The Role of a Novel Long Noncoding RNA TUC40- in Cardiomyocyte Induction and Maturation in P19 Cells

Huijuan Li, Li Jiang, Zhangbin Yu, Shuping Han, Xuehua Liu, Mengmeng Li, Chun Zhu, Lixing Qiao, Li Huang

Research output: Contribution to journalArticle

Abstract

BACKGROUND: In previous studies, TUC40-, a new long noncoding RNA, was found to be overexpressed in human ventricular septal defect (VSD) embryonic heart samples. In this article, we carried out experiments on the P19 cell line to elucidate the effects of TUC40- overexpression on cardiomyocyte development relevant to VSD pathogenesis.

METHODS: We established the overexpression cell model by plasmid transfection, and explored the expression profile of Pbx1, the sense gene of TUC40-, and the marker genes of cardiomyocyte linage commitment (Nkx2.5 and GATA4) and maturation (cardiac troponin T). In addition, we combined cell cycle and Cell Counting Kit-8 analysis to detect cell proliferation and used flow cytometry and caspase-3 assays to test apoptosis. At last, bioinformatics analysis was performed to show the possible role of TUC40-.

RESULTS: In the control group, Pbx1 elevated steadily during cardiomyocyte induction; whereas in the overexpression group, it showed significantly lower expression at day 6, 8 and 10 of induction. Cells in the overexpression group failed to induce cardiomyocytes indicated by GATA4 and cardiac troponin T. Proliferation was inhibited possibly owing to G2/M cell cycle arrest and the induced apoptosis rate was higher in the overexpression group.

CONCLUSIONS: TUC40- overexpression reduced Pbx1 expression, cardiomyocyte induction and differentiation, inhibited proliferation and promoted apoptosis. Combining the results and previous studies, we propose TUC40- as a potential pathologic factor for VSD.

Original languageEnglish (US)
Pages (from-to)608-616
Number of pages9
JournalThe American journal of the medical sciences
Volume354
Issue number6
DOIs
StatePublished - Dec 1 2017
Externally publishedYes

Fingerprint

Long Noncoding RNA
Cardiac Myocytes
Ventricular Heart Septal Defects
Troponin T
Apoptosis
G2 Phase Cell Cycle Checkpoints
Computational Biology
Caspase 3
Genes
Transfection
Cell Cycle
Flow Cytometry
Plasmids
Cell Proliferation
Cell Line
Control Groups

Keywords

  • Cardiomyocyte
  • Long noncoding RNA
  • Pbx1
  • TUC40-
  • Ventricular septal defect

ASJC Scopus subject areas

  • Medicine(all)

Cite this

The Role of a Novel Long Noncoding RNA TUC40- in Cardiomyocyte Induction and Maturation in P19 Cells. / Li, Huijuan; Jiang, Li; Yu, Zhangbin; Han, Shuping; Liu, Xuehua; Li, Mengmeng; Zhu, Chun; Qiao, Lixing; Huang, Li.

In: The American journal of the medical sciences, Vol. 354, No. 6, 01.12.2017, p. 608-616.

Research output: Contribution to journalArticle

Li, Huijuan ; Jiang, Li ; Yu, Zhangbin ; Han, Shuping ; Liu, Xuehua ; Li, Mengmeng ; Zhu, Chun ; Qiao, Lixing ; Huang, Li. / The Role of a Novel Long Noncoding RNA TUC40- in Cardiomyocyte Induction and Maturation in P19 Cells. In: The American journal of the medical sciences. 2017 ; Vol. 354, No. 6. pp. 608-616.
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AU - Li, Huijuan

AU - Jiang, Li

AU - Yu, Zhangbin

AU - Han, Shuping

AU - Liu, Xuehua

AU - Li, Mengmeng

AU - Zhu, Chun

AU - Qiao, Lixing

AU - Huang, Li

PY - 2017/12/1

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N2 - BACKGROUND: In previous studies, TUC40-, a new long noncoding RNA, was found to be overexpressed in human ventricular septal defect (VSD) embryonic heart samples. In this article, we carried out experiments on the P19 cell line to elucidate the effects of TUC40- overexpression on cardiomyocyte development relevant to VSD pathogenesis.METHODS: We established the overexpression cell model by plasmid transfection, and explored the expression profile of Pbx1, the sense gene of TUC40-, and the marker genes of cardiomyocyte linage commitment (Nkx2.5 and GATA4) and maturation (cardiac troponin T). In addition, we combined cell cycle and Cell Counting Kit-8 analysis to detect cell proliferation and used flow cytometry and caspase-3 assays to test apoptosis. At last, bioinformatics analysis was performed to show the possible role of TUC40-.RESULTS: In the control group, Pbx1 elevated steadily during cardiomyocyte induction; whereas in the overexpression group, it showed significantly lower expression at day 6, 8 and 10 of induction. Cells in the overexpression group failed to induce cardiomyocytes indicated by GATA4 and cardiac troponin T. Proliferation was inhibited possibly owing to G2/M cell cycle arrest and the induced apoptosis rate was higher in the overexpression group.CONCLUSIONS: TUC40- overexpression reduced Pbx1 expression, cardiomyocyte induction and differentiation, inhibited proliferation and promoted apoptosis. Combining the results and previous studies, we propose TUC40- as a potential pathologic factor for VSD.

AB - BACKGROUND: In previous studies, TUC40-, a new long noncoding RNA, was found to be overexpressed in human ventricular septal defect (VSD) embryonic heart samples. In this article, we carried out experiments on the P19 cell line to elucidate the effects of TUC40- overexpression on cardiomyocyte development relevant to VSD pathogenesis.METHODS: We established the overexpression cell model by plasmid transfection, and explored the expression profile of Pbx1, the sense gene of TUC40-, and the marker genes of cardiomyocyte linage commitment (Nkx2.5 and GATA4) and maturation (cardiac troponin T). In addition, we combined cell cycle and Cell Counting Kit-8 analysis to detect cell proliferation and used flow cytometry and caspase-3 assays to test apoptosis. At last, bioinformatics analysis was performed to show the possible role of TUC40-.RESULTS: In the control group, Pbx1 elevated steadily during cardiomyocyte induction; whereas in the overexpression group, it showed significantly lower expression at day 6, 8 and 10 of induction. Cells in the overexpression group failed to induce cardiomyocytes indicated by GATA4 and cardiac troponin T. Proliferation was inhibited possibly owing to G2/M cell cycle arrest and the induced apoptosis rate was higher in the overexpression group.CONCLUSIONS: TUC40- overexpression reduced Pbx1 expression, cardiomyocyte induction and differentiation, inhibited proliferation and promoted apoptosis. Combining the results and previous studies, we propose TUC40- as a potential pathologic factor for VSD.

KW - Cardiomyocyte

KW - Long noncoding RNA

KW - Pbx1

KW - TUC40-

KW - Ventricular septal defect

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