Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats
Abstract Background Previous in vitro studies demonstrated that suppression of microRNAs might protect cardiomyocytes and neurons against oxygen–glucose deprivation and reoxygenation (OGD/R)-induced cell apoptosis. However, whether the protective effect of miR-153-inhibition on cardiomyocytes can be...
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| Format: | Article |
| Language: | English |
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BMC
2020-03-01
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| Series: | BioMedical Engineering OnLine |
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| Online Access: | http://link.springer.com/article/10.1186/s12938-020-0759-6 |
| _version_ | 1819066489150373888 |
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| author | Wei Hou Xianting Zhu Juan Liu Jiaguo Map |
| author_facet | Wei Hou Xianting Zhu Juan Liu Jiaguo Map |
| author_sort | Wei Hou |
| collection | DOAJ |
| description | Abstract Background Previous in vitro studies demonstrated that suppression of microRNAs might protect cardiomyocytes and neurons against oxygen–glucose deprivation and reoxygenation (OGD/R)-induced cell apoptosis. However, whether the protective effect of miR-153-inhibition on cardiomyocytes can be observed in the animal model is unknown. We aimed to address this question using a rat model of ischemia–reperfusion (I/R). Methods Rats were received the intramyocardial injection of saline or adenovirus-carrying target or control gene, and the rats were subjected to ischemia/reperfusion (I/R) treatment. The effects of miR-153 on I/R-induced inflammatory response and oxidative stress in the rat model were assessed using various assays. Results We found that suppression of miR-153 decreased cleaved caspase-3 and Bcl-2-associated X (Bax) expression, and increased B cell lymphoma 2 (Bcl-2) expression. We further confirmed that Nuclear transcription factor erythroid 2-like 2 (Nrf2) is a functional target of miR-153, and Nrf2/Heme oxygenase-1 (HO-1) signaling was involved in miR-153-regulated I/R-induced cardiomyocytes apoptosis. Inhibition of miR-153 reduced I/R-induced inflammatory response and oxidative stress in rat myocardium. Conclusion Suppression of miR-153 exerts a cardioprotective effect against I/R-induced injury through the regulation of Nrf2/HO-1 signaling, suggesting that targeting miR-153, Nrf2, or both may serve as promising therapeutic targets for the alleviation of I/R-induced injury. |
| first_indexed | 2024-12-21T16:03:10Z |
| format | Article |
| id | doaj.art-ecaefa47860b484a91aaef12a358fd12 |
| institution | Directory Open Access Journal |
| issn | 1475-925X |
| language | English |
| last_indexed | 2024-12-21T16:03:10Z |
| publishDate | 2020-03-01 |
| publisher | BMC |
| record_format | Article |
| series | BioMedical Engineering OnLine |
| spelling | doaj.art-ecaefa47860b484a91aaef12a358fd122022-12-21T18:57:58ZengBMCBioMedical Engineering OnLine1475-925X2020-03-0119111410.1186/s12938-020-0759-6Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in ratsWei Hou0Xianting Zhu1Juan Liu2Jiaguo Map3Department of Emergency, Yidu Central Hospital of Wei FangDepartment of Nursing, Yidu Central Hospital of Wei FangDepartment of Pediatrics, Ward 1, Yidu Central Hospital of Wei FangDepartment of Cardiology, Qing Zhou Traditional Chinese HospitalAbstract Background Previous in vitro studies demonstrated that suppression of microRNAs might protect cardiomyocytes and neurons against oxygen–glucose deprivation and reoxygenation (OGD/R)-induced cell apoptosis. However, whether the protective effect of miR-153-inhibition on cardiomyocytes can be observed in the animal model is unknown. We aimed to address this question using a rat model of ischemia–reperfusion (I/R). Methods Rats were received the intramyocardial injection of saline or adenovirus-carrying target or control gene, and the rats were subjected to ischemia/reperfusion (I/R) treatment. The effects of miR-153 on I/R-induced inflammatory response and oxidative stress in the rat model were assessed using various assays. Results We found that suppression of miR-153 decreased cleaved caspase-3 and Bcl-2-associated X (Bax) expression, and increased B cell lymphoma 2 (Bcl-2) expression. We further confirmed that Nuclear transcription factor erythroid 2-like 2 (Nrf2) is a functional target of miR-153, and Nrf2/Heme oxygenase-1 (HO-1) signaling was involved in miR-153-regulated I/R-induced cardiomyocytes apoptosis. Inhibition of miR-153 reduced I/R-induced inflammatory response and oxidative stress in rat myocardium. Conclusion Suppression of miR-153 exerts a cardioprotective effect against I/R-induced injury through the regulation of Nrf2/HO-1 signaling, suggesting that targeting miR-153, Nrf2, or both may serve as promising therapeutic targets for the alleviation of I/R-induced injury.http://link.springer.com/article/10.1186/s12938-020-0759-6Ischemia–reperfusionRatMiR-153Nrf2Adenoviral delivery |
| spellingShingle | Wei Hou Xianting Zhu Juan Liu Jiaguo Map Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats BioMedical Engineering OnLine Ischemia–reperfusion Rat MiR-153 Nrf2 Adenoviral delivery |
| title | Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats |
| title_full | Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats |
| title_fullStr | Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats |
| title_full_unstemmed | Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats |
| title_short | Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats |
| title_sort | inhibition of mir 153 ameliorates ischemia reperfusion induced cardiomyocytes apoptosis by regulating nrf2 ho 1 signaling in rats |
| topic | Ischemia–reperfusion Rat MiR-153 Nrf2 Adenoviral delivery |
| url | http://link.springer.com/article/10.1186/s12938-020-0759-6 |
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