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ALDOA protects cardiomyocytes against H/R-induced apoptosis and oxidative stress by regulating the VEGF/Notch 1/Jagged 1 pathway

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Abstract

Myocardial infarction (MI) is a myocardial necrosis disease caused by continuous ischemia and hypoxia. Abnormal expression of aldolase A (ALDOA) has been reported in cardiac hypertrophy, heart failure and other cardio-cerebrovascular diseases. The present study aims to explore the effects of ALDOA on hypoxia/reperfusion (H/R)-induced oxidative stress, and investigate the underlying mechanisms. ALDOA was expressed at a low level in blood samples from MI patients and H/R-induced H9C2 cardiomyocytes. Overexpression of ALDOA suppressed H/R-induced oxidative stress and apoptosis. Using co-immunoprecipitation and protein blots, we demonstrated that ALDOA modulates the Notch 1–Jagged 1 signalling pathway by upregulating VEGF. Taken together, our data reveal that ALDOA protects cardiomyocytes from H/R-induced oxidative stress through the VEGF/Notch 1/Jagged 1 axis, and should be investigated as a therapeutic target for the treatment of MI in future.

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Authors and Affiliations

  1. Department of Clinical Laboratory, Xi’an No 5 Hospital, No. 112 West Main Street, Lianhu District, Xi’an, 710082, Shaanxi, China

    Gaiying Luo & Xiaoling Liu

  2. The Five Ward of Internal Medicine, Xi’an No 5 Hospital, Xi’an, 710082, Shaanxi, China

    Rui Wang & Hui Zhou

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  1. Gaiying Luo
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  2. Rui Wang
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  4. Xiaoling Liu
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XLL conceived and designed the study. GYL, RW and HZ performed the experiments. GYL provided the statistical analysis and wrote the paper. XLL reviewed and edited the manuscript.

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Correspondence to Xiaoling Liu.

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Luo, G., Wang, R., Zhou, H. et al. ALDOA protects cardiomyocytes against H/R-induced apoptosis and oxidative stress by regulating the VEGF/Notch 1/Jagged 1 pathway. Mol Cell Biochem 476, 775–783 (2021). https://doi.org/10.1007/s11010-020-03943-z

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  • DOI: https://doi.org/10.1007/s11010-020-03943-z

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