MiR-21 suppresses ox-LDL-induced HUVECs apoptosis by targeting PDCD4

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• Cellular Biology

Background:

• Oxidized low-density lipoprotein (ox-LDL) is implicated in endothelial dysfunction and atherosclerosis.
• MicroRNAs (miRNAs) play crucial roles in regulating cellular processes, including apoptosis.
• Endothelial cell apoptosis contributes to the pathogenesis of cardiovascular diseases.

Purpose of the Study:

• To investigate the role of microRNA-21 (miR-21) in ox-LDL-induced apoptosis of human umbilical vein endothelial cells (HUVECs).
• To elucidate the molecular mechanisms by which miR-21 affects endothelial cell apoptosis in response to ox-LDL.

Main Methods:

• Cell proliferation was assessed using MTT assays.
• Quantitative RT-PCR was employed to measure miR-21 expression levels.
• Western blotting was utilized to determine protein expression.
• Annexin V/propidium iodide double staining was performed to detect and quantify cell apoptosis.

Main Results:

• Ox-LDL significantly induced HUVECs apoptosis and concurrently reduced miR-21 expression.
• Overexpression of miR-21 (using miR-21 mimic) attenuated ox-LDL-induced HUVECs apoptosis.
• Inhibition of miR-21 (using miR-21 inhibitors) exacerbated ox-LDL-induced HUVECs apoptosis.
• MiR-21 was found to directly target Programmed Cell Death 4 (PDCD4).
• MiR-21 modulated the expression of key apoptotic proteins including Bax, Bad, Bcl-2, and Caspase-3.
• MiR-21 enhanced the phosphorylation of Extracellular signal-regulated kinase (ERK).

Conclusions:

• MiR-21 plays a protective role against ox-LDL-induced apoptosis in HUVECs.
• The mechanism involves the direct targeting of PDCD4 and regulation of downstream apoptotic pathways.
• MiR-21 may represent a potential therapeutic target for preventing ox-LDL-mediated endothelial injury in cardiovascular diseases.