2022/08/31 by Magdalena Nowaczyk, Agnieszka Malcher, Agnieszka Zimna +2 · 3 citations
Biochemistry, Genetics and Molecular Biology · Medicine · #Biology #C2C12 #Cell biology #Immunology #Internal medicine #Medicine #Mesenchymal stem cell research #MicroRNA in disease regulation #Molecular biology #Muscle Physiology and Disorders #MyoD #Myocyte #Myogenesis #Population #Progenitor cell #Skeletal muscle #Stem cell
paper · pdf · doi:10.33963/kp.a2022.0127
published in Kardiologia Polska 80(7-8), 813-824 (Via Medica)
crossref issued 2022/08/31 · crossref published 2022/08/31 · crossref published-online 2022/08/31 · openalex publication_date 2022/08/31 · crossref created 2022/09/02 · crossref deposited 2022/09/02 · openalex created_date 2025/10/10 · crossref indexed 2026/08/04 · openalex updated_date 2026/08/05
BACKGROUND: The application of a circulating miR-195 inhibitor could be a helping factor in the in vitro model of human skeletal muscle-derived stem/progenitor cells (SkMDS/PCs). Previously, microRNA-195 (miR-195) expression has been reported to be a negative factor for myogenesis. AIMS: The study aimed to obtain anti-apoptotic and anti-aging effects in in vitro cultured myoblasts and to improve their ability to form myotubes by suppressing miR-195 expression. METHODS: Human wild-type (WT) SkMDS/PC cells incubated with control (nonspecific) miRNA inhibitor and miR-195-inhibited SkMDS/PCs were studied. Functional assays (myotube formation and cell aging), antioxidant, and myogenic gene expression analyses were performed at two time points, at the seventh and eleventh cell passages. RESULTS: Myotube formation was found to be almost 2-fold higher in the miR-195-inhibited SkMDS/PCs population (P < 0.05) compared to WT cells. miR-195 inhibition did not appear to affect cell aging or rejuvenate human SkMDS/PCs. Antioxidant (SOD3 and FOXO) gene expression was augmented in the miR-195-inhibited SkMDS/PCs population, but no positive effect on the remaining antioxidant genes (SOD1, SOD2, and catalase) was observed. A significant increase in MyoD gene expression with a concomitant decrease in MyoG (P < 0.05) was further documented in miR-195- -inhibited SkMDS/PCs compared to WT cells (the eleventh cell passage). CONCLUSIONS: The performed studies may lead to the preconditioning of myogenic stem cells to extend their potential for pro-regenerative activity. The miR-195 inhibitor may serve as a conditioning factor augmenting selective antioxidant gene expression and proliferative potential of SkMDS/PCs, but it does not have an impact on cell aging and/ or apoptosis.