miR‐324‐5p protects against oxidative stress‐induced endothelial progenitor cell injury by targeting Mtfr1

Abstract

Endothelial progenitor cells (EPCs) belong to bone marrow-derived myeloid progenitor cells that have strong proliferative ability. Dysregulation of miRNAs after acute myocardial infarction (AMI) can result in EPCs injury, thus we hypothesize that correction of miRNA expression may contribute to the tolerance of EPCs against oxidative stress. The peripheral blood of healthy volunteers and patients with ST-segment elevation myocardial infarction (STEMI) was clinically collected. EPCs derived from peripheral blood were transfected by miR-324-5p mimic and simultaneously handled with hydrogen peroxide (H 2 O 2 ) to inducing EPCs injury. At 24 hrs after the H 2 O 2 treatment, cell viability, the uptake capacity on DiI-Ac-LDL, and carrying ability on FITC-UEA-l and multiplication capacity were analyzed. The mechanism process was carefully researched by valued the characteristics of the mitochondrion morphology, membrane potential, ATP levels, and the expressing of apoptosis pathways. Small RNA sequencing indicated that the expression level of miR-324-5p in peripheral blood EPCs of patients with STEMI was significantly lower compared with the healthy volunteers. The Mtfr1 has been confirmed as a targeted gene of miR-324-5p through miRTarBase software and western blot. The miR-324-5p mimic units could be contributed for the improvement of viability, the uptake capacity on DiI-Ac-LDL and carrying ability on FITC-UEA-l and multiplication capacity on oxidative stress-injured EPCs. miR-324-5p could suppress mitochondrial fragmentation, promote membrane potential, and ATP levels, as well as protect against oxidative stress-induced EPCs apoptosis. Our results suggested that miR-324-5p protects against oxidative stress-induced EPCs injury by regulating Mtfr1. K E Y W O R D SEPCs, injury, miR-324-5p, Mtfr1, oxidative stress

Inhibition of the LncRNA Gpr19 attenuates ischemia‐reperfusion injury after acute myocardial infarction by inhibiting apoptosis and oxidative stress via the miR‐324‐5p/Mtfr1 axis

“…Mtfr1, as a mitochondrial protein, contains a short polyformaldehyde‐rich region . The function of Mtfr1 is mainly related to the mitochondrial inner membrane . Recent findings indicate that Mtfr1 has a close relationship with apoptosis and oxidative stress .…”

“…26 The function of Mtfr1 is mainly related to the mitochondrial inner membrane. 26,27 Recent findings indicate that Mtfr1 has a close relationship with apoptosis and oxidative stress. 15 In the present study, we demonstrated that overexpression of Mtfr1 could partially block the role of Gpr19 inhibition in suppressing oxidative stress and apoptosis in NRCMs induced by OGD/R.…”

CircRNA-006258 Sponge-Adsorbs miR-574-5p to Regulate Cell Growth and Milk Synthesis via EVI5L in Goat Mammary Epithelial Cells

“…Recently, researchers found that miRNAs can bind to 3’ untranslated region (3’ UTR) of target messenger RNAs (mRNAs) and negatively regulate gene expression by transcriptional or translational inhibition [ 1 , 2 , 3 ]. MiR-574-5p are implicated in the pathophysiology of many tumors, including breast cancer, colorectal cancer and other oncoma [ 4 , 5 , 6 ]. In addition, miR-574-5p is a very important regulator for cell migration and proliferation [ 7 , 8 , 9 ].…”

Identification and validation of hub genes for diabetic retinopathy

“…MTFR1, a target gene of miR-324-5p ( Ye et al, 2019 ), encodes a mitochondrial protein that can promote mitochondrial fission and is crucially involved in oxidative stress. Suppressing MTFR1 translation attenuates mitochondrial fission, apoptosis and myocardial infarction ( Wang et al, 2015 ), which indicates that excessive expression of MTFR1 aggravates mitochondrial fission and apoptosis, meanwhile regulating MTFR1might afford protection against oxidative stress-induced endothelial progenitor cell injury ( Chen et al, 2019 ). Mitochondrial function has a profound effect on DR ( Shao et al, 2019 ), among these influences, MTFR1 in all probability might play a vital role in the mechanism of DR. ACADL belongs to the mitochondrial flavoenzyme family that are commonly involved in fatty acid.…”