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논문 기본 정보

자료유형
학술저널
저자정보
Chai Qiaoying (the First Hospital of Hebei Medical University) Zheng Mingqi (the First Hospital of Hebei Medical University) Wang Le (the First Hospital of Hebei Medical University) Wei Mei (the First Hospital of Hebei Medical University) Yin Yajuan (the First Hospital of Hebei Medical University) Ma Fangfang (the First Hospital of Hebei Medical University) Li Xinping (Han Dan First Hospital) Zhang Haijun (Han Dan First Hospital) Liu Gang (the First Hospital of Hebei Medical University)
저널정보
한국조직공학과 재생의학회 조직공학과 재생의학 조직공학과 재생의학 제17권 제5호
발행연도
2020.1
수록면
659 - 670 (12page)

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Background: The cardiomyocyte apoptosis is considered as one of major contributions to cardiac remodeling after myocardial infarction (MI). Numerous studies find that circular RNAs (circRNAs) play pivotal roles in a variety of biological functions. However, the role of circ_0068655 in MI and human induced pluripotent stem-derived cardiomyocytes (HCMs) remains unknown. Methods: The expression of circ_0068655, miR-498, and PRKC apoptosis WT1 regulator (PAWR) in human MI heart tissues and hypoxia subjected HCMs was evaluated with qRT-PCR and Western blot. The effects of circ_0068655 on hypoxia-induced apoptotic death and cell migration in HCMs were evaluated with qRT-PCR, cell viability, cell death ELISA (POD), and Caspase-3 activity assay, and Trans-well assay, respectively. Furthermore, luciferase assay, qRT-PCR, biotin-labeled miRNA pulldown assay, and Western blot were employed in the functional studies. Results: We found that the expression of circ_0068655 and PAWR was enhanced in MI patients and hypoxia subjected HCMs; by contrast, the expression of miR-498 decreased. Inhibited expression of circ_0068655 in HMCs counteracted hypoxia-induced apoptotic death and impaired cell migration, in sharp contrast to circ_0068655 knockdown. We identified that circ_0068655 sponged an endogenous miR-498 to sequester and inhibit its activity, leading to the increased PAWR expression. Conclusions: Our findings reveal that the expression of circ_0068655 can promote cardiomyocyte apoptosis through the modulation of miR-498-PAWR axis in vitro, which highlights the diagnostic and therapeutic value of circ_0068655 in patients with MI.

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