[目的]探讨微小 RNA(microRNA,miR)-210-3p 转染大鼠骨髓基质干细胞(bone marrow mesenchymal stem cells,BMMSCs)对成骨活性的影响.[方法]体外培养大鼠BMMSCs,随机分3组,分别为空白对照组、miR-210-3p增强组(增强组)、miR-210-3p抑制组(抑制组),给予相应体外转染处理.检测细胞增殖、凋亡和迁移,以及诱导成骨分化和诱导成脂分化情况;采用qRT-PCR检测相应标志物的mRNA表达水平.[结果]第3代BMMSCs的CD44和CD90呈阳性表达,CD34和CD45呈阴性表达,符合间充质干细胞的表面抗原特征.与空白对照组对比,增强组的miR-210-3p的mRNA表达显著增加(P＜0.05),而抑制组的miR-210-3p的mRNA表达显著抑制(P＜0.05).细胞增殖OD值、Transwell细胞迁移、茜素红染色钙盐沉积计数由高至低依次均为增强组＞空白对照组＞抑制组(P＜0.05);而凋亡率和油红O染色脂滴计数由低至高依次为增强组＜空白对照组＜抑制组(P＜0.05).qRT-PCR检测,成骨表达基因,包括ALP和Bglap-2的mRNA相对表达量由高至低依次为增强组＞空白对照组＞抑制组(P＜0.05);而成脂表达基因,包括PPARγ和LPL的mRNA相对表达量由低至高依次为增强组＜空白对照组＜抑制组(P＜0.05).[结论]本研究表明miR-210-3p可促进大鼠BMMSCs成骨分化,抑制成脂分化,减少细胞凋亡并促进细胞增殖和迁移.

关节透明软骨自我修复能力有限,其再生仍然是临床医生和研究人员面临的巨大挑战.尽管多种传统临床治疗方法显示出一定的疗效,但各自均存在其局限性和不足.近些年来,基于细胞的再生医学为软骨病损提供了一种很有希望的治疗策略.间充质干细胞作为一种多能祖细胞,具有来源广泛、多向分化及自我更新等特征,除增殖及成软骨分化外,其免疫调节、抗炎作用和旁分泌效应亦是其促进软骨修复再生的重要机制.目前,间充质干细胞在多项体内外研究中显示出较好的软骨修复效果.本文就近些年来应用于软骨修复再生的间充质干细胞生物学特征、常见组织来源、实际应用情况、各自的优缺点、最终去向和转归及促软骨修复再生机制等方面的研究进展进行综述.

Cartilage injury of the knee joint is very common. Due to the limited self-healing ability of articular cartilage, osteoarthritis is very likely to occur if left untreated. Bone marrow mesenchymal stem cells (BMMSCs) are widely used in the study of cartilage injury due to their low immunity and good amplification ability, but they still have disadvantages, such as heterogeneous undifferentiated cells. MicroRNAs can regulate the chondrogenic differentiation ability of MSCs by inhibiting or promoting mRNA translation and degradation. In this research, we primarily investigated the effect of microRNA-210-3p (miR-210-3p) on chondrogenic and adipogenic differentiation of BMMSCs in vitro. Our results demonstrate that miR-210-3p promoted chondrogenic differentiation and inhibited adipogenic differentiation of rat BMMSCs, which was related to the HIF-3α signalling pathway. Additionally, miR-210-3p promotes mRNA and protein levels of the chondrogenic expression genes COLII and SOX9 and inhibits mRNA and protein levels of the adipogenic expression genes PPARγ and LPL. Thus, miR-210-3p combined with BMMSCs is a candidate for future clinical applications in cartilage regeneration and could represent a promising new therapeutic target for OA.

背景:假体无菌性松动与假体周围骨溶解严重影响人工关节假体的使用寿命,影响置换效果,增加治疗费用.假体无菌性松动与假体周围骨溶解的机制研究为其治疗提供了新的方向.目的:针对人工关节假体周围骨溶解的机制和治疗做一综述.方法:应用计算机在PubMed、Web of Science和知网数据库检索涉及假体无菌性松动与假体周围骨溶解的相关研究,检索关键词为"periprosthetic osteolysis""aseptic loosening""假体周围骨溶解""假体无菌性松动",检索时间为2000年3月至2020年9月,最终纳入文献69篇.结果与结论:①可能改变植入物诱导反应的关键点是:巨噬细胞极化,假体周围细胞的促破骨细胞信号,核因子κB受体活化因子配体介导的破骨细胞生成,参与炎症/破骨细胞生成的核因子κB和丝裂原活化蛋白激酶途径,假体周围膜坏死与凋亡的延伸;②机械因素,如重复应力/应变也可能导致假体周围骨溶解,但是这些因素难以改变;③对假体周围骨溶解病理生理学的详细了解为其预防措施提供了新的可能性,可在未来显著降低人工关节置换后假体周围骨溶解和无菌性松动的发生率.