| 刘轶宁,孙海建,崔 敏,周佳雯,苗登顺.Bmi1过表达通过促进增殖、抑制凋亡纠正活性维生素D缺乏引起的骨量降低[J].,2022,(5):801-807 |
| Bmi1过表达通过促进增殖、抑制凋亡纠正活性维生素D缺乏引起的骨量降低 |
| Overexpression of Bmi1 Corrects Bone Loss Caused by Active Vitamin D Deficiency by Promoting Proliferation and Inhibiting Apoptosis |
| 投稿时间：2021-09-27 修订日期：2021-10-23 |
| DOI：10.13241/j.cnki.pmb.2022.05.001 |
| 中文关键词: 骨髓间充质干细胞 抑制凋亡 促进增殖 骨质疏松症 |
| 英文关键词: Bone marrow mesenchyml stem cell Inhibition of apoptosis Promote proliferation Osteoporosis |
| 基金项目:国家自然科学基金项目（81730066） |
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| 中文摘要: |
| 摘要 目的：探索B淋巴瘤Mo-MLV插入区1（B cell-specific MLV integration site-1, Bmi-1）过表达能否通过促进增殖、抑制凋亡改善1,25-二羟基维生素D (1,25-dihydroxy vitamin d，1,25(OH) 2D)缺乏引起的小鼠骨质骨量丢失。方法：取8月龄Bmi-1 Tg 、Bmi1 Tg 1α(OH)ase+/-与 1α(OH)ase+/-小鼠以及同窝野生型（wild type, WT）小鼠椎骨组织，通过流式细胞术及TUNEL染色检测间充质干细胞周期变化及凋亡水平，通过PCNA染色及免疫组织化学染色检测小鼠椎骨组织中Bcl-2、Caspase-3等指标的变化，通过Western blot检测小鼠椎骨中Caspase-3、CDK4、CDK6、OPN、OCN等蛋白表达量的差异，通过ALP染色检查成骨细胞骨形成水平。结果：在骨髓间充质干细胞中过表达Bmi1可以通过促进增殖，抑制凋亡、增加成骨细胞骨形成来纠正1α(OH)ase+/-小鼠的骨量降低。结论：Bmi1是1,25(OH) 2D的关键下游靶点，在防止1,25(OH) 2D缺乏引起的骨丢失方面起着至关重要的作用。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate whether overexpression of B cell-specific MLV integration site-1 (Bmi-1) can improve the phenotype of osteoporosis caused by 1,25(OH) 2D (1,25-dihydroxy vitamin d) deficiency in mice by promoting proliferation and inhibiting apoptosis. Methods: Vertebral tissues of 8-month-old Bmi-1 Tg , Bmi1 Tg 1α(OH)ase+/- and 1α(OH)ase+/- mice and homogenous Wild type (WT) mice were taken, and the cycle and apoptosis levels of mesenchymal stem cells were detected by flow cytometry and TUNEL staining. The changes of Bcl-2, Caspase-3 and other indexes in mouse vertebral tissues were detected by PCNA staining and immunohistochemical staining. Western blot was used to detect the protein expression levels of Caspase-3, CDK4, CDK6, OPN and OCN in mouse vertebrae, and ALP staining was used to check the level of osteoblast bone formation. Results: Overexpression of Bmi1 in bone marrow mesenchymal stem cells can correct the bone phenotype of 1α(OH)ase+/- mice by promoting proliferation, inhibiting apoptosis and increasing osteoblast bone formation. Conclusion: Bmi1 is a key downstream target of 1,25 (OH) 2D and plays a critical role in preventing bone loss caused by 1,25 (OH) 2D deficiency. |
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