Conclusions
CircRNA circ-GTF2I aggravated MIRI and neonatal rat cardiomyocyte damage in vivo and in vitro by regulating miR-590-5p and the heart development transcription factor KBTBD7.
Methods
The cell experiment was performed by using neonatal rat cardiomyocytes. Moreover, a hypoxia/reoxygenation treatment model was established. Cell Counting Kit-8 assay was conducted, and EdU cell proliferation was detected. Cell apoptosis was detected via flow cytometry and quantitative RT-PCR (RT-qPCR). Binding detection was performed through a double-luciferase reporter assay. Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and lactate dehydrogenase (LDH) were detected via enzyme-linked immunosorbent assay (ELISA).
Purpose
We investigated the effect of the circular RNA (circRNA) general transcription factor IIi (GTF2I) on myocardial ischemia (MI) deterioration and neonatal rat cardiomyocyte damage.
Results
Compared with that in the sham and control groups, circ-GTF2I expression in MIRI and the hypoxia/reoxygenation treatment model was significantly upregulated in vivo and in vitro. The knockdown of circ-GTF2I relieved neonatal rat cardiomyocyte damage and MI. Further detection through the double-luciferase reporter assay confirmed that the binding site of circ-GTF2I to miR-590-5p and miR-590-5p was Kelch repeat and BTB domain-containing protein 7 (KBTBD7). ELISA and RT-qPCR results showed that circ-GTF2I induced the abnormal expressions of IL-6 TNF-α, LDH, Bax, Bcl-2, and Cyt-c in MIRI and the hypoxia/reoxygenation treatment models by regulating miR-590-5p and the heart development transcription factor KBTBD7. Conclusions: CircRNA circ-GTF2I aggravated MIRI and neonatal rat cardiomyocyte damage in vivo and in vitro by regulating miR-590-5p and the heart development transcription factor KBTBD7.