Up-regulation of CTRP12 ameliorates hypoxia/re-oxygenation-induced cardiomyocyte injury by inhibiting apoptosis, oxidative stress, and inflammation via the enhancement of Nrf2 signaling

Zhang, Qian-Rong; Yang, Cuiling; Sha, Ye; Cheng, Haijuan; Zheng, Yuanyuan

doi:10.1177/09603271211021880

Cited by 6 publications

(2 citation statements)

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“…CCK-8 assays and the determination of LDH activity are sensitive tools for evaluating myocardial cell viability and injury, respectively ( 35 ). In the present study, following CTRP12 overexpression, cell viability was significantly improved and LDH activity was significantly reduced, supporting the hypothesis that CTRP12 has a protective effect against I/R-induced cardiomyocyte injury, which is consistent with previous studies ( 17 , 36 ).…”

Section: Discussionsupporting

confidence: 93%

“…Moreover, Fadaei et al ( 16 ) reported that the serum levels of CTRP12 were decreased and negatively associated with TNF-α and IL-6 in patients with coronary artery disease. Consistent with previously published findings ( 36 ), the results of the present study demonstrated that the secretory levels of TNF-α, IL-1β and IL-6 were significantly increased in cell culture supernatants from H/R-treated cells, whereas CTRP12 overexpression significantly abrogated this effect. These findings indicated that CTRP12 overexpression may protect cardiomyocytes against H/R-induced inflammation.…”

Section: Discussionsupporting

confidence: 93%

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CTRP12 alleviates cardiomyocyte ischemia‑reperfusion injury via regulation of KLF15

Liao

Tian

2022

Mol Med Rep

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Myocardial ischemia-reperfusion (I/R) serves a crucial role in myocardial infarction. C1q/TNF-related protein 12 (CTRP12) is a secretory protein involved in metabolism. It has been reported that CTRP12 participates in the regulation of numerous cardiovascular diseases. However, its role in myocardial I/R injury remains unclear. In the present study, the left anterior descending coronary artery in mice was ligated to establish a mouse I/R model. A myocardial hypoxia-reoxygenation (H/R) cell model was also established. Cardiomyocyte injury was evaluated using hematoxylin and eosin staining, Cell Counting Kit-8 and a lactate dehydrogenase (LDH) kit. The expression levels of CTRP12 and Krueppel-like factor 15 (KLF15) in murine myocardial tissues and H9c2 cells were determined using reverse transcription-quantitative PCR and western blotting, as KLF15 was previously reported to protect against I/R-induced cardiomyocyte damage. Furthermore, inflammatory factors TNF-α, IL-1β and IL-6 were analyzed using ELISA while apoptosis was assessed using TUNEL assays and western blotting. Moreover, the activity of the CTRP12 promoter was determined using a dual-luciferase reporter assay. The results demonstrated that I/R surgery markedly exacerbated myocardial tissue damage, whereas H/R treatment significantly reduced cell viability and significantly increased LDH activity as well as the release of inflammatory factors and apoptosis. I/R and H/R induction significantly reduced the expression levels of CTRP12 and KLF15. CTRP12 overexpression significantly alleviated H/R-induced cell injury and significantly inhibited inflammation and apoptosis. Further analysis demonstrated that KLF15 could significantly promote the activity of the CTRP12 promoter. However, following CTRP12 knockdown, KLF15 overexpression exacerbated cell injury, inflammation and apoptosis. In conclusion, the present study demonstrated that CTRP12 may mitigate inflammation and apoptosis in H/R-induced cardiomyocytes, possibly via the regulation of KLF15, which provided a theoretical basis for the potential treatment of I/R-induced myocardial infarction.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%