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• W3020170123 abstract "Purpose: Placenta-derived Mesenchymal stromal cells (PMSCs) have been widely explored for tissue engineering applications and have demonstrated high proliferation and capacity for chondrogenic differentiation in vitro. However, rapid induction of PMSC chondrogenic differentiation during therapeutic transplantation remains extremely challenging. Our previous studies discovered that transcription factor Twist1 plays a crucial role in stem cell maintenance, proliferation and lineage commitment. Particularly, gene silencing Twist1 increased formation of chondrogenic nodules and expression of chondrogenic markers in micromass culture of murine limb bud mesenchymal cells [1]. The purpose of this study is to determine if Twist1 inhibition by shRNA could be utilized to accelerate human PMSC-mediated cartilage repair in a mouse cartilage defect model. Methods: In this study, PMSCs were isolated from human placenta delivered from normal term. PMSC stemness phenotype was evaluated by colony formation and flow cytometry. In vitro osteogenic, chondrogenic and adipogenic differentiation assays were performed to determine the multipotency. Lentivirus-mediated gene silence was used to test whether Twist1 inhibition could enhance chondrogenesis in PMSC pellet culture. A mouse knee joint cartilage defect model was used for in vivo study. Wild type and Twist1 deficient PMSC pellets were generated and inserted to fill the cartilage defects. After 4 weeks postoperatively, animals were euthanized and osteochondral units containing the defects were harvested. Alcian Blue/Orange G staining, Immunohistochemical staining (IHC) and RT-PCR analysis for Sox9, type II collagen (Col-II), and Aggrecan was performed to analyze in vitro and in vivo chondrogenesis. All experiments were repeated at least three times independently and data were presented as mean ± standard deviation (s.d.). Statistical significance among the groups was assessed with one-way ANOVA. The level of significance was P<0.05. Results: The flow cytometry results indicated that human stromal cell markers CD29, CD73, CD90 and proliferation marker Ki-67 were highly expressed in the 3rd generation PMSCs, and these cells could be induced into osteoblastic cells, adipocytes and chondrocytes when cultured in specific conditional media. Particularly, in PMSC chondrogenic cell pellet cultures, silencing Twist1 significantly enhanced chondrogenesis by showing increased Alcian blue staining, enhanced Col-II expression when compared to control wild type PMSCs (Fig. 1). Importantly, the in vivo transplantation of Twist1 deficient PMSCs into knee joint cartilage defects had a significantly enhanced cartilage formation by showing stronger Alcian blue and Col-II staining in cartilage defect area when compared with wild type PMSCs at 4 weeks after operation (Fig. 2). Finally, our PCR data showed an increased expression of chondrogenic markers Sox9, Col-II and aggrecan in knee joint tissue with transplantation of Twist1 deficient PMSCs when compared with wild type PMSCs. Conclusions: In this study, PMSCs were observed to have high proliferation and chondrogenic ability, especially when anti-chondrogenic gene Twist1 was silenced. This is in agreement with published studies that have similarly demonstrated the superior chondrogenic differentiation potential of PMSCs compared to other types of MSCs [2]. Collectively, these findings demonstrate that 1) PMSCs are a favorable cell source for cartilage repair. 2) Silencing transcript factor Twist1 could accelerate PMSC differentiation into chondrocyte under the cartilage microenvironment in vivo. Our Results strongly suggest that silencing Twist1 in stromal cells may be a promising strategy for cartilage regeneration." @default.
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• W3020170123 date "2020-04-01" @default.
• W3020170123 modified "2023-09-27" @default.
• W3020170123 title "Targeting Twist1 to promote stromal cell-mediated cartilage repair" @default.
• W3020170123 doi "https://doi.org/10.1016/j.joca.2020.02.788" @default.
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