Matrix replenishing by BMSCs is beneficial for osteoarthritic temporomandibular joint cartilage
Matrix replenishing by BMSCs is beneficial for osteoarthritic temporomandibular joint cartilage
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BMSCs补充基质有利于骨关节炎颞下颌关节软骨。
DOI：
10.1016/j.joca.2017.05.007
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发表时间：
2017
影响因子：
7
通讯作者：
Wang M.
中科院分区：
文献类型：
--
作者：
Zhang M.;Yang H.;Lu L.;Wan X.;Zhang J.;Zhang H.;Liu X.;Huang X.;Xiao G.;Wang M.
目的探讨基质补充是否是骨关节炎（OA）软骨的主要需求。方法将猪颞下颌关节（TMJ）浅层和深层软骨细胞置于流体剪切应力（FFSS）下。检测基质生成和细胞分化的差异。单侧前牙合（UAC）应用于C57BL/6J雌性小鼠。每周将绿色荧光蛋白标记的外源性骨髓基质细胞（GFP-BMSCs）注射到TMJs中，从UAC刺激3周开始，持续4、8和12周。另一个GFP-BMSCs注射UAC组在注射8周后停止注射4周。评估的重点是UAC小鼠TMJ软骨的形态学改变、anoikis标志物DAP3、清除率受体家族成员CD163和增殖指标ki67的表达水平。结果ffss可下调ii型胶原蛋白的表达，但可促进深层软骨细胞的终末分化。它可以下调聚集蛋白的表达，但上调I型胶原蛋白的表达。UAC在不影响细胞增殖的情况下，引起基质损失和损伤，增强了深区软骨细胞的清除活性。晚期有明显的浅纤维性颤动。每周注射骨髓间充质干细胞在很大程度上恢复了这些变化。移植的骨髓间充质干细胞表达了高水平的CD163蛋白，但没有表现出显著的细胞增殖。终止外源性骨髓间充质干细胞的供应逆转了这种恢复作用。结论清除降解基质和补充纤维化发育基质是OA软骨修复的首要条件。
ObjectivesThe present goal was to explore whether matrix replenishment is the primary requirement for osteoarthritic (OA) cartilage.MethodsCells isolated from the superficial and deep zone cartilage of a pig temporomandibular joint (TMJ) were exposed to fluid flow shear stress (FFSS). Differences in matrix production and cellular differentiation were detected. Unilateral anterior crossbite (UAC) was applied to C57BL/6J female mice. Green fluorescent protein-labeled exogenous bone marrow stromal cells (GFP-BMSCs) were injected weekly into TMJs, starting from 3 weeks of UAC stimulation and continuing for 4-, 8- and 12-weeks. Another GFP-BMSCs injection UAC group stopped receiving injections for 4-weeks after 8-weeks of injections. Assessments were focused on morphological alterations in UAC mouse TMJ cartilage, the expression levels of DAP3, an anoikis marker, CD163, a scavenger receptor family member, and ki67, a proliferation indicator.ResultsFFSS down-regulated type-II collagen expression but stimulated terminal differentiation in cells isolated from deep zone cartilage. It down-regulated aggrecan expression but up-regulated type I collagen in cells isolated from both superficial and deep zones. UAC caused matrix loss and anoikis and enhanced scavenging activity in deep zone chondrocytes without affecting cell proliferation. Superficial fibrillation was obvious in the late stage. Weekly injections of BMSCs largely restored these changes. The implanted BMSCs expressed a high level of CD163 protein but did not show remarkable cell proliferation. Terminating the supply of exogenous BMSCs reversed the restorative effects.ConclusionsScavenging the degraded matrix and replenishing the fibrosis-developmental matrix are the primary requirements for the repair of OA cartilage.