Abstract
Rationale
Ischemic heart disease is one of leading causes of death worldwide. Prompt restoration of blood flow can resuscitate post-ischemic myocardium but paradoxically aggravates myocardial injury, termed as ischemia/reperfusion injury (IRI). HSP70, encoded by Hspa1b, was significantly increased upon myocardial ischemia and protected against IRI. However, the underlying mechanisms are largely unknown.
Objective
To investigate if Hspa1b protects against hypoxia/reoxygenation (H/R)-induced cell injury and the molecular mechanisms in H9C2 cardiomyocytes.
Method
Knockdown of Hspa1b model was established using siRNA technology in H9C2 cells, followed by H/R treatment. Cell injury was evaluated by LDH release and CCK8 assay. Cell apoptosis was assessed by TUNEL assay and pro-apoptotic markers (cleaved caspase 3, Bax).
Result
Hspa1b mRNA level was significantly enhanced in the post-ischemic rat myocardium and H/R-treated H9C2 cells. Knockdown of Hspa1b significantly exacerbated H/R-induced cell injury and apoptosis. A significant enhancement of p53 was observed in the Hspa1b knockdown cells upon H/R treatment, while PFTα (p53 inhibitor) alleviated H/R-induced cell injury in Hspa1b knockdown cells.
Conclusion:
Upon H/R stimulation, knockdown of Hspa1b significantly aggravates cell injury and apoptosis via activation of p53 in H9C2 cells.
Ischemic heart disease is one of leading causes of death worldwide. Prompt restoration of blood flow can resuscitate post-ischemic myocardium but paradoxically aggravates myocardial injury, termed as ischemia/reperfusion injury (IRI). HSP70, encoded by Hspa1b, was significantly increased upon myocardial ischemia and protected against IRI. However, the underlying mechanisms are largely unknown.
Objective
To investigate if Hspa1b protects against hypoxia/reoxygenation (H/R)-induced cell injury and the molecular mechanisms in H9C2 cardiomyocytes.
Method
Knockdown of Hspa1b model was established using siRNA technology in H9C2 cells, followed by H/R treatment. Cell injury was evaluated by LDH release and CCK8 assay. Cell apoptosis was assessed by TUNEL assay and pro-apoptotic markers (cleaved caspase 3, Bax).
Result
Hspa1b mRNA level was significantly enhanced in the post-ischemic rat myocardium and H/R-treated H9C2 cells. Knockdown of Hspa1b significantly exacerbated H/R-induced cell injury and apoptosis. A significant enhancement of p53 was observed in the Hspa1b knockdown cells upon H/R treatment, while PFTα (p53 inhibitor) alleviated H/R-induced cell injury in Hspa1b knockdown cells.
Conclusion:
Upon H/R stimulation, knockdown of Hspa1b significantly aggravates cell injury and apoptosis via activation of p53 in H9C2 cells.
| Original language | English |
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| Publication status | Published - 26 Jun 2023 |
| Event | SHVM 2023 - Graz, Austria Duration: 25 Jun 2023 → 28 Jul 2023 |
Conference
| Conference | SHVM 2023 |
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| Country/Territory | Austria |
| City | Graz |
| Period | 25/06/23 → 28/07/23 |