Curcumin-primed human BMSC-derived extracellular vesicles reverse IL-1β-induced catabolic responses of OA chondrocytes by upregulating miR-126-3p.
Shushan LiSabine StöcklChristoph LukasMarietta HerrmannChristoph BrochhausenMatthias A KönigBrian JohnstoneSusanne GrässelPublished in: Stem cell research & therapy (2021)
Cur-EVs alleviated IL-1β-induced catabolic effects on OA-CH by promoting viability and migration, reducing apoptosis and phosphorylation of Erk1/2, PI3K/Akt, and p38 MAPK thereby modulating pro-inflammatory signaling pathways. Treatment of OA-CH with Cur-EVs is followed by upregulation of expression of hsa-miR-126-3p which is involved in modulation of anabolic response of OA-CH. EVs may be considered as promising drug delivery vehicles of curcumin helping to alleviate OA.
Keyphrases
- signaling pathway
- pi k akt
- cell cycle arrest
- knee osteoarthritis
- cell proliferation
- high glucose
- drug delivery
- poor prognosis
- diabetic rats
- endothelial cells
- room temperature
- epithelial mesenchymal transition
- induced apoptosis
- oxidative stress
- cell death
- drug induced
- protein kinase
- long non coding rna
- binding protein
- drug release