Adenylate cyclase 1 knockdown attenuates pirarubicin‐induced cardiotoxicity

This study aimed to investigate the effects and possible mechanisms of adenylate cyclase 1 (ADCY1) on pirarubicin-induced cardiomyocyte injury. HL-1 cells were treated with pirarubicin (THP) to induce intracellular toxicity, and the extent of damage to mouse cardiomyocytes was assessed using CCK-8, Edu, flow cytometry, ROS, ELISA, RT-qPCR and western blotting. THP treatment reduced the viability of HL-1 cells, inhibited proliferation, induced apoptosis and triggered oxidative stress. In addition, the RT-qPCR results revealed that ADCY1 expression was significantly elevated in HL-1 cells, and molecular docking showed a direct interaction between ADCY1 and THP. Western blotting showed that ADCY1, phospho-protein kinase A and GRIN2D expression were also significantly elevated. Knockdown of ADCY1 attenuated THP-induced cardiotoxicity, possibly by regulating the ADCY1/PKA/GRIN2D pathway.

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Publication Details

Journal
Clinical and Experimental Pharmacology and Physiology
Published
2024-09-03
DOI
https://doi.org/10.1111/1440-1681.13920
Primary Topic
Chemotherapy-induced cardiotoxicity and mitigation
Type
article
Field-Weighted Citation Impact
0.00

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article

Adenylate cyclase 1 knockdown attenuates pirarubicin‐induced cardiotoxicity

Dexian Wei, Jiahua Ji, Liqun Ren, Wenqing Zhang et al.
Clinical and Experimental Pharmacology and Physiology
Chemotherapy-induced cardiotoxicity and mitigation
article

Adenylate cyclase 1 knockdown attenuates pirarubicin‐induced cardiotoxicity

Dexian Wei, Jiahua Ji, Liqun Ren, Wenqing Zhang, Peng Huang, HongYuan Cheng, Zhiyun Shu
article en

Abstract

This study aimed to investigate the effects and possible mechanisms of adenylate cyclase 1 (ADCY1) on pirarubicin-induced cardiomyocyte injury. HL-1 cells were treated with pirarubicin (THP) to induce intracellular toxicity, and the extent of damage to mouse cardiomyocytes was assessed using CCK-8, Edu, flow cytometry, ROS, ELISA, RT-qPCR and western blotting. THP treatment reduced the viability of HL-1 cells, inhibited proliferation, induced apoptosis and triggered oxidative stress. In addition, the RT-qPCR results revealed that ADCY1 expression was significantly elevated in HL-1 cells, and molecular docking showed a direct interaction between ADCY1 and THP. Western blotting showed that ADCY1, phospho-protein kinase A and GRIN2D expression were also significantly elevated. Knockdown of ADCY1 attenuated THP-induced cardiotoxicity, possibly by regulating the ADCY1/PKA/GRIN2D pathway.

Clinical and Experimental Pharmacology and PhysiologyVol. 51(10)
Jilin University (CN)
National Natural Science Foundation of China
Good health and well-being
Openalex Percentile: Top 74%
Chemotherapy-induced cardiotoxicity and mitigation
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