| 颅骨缺损山羊模型中miR-196b调节破骨细胞分化的作用机制 |
| 投稿时间：2015-12-29 修订日期：2016-01-22 点此下载全文 |
| 引用本文：崔阳,张春阳,杨文典,朱东,李鲁.颅骨缺损山羊模型中miR-196b调节破骨细胞分化的作用机制[J].医学研究杂志,2016,45(8):59-62 |
| DOI：
10.11969/j.issn.1673-548X.2016.08.016 |
| 摘要点击次数: 1059 |
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| 基金项目:国家自然科学基金资助项目（81360164） |
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| 中文摘要:目的 研究miR-196b在调节破骨细胞分化过程中的作用机制。方法 通过构建山羊颅骨缺损模型，分别选取颅骨缺损山羊的颅骨组织和发育正常山羊的颅骨组织作为样本。将收集样本进行基因测序分析，得到两样本中明显差异表达的miRNAs。以这些差异表达的miRNA为对象进行KEGG pathway功能分析，并通过靶基因预测软件预测miR-196b的靶基因，研究miR-196b在破骨细胞分化过程中的作用及其与靶基因的关系。结果 miR-196b在颅骨缺损组中呈高表达（P<0.05），两样本中差异表达的miRNA在破骨细胞分化通路中富集，miR-196b调控的靶基因参与破骨细胞分化的调控通路。结论 高表达的miR-196b参与破骨细胞分化通路中对AKT、JNK、STAT2等靶基因的调控过程。其作用可能对骨组织的代谢产生影响。 |
| 中文关键词:miR-196b 破骨细胞 调控通路 靶基因 |
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| Mechanism of MiR-196b Regulate Osteoclast Differentiation in Goat Skull Defects |
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| Abstract:Objective To investigate the modulation mechanism of miR-196b in osteoclast differentiation. Methods After the establishing the goat models with skull defects, the skull tissues were collected from both goats with skull defects and healthy goats with normal development as samples. Gene sequencing analysis was then performed for the skull tissue samples, and the miRNAs with obvious differential expressions were acquired. KEGG pathway analysis was carried out with the miRNAs as the object, and the target genes of miR-196b were predicted by gene target prediction software, and the function of miR-196b in osteoclast differentiation and the its relationship with the target genes. Results miR-196b presented high expression in the skull tissues of the skull defect group; the miRNAs with obvious differential expressions in the two samples presented enrichment in the osteoclast differentiation pathway; and the miR-196b modulated target genes play a role in the modulation pathway of osteoclast differentiation. Conclusion The highly-expressed miR-196b participates in the modulation of the target genes including AKT, JNK, STAT2 in the osteoclast differentiation pathway, and this modulation function may have influences on the metabolism of bone tissues. |
| keywords:MiR-196b Osteoclasts Regulation pathways Target genes |
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