MicroRNA‑301a‑3p increases oxidative stress, inflammation and apoptosis in ox‑LDL‑induced HUVECs by targeting KLF7
Affiliations: Cardiac Function Examination Room, Quanzhou First Hospital, Quanzhou, Fujian 362000, P.R. China
- Published online on: March 29, 2021 https://doi.org/10.3892/etm.2021.10001
Copyright: © Jiang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Arteriosclerotic cardiovascular disease is an inflammatory disease of ischemia or endothelial dysfunction caused by atherosclerosis, thereby causing high mortality. The viability and apoptosis of human umbilical vein endothelial cells (HUVECs) following oxidized low‑density lipoprotein (ox‑LDL) induction or transfection was detected by Cell Counting Kit‑8 (CCK‑8) assay and flow cytometry analysis. MicroRNA (miR)‑301a‑3p and Krueppel‑like factor 7 (KLF7) mRNA expression was determined by reverse transcription‑quantitative PCR (RT‑qPCR). The levels of monocyte chemoattractant protein‑1 (MCP‑1) and IL‑6, activities of reactive oxygen species and superoxide dismutase and lactate dehydrogenase leakage were analyzed by respective commercial assay kits. The protein expression of IL‑6, MCP‑1, Bcl2, Bax, poly (ADP‑ribose) polymerase (PARP), cleaved PARP, pro‑caspase3 and cleaved caspase‑3 was detected by western blotting. miR‑301a‑3p expression is highly expressed in ox‑LDL‑induced HUVECs. miR‑301a‑3p is also a target of KLF7. Inhibition of miR‑301a‑3p suppressed oxidative stress, inflammation and apoptosis in ox‑LDL‑induced HUVECs, which was reversed by KLF7 inhibition. In conclusion, miR‑301a‑3p promotes oxidative stress, inflammation and apoptosis in ox‑LDL‑induced HUVECs via decreasing KLF7 expression.