Folic acid pretreatment and its sustained delivery for chondrogenic differentiation of MSCs

软骨发生 阿格里坎 软骨寡聚基质蛋白 间充质干细胞 化学 软骨 糖胺聚糖 II型胶原 细胞生物学 生物化学 骨关节炎 关节软骨 医学 生物 解剖 病理 替代医学
作者
Yuna Moon,Madhumita Patel,Soyoun Um,Hyun Jung Lee,Sohee Park,Soo-Bong Park,Sun‐Shin Cha,Byeongmoon Jeong
出处
期刊:Journal of Controlled Release [Elsevier]
卷期号:343: 118-130 被引量:5
标识
DOI:10.1016/j.jconrel.2022.01.018
摘要

Dietary uptake of folic acid (FA) improves cartilage regeneration. In this work, we discovered that three days of FA treatment is highly effective for promoting chondrogenic differentiation of tonsil-derived mesenchymal stem cells (TMSCs). In a three-dimensional pellet culture, the levels of typical chondrogenic biomarkers, sulfated glycosaminoglycan, proteoglycan, type II collagen (COL II), SRY box transcription factor 9 (SOX 9), cartilage oligomeric matrix protein (COMP), and aggrecan (ACAN) increased significantly in proportion to FA concentration up to 30 μM. At the mRNA expression level, COL II, SOX 9, COMP, and ACAN increased 3.6-6.0-fold with FA treatment at 30 μM compared with the control system that did not receive FA treatment, and the levels with FA treatment were 1.6-2.5 times greater than those in the kartogenin-treated positive control system. FA treatment did not increase type I collagen α1 (COL I α1), an osteogenic biomarker which is a concern with most chondrogenic promoters. At the high FA concentration of 100 μM, significant decreases in chondrogenic biomarkers were observed, which might be related to DNA methylation. A thermogel system incorporating TMSCs and FA provided sustained release of FA over several days, similar to the FA treatment. The thermogel system confirmed the efficacy of FA in promoting chondrogenic promotion of TMSCs. The increased nuclear translocation of core-binding factor β subunit (CBFβ) and the runt-related transcription factor 1 (RUNX1) expression after FA treatment, together with molecular docking studies, suggest that the chondrogenic enhancement mechanism of FA is mediated by CBFβ and RUNX1.
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