Chen Xia, Zhang Ruhong, Zhang Qun, Xu Zhicheng, Xu Feng, Li Datao, Li Yiyuan
Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
Aging (Albany NY). 2019 Sep 6;11(17):7070-7082. doi: 10.18632/aging.102237.
Stable cartilage regeneration has always been a challenge in both tissue engineering research and clinical practice. This study explored the feasibility of using a chondrocyte sheet technique stimulated by microRNAs to regenerate cartilage. We tested the involvement of hsa-miR-193b-3p in the microtia patient remnant auricular chondrocyte extracellular matrix (ECM). We observed chondrocyte proliferation, ECM synthesis, as well as the increase in the expression of type II collagen (COL2A1) and decrease in the expression of matrix metalloproteinase 16 (MMP16) of the chondrocyte sheets. COL2A1 deposition and MMP16 degradation of regenerative cartilage tissue were examined . A dual-luciferase reporter showed that the MMP16 gene was the direct target of miR-193b-3p. These results suggested that miR-193b-3p promotes chondrocyte sheet ECM synthesis by inhibiting MMP16. Since the evidence suggests that MMP16 is a critical regulator of chondrocyte ECM, this finding points the way towards a method that both strengthens the ECM and inhibits MMPs.
在组织工程研究和临床实践中，稳定的软骨再生一直是一项挑战。本研究探索了利用微小RNA刺激的软骨细胞片技术再生软骨的可行性。我们检测了hsa-miR-193b-3p在小耳畸形患者残余耳廓软骨细胞外基质（ECM）中的作用。我们观察到软骨细胞片的软骨细胞增殖、ECM合成，以及II型胶原蛋白（COL2A1）表达增加和基质金属蛋白酶16（MMP16）表达减少。检测了再生软骨组织的COL2A1沉积和MMP16降解情况。双荧光素酶报告基因显示MMP16基因是miR-193b-3p的直接靶标。这些结果表明，miR-193b-3p通过抑制MMP16促进软骨细胞片ECM合成。由于有证据表明MMP16是软骨细胞ECM的关键调节因子，这一发现为一种既能增强ECM又能抑制基质金属蛋白酶的方法指明了方向。
