Synovial fluid mesenchymal stem cell-derived microRNA-127-5p can modulate transforming growth factor-β signaling after in vitro chondrogenic induction

SEMERCİ SEVİMLİ T., İNAN U., Qomi Ekenel E., Ozgul C., Danaci C. O., Cetinkaya S., ...More

Cytotechnology, vol.77, no.1, 2025 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 77 Issue: 1
  • Publication Date: 2025
  • Doi Number: 10.1007/s10616-024-00660-z
  • Journal Name: Cytotechnology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Biotechnology Research Abstracts, CAB Abstracts, EMBASE, Veterinary Science Database
  • Keywords: Cartilage, Chondrogenesis, Mesenchymal stem cells, microRNA-127-5p, TGF-β pathway
  • Middle East Technical University Affiliated: Yes

Abstract

MicroRNA profiling in human cartilage is necessary for chondrogenesis. The study aimed to compare microRNA 127-5p (miR-127-5p) and TGF-β signaling pathway gene expressions of human adipose tissue-derived mesenchymal stem cells (hAT-MSCs) and synovial fluid-derived stem cells (hSF-MSCs) after induced chondrogenesis. MSCs induced into chondrogenic differentiation. Alcian Blue and Safranin O staining were performed to determine chondrogenic differentiation. The RT-qPCR determined the expression levels of miR-127-5p and TGF-β signaling pathway genes. miR-127-5p expression was significantly higher in chondrogenic differentiated hSF-MSCs (dhSF-MSCs) (p < 0.05). TGF-β, SMAD2, and SMAD3 expressions were substantially higher in dhSF-MSCs (all p < 0.001), while SMAD4, and ACAN expressions were downregulated (all p < 0.001). No difference was detected between COL1A2 expression levels. This study suggests that miR-127-5p derived from hSF-MSCs may regulate chondrogenesis, thereby inducing the TGF-β pathway activation, and also presents, for the first time, a comparative analysis of the expression of miR-127-5p and the TGF-β signaling pathway genes of hSF-MSCs and hAT-MSCs concerning differences in chondrogenic potential. Graphical abstract: (Figure presented.)