miR-210 knockdown increased cell apoptosis by inducing caspase activity and regulating the balance between Bcl-2 and Bax levels. The present study demonstrated that miR-210 knockdown induced cell apoptosis using an ex vivo model of ischemic hypoxia (IH). Knockdown of miR-210 represents a potential novel therapeutic approach to combat neonatal IH.
authors.affiliation: Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Jie
authors.initials: J
authors.lastname: Qiu
authors.affiliation: Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Xiao-Yu
authors.initials: XY
authors.lastname: Zhou
authors.affiliation: Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Xiao-Guang
authors.initials: XG
authors.lastname: Zhou
authors.affiliation: Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Rui
authors.initials: R
authors.lastname: Cheng
authors.affiliation: Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
authors.forename: Hai-Ying
authors.initials: HY
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D015687:Cell Hypoxia; D005786:Gene Expression Regulation; D055785:Gene Knockdown Techniques; D020868:Gene Silencing; D005947:Glucose / Q000378:metabolism; D035683:MicroRNAs / Q000235:genetics*; D016716:PC12 Cells; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C546388:MIRN210 microRNA, rat; D035683:MicroRNAs; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D053148:Caspase 3; D053453:Caspase 9; D005947:Glucose