Show pageBacklinksCite current pageExport to PDFFold/unfold allBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. [[Flow cytometry]] was prepared for assessing [[THP-1]]-derived macrophage [[apoptosis]]. The protein and expression levels of miR-34a-5p and [[MDM4]] were examined by [[Western blot]] and RT-qPCR, respectively. They also measured the levels of total [[cholesterol]] (TC) and [[triglyceride]] to determine the [[lipid]] accumulation. Subsequently, the activities of superoxide dismutase, malondialdehyde, and reactive oxygen species revealed the level of oxidative stress injury after miR-34a-5p and MDM4 knockdown. After ox-LDL treatment, cell apoptosis of macrophages increased in a dose-dependent and time-dependent manner. With the increase of ox-LDL treatment and the prolongation of treatment time, the expression level of miR-34a-5p was upregulated. Next, interfering with miR-34a-5p inhibited lipid accumulation and oxidative stress injury in ox-LDL-stimulated macrophages. MDM4 was a target gene of miR-34a-5p and was upregulated in ox-LDL-stimulated macrophages. With the increase of ox-LDL treatment and the prolongation of treatment time, the expression level of MDM4 was downregulated. Importantly, MDM4 knockdown partially counteracted the inhibitory effect of miR-34a-5p on oxidative stress injury. MicroRNA miR-34a-5p[[ knockdown]] suppressed [[oxidative stress]] injury via [[MDM4]] in ox-LDL-treated [[macrophage]]s ((Kong J, Liu L, Song L, Zhao R, Feng Y. MicroRNA miR-34a-5p inhibition restrains oxidative stress injury of macrophages by targeting MDM4. Vascular. 2022 Feb 28:17085381211069447. doi: 10.1177/17085381211069447. Epub ahead of print. PMID: 35226569.)). thp-1.txt Last modified: 2025/04/29 20:23by 127.0.0.1