MicroRNA-200a Regulates the Development of Mandibular Condylar Cartilage
MicroRNA-200a Regulates the Development of Mandibular Condylar Cartilage
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MicroRNA-200a 调节下颌髁软骨的发育
DOI：
10.1177/0022034515577411
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发表时间：
2015
影响因子：
7.6
通讯作者：
M. Umeda
中科院分区：
文献类型：
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作者：
泰江 章博;堀内 信也;木内 奈央;大庭 康雄;横関 雅彦;田中 栄二;M. Umeda
下颌髁突软骨（MCC）属于继发性软骨，其组织学结构不同于原发性软骨。microRNA（miRNA）是一种小的非编码RNA，它与信使RNA（mRNA）靶点结合，抑制其翻译，在细胞分化、增殖和死亡中起重要作用。微阵列分析显示miR-200 a在胚胎发育过程中有特征性表达。我们推测miR-200 a可能参与调控MCC生长过程中软骨的形成。我们通过将抑制剂或模拟物转染到MCC器官和细胞培养物中来研究miR-200 a的功能。组织学检查揭示了miR-200 a模拟物的局部抑制作用和抑制剂对MCC器官培养系统中软骨细胞分化的广泛增强作用。免疫组织化学检查和基因表达分析表明，miR-200 a抑制剂增强软骨形成，而模拟物通过增强细胞增殖具有相反的作用。定量逆转录聚合酶链反应分析显示，miR-200 a下调软骨细胞标志物的基因表达。此外，miR-200 a模拟物转染到ATDC 5细胞中抑制了软骨基质的形成。这些结果表明，miR-200 a通过控制MCC细胞的增殖和分化，在MCC的发育中促进软骨形成。
Mandibular condylar cartilage (MCC) is classified as secondary cartilage, the histologic structure of which is unique from that of primary cartilage. MicroRNA (miRNA) is a small noncoding RNA that binds to the messenger RNA (mRNA) target to repress its translation and plays an important role in cell differentiation, proliferation, and death. Microarray analysis revealed that miR-200a was characteristically expressed during embryonic development. We hypothesized that miR-200a may be involved in regulating the formation of cartilage during MCC growth. We investigated the function of miR-200a by transfecting an inhibitor or mimic into MCC organ and cell cultures. A histologic examination revealed the localized inhibitory effects of the miR-200a mimic and widespread enhancing effects of the inhibitor on chondrocytic differentiation in the MCC organ culture system. An immunohistochemical examination and gene expression analysis demonstrated that the miR-200a inhibitor enhanced chondrogenesis, while the mimic had the opposite effect by enhancing cell proliferation. Quantitative reverse transcription polymerase chain reaction analysis revealed that miR-200a downregulated the gene expression of chondrocyte markers. Moreover, transfection of the miR-200a mimic into ATDC5 cells repressed the formation of the cartilaginous matrix. These results indicate that miR-200a contributed to chondrogenesis in developing MCC by controlling proliferation and differentiation in MCC cells.