未经授权：先天性胫骨假关节（CPT）是一种罕见的先天性畸形和骨不愈合的特殊亚型。CPT来源的间充质干细胞(MSCs)成骨分化能力降低,miR-30a可抑制成骨分化。然而,miR-30a在CPT来源的MSCs中的作用尚不清楚.
UNASSIGNED:通过茜素红S染色和碱性磷酸酶(ALP)活性测试了用miR-30a抑制剂处理的CPT来源的MSCs的成骨分化。通过Westernblot或定量逆转录聚合酶链反应（RT-qPCR）评估蛋白质和mRNA的表达水平。分别。miR-30a和HOXD8之间的相互作用通过双荧光素酶报告基因测定进行研究。进行染色质免疫沉淀(ChIP)以评估HOXD8和RUNX2启动子之间的结合关系。
UNASSIGNED：CPT来源的MSCs显示出比正常MSCs更低的成骨分化能力。miR-30a在CPT来源的MSCs中增加，miR-30a下调可促进CPT来源MSCs的成骨分化。同时,HOXD8是miR-30a的直接靶标，HOXD8可以转录激活RUNX2。此外,miR-30a通过负调控HOXD8抑制CPT来源MSCs的成骨分化。
未授权：miR-30a通过靶向HOXD8抑制CPT来源的MSCs的成骨分化。因此，这项研究可能为对抗CPT提供一种新的策略。
UNASSIGNED: Congenital pseudarthrosis of the tibia (CPT) is an uncommon congenital deformity and a special subtype of bone nonunion. The lower ability of osteogenic differentiation in CPT-derived mesenchymal stem cells (MSCs) could result in progression of CPT, and miR-30a could inhibit osteogenic differentiation. However, the role of miR-30a in CPT-derived MSCs remains unclear.
UNASSIGNED: The osteogenic differentiation of CPT-derived MSCs treated with the miR-30a inhibitor was tested by Alizarin Red S staining and alkaline phosphatase (ALP) activity. The expression levels of protein and mRNA were assessed by Western blot or quantitative reverse transcription-polymerase chain reaction (RT-qPCR), respectively. The interplay between miR-30a and HOXD8 was investigated by a dual-luciferase reporter assay. Chromatin immunoprecipitation (ChIP) was conducted to assess the binding relationship between HOXD8 and RUNX2 promoter.
UNASSIGNED: CPT-derived MSCs showed a lower ability of osteogenic differentiation than normal MSCs. miR-30a increased in CPT-derived MSCs, and miR-30a downregulation promoted the osteogenic differentiation of CPT-derived MSCs. Meanwhile, HOXD8 is a direct target for miR-30a, and HOXD8 could transcriptionally activate RUNX2. In addition, miR-30a could inhibit the osteogenic differentiation of CPT-derived MSCs by negatively regulating HOXD8.
UNASSIGNED: miR-30a inhibits the osteogenic differentiation of CPT-derived MSCs by targeting HOXD8. Thus, this study might supply a novel strategy against CPT.
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