Re-enforcing hypoxia-induced polyploid cardiomyocytes enter cytokinesis through activation of β-catenin.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
28 11 2019
Historique:
received: 14 05 2019
accepted: 08 11 2019
entrez: 30 11 2019
pubmed: 30 11 2019
medline: 5 11 2020
Statut: epublish

Résumé

Cardiomyocyte (CM) loss is a characteristic of various heart diseases, including ischaemic heart disease. Cardiac regeneration has been suggested as a promising strategy to address CM loss. Although many studies of regeneration have focused mainly on mononucleated or diploid CM, the limitations associated with the cytokinesis of polyploid and multinucleated CMs remain less well known. Here, we show that β-catenin, a key regulator in heart development, can increase cytokinesis in polyploid multinucleated CMs. The activation of β-catenin increases the expression of the cytokinesis-related factor epithelial cell transforming 2 (ECT2), which regulates the actomyosin ring and thus leads to the completion of cytokinesis in polyploid CMs. In addition, hypoxia can induce polyploid and multinucleated CMs by increasing factors related to the G1-S-anaphase of the cell cycle, but not those related to cytokinesis. Our study therefore reveals that the β-catenin can promote the cytokinesis of polyploid multinucleated CMs via upregulation of ECT2. These findings suggest a potential field of polyploid CM research that may be exploitable for cardiac regeneration therapy.

Identifiants

pubmed: 31780774
doi: 10.1038/s41598-019-54334-4
pii: 10.1038/s41598-019-54334-4
pmc: PMC6883062
doi:

Substances chimiques

Ect2 protein, mouse 0
Proto-Oncogene Proteins 0
beta Catenin 0
Actomyosin 9013-26-7
Oxygen S88TT14065

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

17865

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Auteurs

Yun-Han Jiang (YH)

Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Chongqing, 400037, P. R. China.

Yu Zhu (Y)

Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Chongqing, 400037, P. R. China.

Sai Chen (S)

Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Chongqing, 400037, P. R. China.

Hai-Long Wang (HL)

Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Chongqing, 400037, P. R. China.

Yang Zhou (Y)

Department of Cardiothoracic Surgery, The People's Hospital of Leshan, Leshan, Sichuan Province, 614000, P. R. China.

Fu-Qin Tang (FQ)

Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Chongqing, 400037, P. R. China.

Zhao Jian (Z)

Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Chongqing, 400037, P. R. China.

Ying-Bin Xiao (YB)

Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Chongqing, 400037, P. R. China. xiaoyb@tmmu.edu.cn.

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