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软骨分化的脂肪来源间充质干细胞片对实验性兔模型中退变关节软骨的软骨保护作用

Chondroprotective Effects of Chondrogenic Differentiated Adipose-Derived Mesenchymal Stem Cells Sheet on Degenerated Articular Cartilage in an Experimental Rabbit Model.

作者信息

Taninaka Atsushi, Kabata Tamon, Hayashi Katsuhiro, Kajino Yoshitomo, Inoue Daisuke, Ohmori Takaaki, Ueoka Ken, Yamamuro Yuki, Kataoka Tomoyuki, Saiki Yoshitomo, Yanagi Yu, Ima Musashi, Iyobe Takahiro, Tsuchiya Hiroyuki

机构信息

Department of Orthopaedic Surgery, Graduate School of Medical Sciences, Kanazawa University, Ishikawa 920-8641, Japan.

出版信息

Bioengineering (Basel). 2023 May 10;10(5):574. doi: 10.3390/bioengineering10050574.

DOI:10.3390/bioengineering10050574
PMID:37237645
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10215072/
Abstract

Adipose-derived stem cells (ADSCs) have been studied for many years as a therapeutic option for osteoarthritis (OA); however, their efficacy remains insufficient. Since platelet-rich plasma (PRP) induces chondrogenic differentiation in ADSCs and the formation of a sheet structure by ascorbic acid can increase the number of viable cells, we hypothesized that the injection of chondrogenic cell sheets combined with the effects of PRP and ascorbic acid may hinder the progression of OA. The effects of induction of differentiation by PRP and formation of sheet structure by ascorbic acid on changes in chondrocyte markers (collagen II, aggrecan, Sox9) in ADSCs were evaluated. Changes in mucopolysaccharide and VEGF-A secretion from cells injected intra-articularly in a rabbit OA model were also evaluated. ADSCs treated by PRP strongly chondrocyte markers, including type II collagen, Sox9, and aggrecan, and their gene expression was maintained even after sheet-like structure formation induced by ascorbic acid. In this rabbit OA model study, the inhibition of OA progression by intra-articular injection was improved by inducing chondrocyte differentiation with PRP and sheet structure formation with ascorbic acid in ADSCs.

摘要

脂肪来源干细胞（ADSCs）作为骨关节炎（OA）的一种治疗选择已被研究多年；然而，其疗效仍然不足。由于富血小板血浆（PRP）可诱导ADSCs向软骨细胞分化，且抗坏血酸诱导形成的片状结构可增加活细胞数量，我们推测注射软骨细胞片结合PRP和抗坏血酸的作用可能会阻碍OA的进展。评估了PRP诱导分化和抗坏血酸形成片状结构对ADSCs中软骨细胞标志物（胶原蛋白II、聚集蛋白聚糖、Sox9）变化的影响。还评估了在兔OA模型中关节内注射细胞后黏多糖和VEGF - A分泌的变化。经PRP处理的ADSCs强烈表达软骨细胞标志物，包括II型胶原蛋白、Sox9和聚集蛋白聚糖，并且即使在抗坏血酸诱导形成片状结构后，它们的基因表达仍得以维持。在这项兔OA模型研究中，通过PRP诱导软骨细胞分化和抗坏血酸在ADSCs中形成片状结构，关节内注射对OA进展的抑制作用得到了改善。

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