We have located links that may give you full text access.
microRNA-451 protects neurons against ischemia/reperfusion injury-induced cell death by targeting CELF2.
Objectives: miRNAs are a family of non-coding RNAs that affect cell growth, migration and apoptosis. However, little is known on the behavior of miRNAs in neurons. Hence, this work aimed to investigate the functions and roles of miRNA-451 in neurons induced by ischemia/reperfusion injury.
Materials and methods: In this study, we established a 12- or 24-hour oxygen and glucose deprivation/reoxygenation (OGD/R) cell model. miR-451 mimic, si-CUGBP Elav-like family member 2 (siCELF2), oeCELF2 and the corresponding negative controls were transfected into the 24-hour OGD/R cells. The transfection efficiency and the relative expression of miR-451 and CELF2 were measured using quantitative reverse transcription PCR and Western blot analysis. Cell viability, apoptosis, oxidative stress and cleaved-caspase-3 expression were assessed using Cell Counting Kit-8, LDH, SOD, malondialdehyde, ROS assays, flow cytometry and Western blot analysis upon miR-451 overexpression, CELF2 silencing or overexpression of both. Bioinformatics analysis and the dual-luciferase reporter assay were used to examine the relationship between CELF2 and miR-451 in the OGD/R cells.
Results: The results showed that miR-451 was downregulated in the OGD/R cells. The overexpression of miR-451 increased cell viability and SOD activity, but decreased apoptosis rate, levels of LDH, MDA, ROS and cleaved caspase-3 expression. CELF2 silencing inhibited apoptosis and oxidative stress. The results suggested that CELF2 was a target of miR-451, and that CELF2 overexpression alleviated the inhibitory effect of miR-451 on apoptosis and oxidative stress of the OGD/R cells.
Conclusion: The results demonstrated that miR-451 could protect cells against OGD/R-induced apoptosis and oxidative stress by targeting CELF2.
Materials and methods: In this study, we established a 12- or 24-hour oxygen and glucose deprivation/reoxygenation (OGD/R) cell model. miR-451 mimic, si-CUGBP Elav-like family member 2 (siCELF2), oeCELF2 and the corresponding negative controls were transfected into the 24-hour OGD/R cells. The transfection efficiency and the relative expression of miR-451 and CELF2 were measured using quantitative reverse transcription PCR and Western blot analysis. Cell viability, apoptosis, oxidative stress and cleaved-caspase-3 expression were assessed using Cell Counting Kit-8, LDH, SOD, malondialdehyde, ROS assays, flow cytometry and Western blot analysis upon miR-451 overexpression, CELF2 silencing or overexpression of both. Bioinformatics analysis and the dual-luciferase reporter assay were used to examine the relationship between CELF2 and miR-451 in the OGD/R cells.
Results: The results showed that miR-451 was downregulated in the OGD/R cells. The overexpression of miR-451 increased cell viability and SOD activity, but decreased apoptosis rate, levels of LDH, MDA, ROS and cleaved caspase-3 expression. CELF2 silencing inhibited apoptosis and oxidative stress. The results suggested that CELF2 was a target of miR-451, and that CELF2 overexpression alleviated the inhibitory effect of miR-451 on apoptosis and oxidative stress of the OGD/R cells.
Conclusion: The results demonstrated that miR-451 could protect cells against OGD/R-induced apoptosis and oxidative stress by targeting CELF2.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
Perioperative echocardiographic strain analysis: what anesthesiologists should know.Canadian Journal of Anaesthesia 2024 April 11
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app