Background
Pressure ulcer (PU) is a common complication of acute and long-time hospitalization, especially in elderly patients. The incidence and prevalence of PU are swiftly fortifying. Currently, our
Conclusion
Our data suggested that circ-Ttc3 alleviated hypoxic injury and activated NF-κB and PI3K/AKT pathways by downregulating miR-449a in HaCaT cells.
Methods
HaCaT cells were pretreated under hypoxia condition. Cell counting kit 8 assay and flow cytometry were utilized to test HaCaT cell viability and apoptosis. Quantitative reverse transcription polymerase chain reaction was utilized to determine circ-Ttc3 and miR-449a expression. Western blot was performed to examine apoptosis-associated proteins expression. Subsequently, the above-described investigations were reperformed after miR-449a upregulation.
Results
Hypoxia induced apoptosis and declined viability in HaCaT cells. Circ-Ttc3 expression was enhanced after transfection with circ-Ttc3 expressing vector. Overexpressing circ-Ttc3 raised viability and reduced apoptosis in HaCaT cells. Moreover, miR-449a expression was elevated by hypoxia and reversed by overexpressing circ-Ttc3. And circ-Ttc3 exerted its effect via downregulating miR-449a. Finally, overexpressing circ-Ttc3 activated nuclear factor kappa-B (NF-κB) and phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) pathways via downregulating miR-449a.