期刊文献+

miR-21调控TGF-β1诱导的大鼠BMSCs向肌成纤维细胞分化的机制研究 被引量:1

TGF-β1 induced mi R-21 overexpression regulates myofibroblast differentiation of rat mesenchymal stem cells and contributes to radiation-induced fibroatrophic process
原文传递
导出
摘要 目的:在细胞水平探索mi R-21在调控TGF-β1诱导的大鼠骨髓间充质干细胞向肌成纤维细胞分化中的作用。方法:全髓培养法培养原代大鼠骨髓间充质干细胞,培养至第三代时用TGF-β1分组诱导培养,检测TGF-β1对大鼠BMSCs促纤维化的作用及该过程中不同浓度梯度TGF-β1诱导以及不同时间段mi R-21的表达变化;通过转染mi R-21 mimics(高表达)不同时间点检测其对α-SMA表达的影响。结果:TGF-β1能促进大鼠骨髓间充质干细胞向成纤维,肌成纤维细胞分化;大鼠骨髓间充质干细胞向成纤维,肌成纤维细胞分化后mi R-21表达上调;上调mi R-21能促进大鼠BMSCs的纤维化作用。结论:mi R-21 mimics能够促进大鼠BMSCs的纤维化作用。 Objective:To investigate the role of miR-21 in the jaw of fibrosis in vitro. Method:Whole bone marrow adherence on plastic was used to isolation and culture rat mesenchymal stem cells. When passage 3, the cells were treated with TGF-β1 for different periods of time and concentration. The target gene expression of miR-21 was detected by real-time PCR;Over-expression of miR-21 by niR-21 mimics,to study whether up-regulated miR-21 enhances myfibroblast differentiation of rat mesenchymal stem cells by immunohistochemistry. Result:Real-time PCR demonstrated that TGF-β1 induced miR-21 expression in a time-dependent and dosage-dependent manner,peaking at 48h with an optimal dose at 5 ng/mL. The protein expression of α-SMA was up-regulated. Conclusion:miR-21 could promote myfibroblast differentia-tion of BMSCs in vitro. Inhibition of miR-21 may be a therapeutic approach to suppress renal fibrosis.
出处 《临床口腔医学杂志》 2015年第4期213-216,共4页 Journal of Clinical Stomatology
基金 国家自然科学基金(NSFC:81271112) 上海市人才发展资助项目(201312) 上海交通大学晨星计划(a)
关键词 颌骨纤维化 骨髓间充质干细胞 肌成纤维细胞 TGF-Β1 MIRNA-21 Fibrosis of jaw mesenchymal stem cells myofibroblast
  • 相关文献

参考文献18

  • 1Delanian S,Lefaix JL. The radiation-induced fibroatrophic process." therapeutic perspective via the antioxidant pathway [J]. Radiother Oncol, 2004, 73 (2) : 119-131.
  • 2Gu J, Li HL, Wu HY, et al. Sodium tanshinone IIA sulfonate attenu- ates radiation-induced fibrosis damage in cardiac fibroblasts [J]. J Asian Nat Prod Res, 2014, 16 (9) : 941-952.
  • 3Igaz P, Igaz I,Nagy Z,et al. MicroRNAs in adrenal tumors: rele- vance for pathogenesis, diagnosis, and therapy [J]. Cell Mol Life Sci, 2015,72 (3) : 417-428.
  • 4Wang JY, Gao YB,Zhang N, et al. miR-21 overexpression enhances TGF-betal-induced epithelial-to-mesenchymal transition by target smad7 and aggravates renal damage in diabetic nephropathy [J]. Mol Cell Endocrinol, 2014, 5:392 (1-2) : 163-172.
  • 5Hinz B,Phan SH,Thannickal VJ, et al. The myofibroblast: one function, multiple origins [J]. Am J Pathol,2007, 170 (6): 1807- 1816.
  • 6Ji H,Tang H,Lin H, et al. Rho'Rock cross-talks with transforming growth factor-beta, Smad pathway participates in lung fibroblast-my- ofibroblast differentiation [J]. Biomed Rep, 2014, 2 (6) ; 787-792.
  • 7邱林,金先庆.骨髓间充质干细胞的生物学特性及其临床治疗应用[J].中国组织工程研究与临床康复,2008,12(12):2347-2350. 被引量:19
  • 8Lee CH, Shah B, Moioli EK and Mao JJ. CTGF directs fibroblast dif- ferentiation from human mesenchymal stenCstromal ceils and defines connective tissue healing in a rodent injury model [J]. J Clin Invest, 2010,120 (9) : 3340-3349.
  • 9Guo W, Shan B, Klingsberg RC, et al. Abrogation of TGF-betal -in- duced fibrobtast-myofibroblast differentiation by histone deacetylase inhibition [J]. Am J Physiol Lung Cell Mol Physiol, 2009, 297 (5)." L864-870.
  • 10Evans RA,Tian YC, Steadman R, et al.. TGF-betal-mediated fi- broblast-myofibroblast terminal differentiation-the role of Smad pro- teins[J]. Exp Cell Res, 2003, 15,282 (2) : 90-100.

二级参考文献38

  • 1付小兵,方利君,王玉新,孙同柱,程飚.骨髓间充质干细胞自体移植提高猪皮肤创面修复质量的初步研究[J].中华医学杂志,2004,84(11):920-924. 被引量:37
  • 2孙勇刚,王光和.颌骨放射性骨坏死的临床观察[J].中华口腔医学杂志,1989,24(3):194-196. 被引量:13
  • 3Thom JJ, Hansen HS,Specht L,et al. Osteoradionecrosis of thejaws: clinical characteristics and relation to the field ofirradiation[J]. J Oral Maxillofac Surg, 2000, 58(10): 1088-1095.
  • 4Harris M. The conservative management of osteoradionecrosis ofthe mandible with ultrasound therapy [J]. Br J Oral MaxillofacSurg, 1992, 30(5): 313-318.
  • 5Delanian S,Lefaix JL. The radiation -induced fibroatrophicprocess: therapeutic perspective via the antioxidant pathway [J].Hadiother Oncol, 2004,73(2): 119-131.
  • 6Delanian S, Martin M,Housset M. Iatrogenic fibrosis incancerology(l): descriptive and physiopathological aspects[J]. BullCancer, 1993,80(3): 192-201.
  • 7Lefaix JL, Daburon F. Diagnosis of acute localized irradiationlesions: review of the French experimental experience [J]. HealthPhys, 1998, 75(4): 375-384.
  • 8Canney PA, Dean S. Transforming growth factor P: a promotor oflate connective tissue injury following radiotherapy. [J]. Br JRadiol, 1990,63(752): 620-623.
  • 9Basavaraju SR, Easterly CE. Pathophysiological effects ofradiation on atherosclerosis development and progression, and theincidence of cardiovascular complications [J]. Med Phys,2002,29(10): 2391-2403.
  • 10Vodovotz Y, Lucia MS, DeLucca AM, et al. Reducedhematopoietic function and enhanced radiosensitivity oftransforming growth factor-pl transgenic mice [J]. Int J Cancer,2000, 90(1): 13-21.

共引文献26

同被引文献12

引证文献1

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部