Comparative impact of platelet rich plasma and transforming growth factor-β on chondrogenic differentiation of human adipose derived stem cells.
Roya HesariMina KeshvariniaMahboubeh KabiriIman RadKazem ParivarHoorieh HoseinpoorRezvan TavakoliMasoud SoleimaniFatemeh KouhkanSoheila ZamanlueeHana Hanaee-AhvazPublished in: BioImpacts : BI (2019)
Introduction: Transforming growth factor-beta (TGF-β) is known as standard chondrogenic differentiation agent, even though it comes with undesirable side effects such as early hypertrophic maturation, mineralization, and secretion of inflammatory/angiogenic factors. On the other hand, platelet-rich plasma (PRP) is found to have a chondrogenic impact on mesenchymal stem cell proliferation and differentiation, with no considerable side effects. Therefore, we compared chondrogenic impact of TGF-β and PRP on adipose-derived stem cells (ADSCs), to see if PRP could be introduced as an alternative to TGF-β. Methods: Differentiation of ADSCs was monitored using a couple of methods including glycosaminoglycan production, miRNAs expression, vascular endothelial growth factor (VEGF)/tumor necrosis factor alpha (TNFα) secretion, alkaline phosphatase (ALP) and calcium content assays. Results: Accordingly, the treatment of differentiating cells with 5% (v/v) PRP resulted in higher glycosaminoglycan production, enhanced SOX9 transcription, and lowered TNFα and VEGF secretion compared to the control and TGF-β groups. Besides, the application of PRP to the media up-regulated miR-146a and miR-199a in early and late stages of chondrogenesis, respectively. Conclusion: PRP induces in vitro chondrogenesis, as well as TGF-β with lesser inflammatory and hypertrophic side effects.
Keyphrases
- platelet rich plasma
- transforming growth factor
- vascular endothelial growth factor
- cell proliferation
- epithelial mesenchymal transition
- endothelial cells
- mesenchymal stem cells
- rheumatoid arthritis
- long non coding rna
- stem cells
- oxidative stress
- poor prognosis
- long noncoding rna
- signaling pathway
- magnetic resonance imaging
- binding protein
- high throughput
- cell death
- single cell
- replacement therapy