Ischemia-reperfusion injury in human AC16 cardiomyocytes is modulated by AXIN1 depending on c-Myc regulation

  • Ann Med Surg (Lond). 2023 Aug 7;85(10):4844-4850. doi: 10.1097/MS9.0000000000001139.
Jun Li  1 ,  Hao Wang  1 ,  Li Chen  1 ,  Jialin Zhong  1 ,  Junsheng Wang  1 ,  Jun Xiao  1
Affiliations
  • 1. Department of Cardiovascular Medicine, Chongqing University Center Hospital, Chongqing, People's Republic of China.
PMID: 37811065 DOI: 10.1097/MS9.0000000000001139
Abstract

Objective: A major consequence of acute Myocardial Infarction is myocardial ischemia-reperfusion (I/R) injury. Collecting proof demonstrates that AXIN1 assume a basic part in different disease; however, the role of AXIN1 in I/R injury remains to a great extent obscure.

Methods: The I/R injury model on AC16 cells was constructed. siRNA transfection was used to knockdown AXIN1. The qRT-PCR assays and western blot assays were used to detect the expression level of AXIN1 and other key proteins. CCK-8 assays and cell Apoptosis assays were used to detect cell proliferation and cell Apoptosis.

Results: AXIN1 was significantly overexpressed in an in vitro model of I/R injury. Knockdown of AXIN1 significantly restored the cell proliferation inhibition caused by IR injury, while inhibiting Apoptosis and inflammation. Further mechanistic studies revealed that the transcription factor c-Myc could regulate the expression of AXIN1. The effects of I/R injury on AC16 cells after overexpression of c-Myc were reversed by knockdown of AXIN1. Meanwhile, AXIN1 could regulate the SIRT1/p53/Nrf 2 pathway.

Conclusion: Our results show an important role for AXIN1 and provide new targets for avoiding and treating I/R injury.

Keywords
AXIN1; apoptosis; c-Myc; cell proliferation; myocardial I/R injury.
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