LAUSR.org creates dashboard-style pages of related content for over 1.5 million academic articles. Sign Up to like articles & get recommendations!

MiR‐182‐5p inhibited oxidative stress and apoptosis triggered by oxidized low‐density lipoprotein via targeting toll‐like receptor 4

Photo from wikipedia

MicroRNAs (miRNAs) exhibit various roles in multiple biological processes and abnormal expression of miR‐182‐5p has been involved in many diseases. However, the role miR‐182‐5p in Atherosclerosis (AS) remains poorly understood.… Click to show full abstract

MicroRNAs (miRNAs) exhibit various roles in multiple biological processes and abnormal expression of miR‐182‐5p has been involved in many diseases. However, the role miR‐182‐5p in Atherosclerosis (AS) remains poorly understood. In our current investigation, an AS model was established by using oxidized low‐density lipoprotein (ox‐LDL) in RAW264.7 cells. miR‐182‐5p was markedly decreased in AS model dose‐dependently and time‐dependently. Additionally, CD36, oil‐red staining levels, TC, and TG were inhibited by miR‐182‐5p mimics, meanwhile ROS levels, MDA, and cell apoptosis were also restrained with an enhancement of SOD activity. Consistently, opposite results were exhibited when miR‐182‐5p inhibitors were transfected into RAW264.7 cells. It is well known that toll‐like receptor 4 (TLR4) is responsible for many inflammation diseases. By using bioinformatics analysis, TLR4 was indicated as a potential target of miR‐182‐5p. We observed TLR4 was activated in AS models and miR‐182‐5p could repress AS progression by targeting TLR4 in vitro. In conclusion, we uncovered that miR‐182‐5p played significant roles in AS through inhibiting oxidative stress and apoptosis via inactivating TLR4 expression.

Keywords: toll like; oxidized low; apoptosis; mir 182; density lipoprotein; low density

Journal Title: Journal of Cellular Physiology
Year Published: 2018

Link to full text (if available)


Share on Social Media:                               Sign Up to like & get
recommendations!

Related content

More Information              News              Social Media              Video              Recommended



                Click one of the above tabs to view related content.