title: MicroRNA-1 upregulation promotes myocardiocyte proliferation and suppresses apoptosis during heart development.
abstract: Previous studies have investigated the role of microRNAs (miRs) in heart development to reveal the miRNA mechanism of action in congenital heart disease (CHD) in children. The present study aimed to investigate the role of miR‑1 in heart development in P19 cells. The mRNA level for miR‑1 in P19 cells was detected before or after cardiomyocyte differentiation, using reverse transcription‑quantitative polymerase chain reaction analysis. Expression of cardiomyocyte differentiation markers was also analyzed. The effect of miR‑1 overexpression on the viability and apoptosis of differentiated P19 cells was assessed using MTT and Annexin V‑FITC assays, respectively. Furthermore, the effects of miR-1 on expression of markers of cell proliferation and apoptosis were also analyzed in differentiated P19 cells using western blotting. The results demonstrated that P19 cells were successfully differentiated into cardiomyocytes, and that endogenous miR‑1 expression was significantly decreased in differentiated P19 cells compared with undifferentiated P19 cells. Overexpression of miR‑1 resulted in increased viability in differentiated P19 cells and decreased apoptosis, compared with the normal control. In addition, expression of heart and neural crest derivatives expressed transcript 2 (Hand2) was increased in differentiated cells with miR‑1 overexpressed compared with normal cells, while caspase‑3 cleavage was decreased by miR‑1 overexpression. In conclusion, the present study suggested that miR-1 upregulation may be important in regulating cell proliferation and apoptosis in P19 differentiated cardiomyocytes by increasing Hand2 expression and suppressing caspase‑3 cleavage. The present study aimed to provide a theoretical basis for the explanation of the mechanism of CHD and investigate miR‑1 as a potential therapeutic target for its clinical treatment.
authors.affiliation: Department of Pediatrics, Children's Medical Center, People's Hospital of Hunan, Changsha, Hunan 410005, P.R. China.
authors.forename: Liping
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Pediatrics, Children's Medical Center, People's Hospital of Hunan, Changsha, Hunan 410005, P.R. China.
authors.forename: Yonghua
authors.initials: Y
authors.lastname: Yuan
authors.affiliation: Department of Pediatrics, Children's Medical Center, People's Hospital of Hunan, Changsha, Hunan 410005, P.R. China.
authors.forename: Xuehua
authors.initials: X
authors.lastname: He
authors.affiliation: Department of Ultrasonography, People's Hospital of Hunan, Changsha, Hunan 410005, P.R. China.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Xia
authors.affiliation: Faculty of Life Sciences, Hunan Normal University, Changsha, Hunan 410006, P.R. China.
authors.forename: Xiaoyang
authors.initials: X
authors.lastname: Mo
mesh_terms: D000818:Animals; D000070416:Antagomirs / Q000378:metabolism; D017209:Apoptosis; D051792:Basic Helix-Loop-Helix Proteins / Q000235:genetics / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D002454:Cell Differentiation; D002460:Cell Line; D049109:Cell Proliferation / Q000502:physiology*; D050991:GATA4 Transcription Factor / Q000235:genetics / Q000378:metabolism; D000072576:Homeobox Protein Nkx-2.5 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology*
chemical_list: D000070416:Antagomirs; D051792:Basic Helix-Loop-Helix Proteins; D053148:Caspase 3; D050991:GATA4 Transcription Factor; D000072576:Homeobox Protein Nkx-2.5; D035683:MicroRNAs; C484171:Gata4 protein, mouse; C498766:Hand2 protein, mouse; C517731:Mirn1 microRNA, mouse; C484469:Nkx2-5 protein, mouse