期刊文献+

间歇性张应力对小鼠破骨细胞TRPV5基因表达的影响 被引量:2

Intermittent tensile stress affects the expression of TRPV5 in murine osteoclasts
原文传递
导出
摘要 目的探究在间歇性张应力作用下小鼠破骨细胞内TRPV5的基因表达情况。方法将小鼠破骨细胞分组并施加不同大小的间歇性张应力(A组1 000με、B组3 000με、C组5 000με、D组不做加力处理),通过荧光定量PCR方法检测在应力作用前后TRPV5的mRNA表达水平。结果对小鼠破骨细胞施加不同程度的间歇性张应力之后,TRPV5基因的表达水平相比对照组(D组)均升高,加力组与对照组之间差异有统计学意义(P<0.001),两两比较结果显示,B组与C组之间差异无统计学意义(P>0.05),其余任意两组之间差异均有统计学意义(P<0.05)。结论间歇性张应力可以促进破骨细胞TRPV5基因的表达,在一定范围内加大力值可提高TRPV5基因的表达。 Objective To investigate the expression of transient receptor potential vanilloid receptor V( TRPV5) during the differentiation of osteoclasts mediated by intermittent tensile stress. Methods Murine osteoclasts were divided into4 groups and mediated by different loading stress: group A( 1 000 με),group B( 3 000 με),group C( 5 000 με),and group D( 0 με). The mRNA expression of TRPV5 in the 4 groups was detected with fluorescence quantitative PCR before and after the differentiation. Results Compared with group D,the other 3 groups had higher mRNA expression of TRPV5( P 0. 001). Pairwise comparison results showed that there was no statistical difference between group B and C( P 0. 05),there was statistical difference between any other two groups( P 0. 05). Conclusion Intermittent tensile stress promotes the expression of TRPV5 channel gene in osteoclasts within a certain range.
出处 《山东大学学报(医学版)》 CAS 北大核心 2017年第11期22-26,共5页 Journal of Shandong University:Health Sciences
基金 山东省医药卫生科技发展计划(2013WS0014) 青岛市科技计划基础研究项目[(12-1-4-16-(8)-jch)] 青岛市医疗卫生优秀人才培养项目(VDTR2016Y08)
关键词 瞬时电位感受器香草精家族受体V 间歇性张应力 破骨细胞 荧光定量PCR Transient receptor potential vanilloid receptor 5 Intermittent tensile stress Osteoclast Fluorescence quan-titative PCR
  • 相关文献

参考文献7

二级参考文献232

  • 1王晓楠,孙联文,樊瑜波.微重力对骨组织细胞功能的影响[J].中华航空航天医学杂志,2012,23(2):151-156. 被引量:4
  • 2邹世恩,张绍芬.雌激素对成骨细胞和破骨细胞凋亡的调节机制[J].现代妇产科进展,2006,15(7):547-548. 被引量:18
  • 3李晓红,司红羚,刘啸晨.雌激素对骨质疏松大鼠牙槽骨改建过程中IL-1表达的影响[J].实用口腔医学杂志,2006,22(5):684-687. 被引量:10
  • 4Hoenderop JG,van der Kemp AW,Hartog A,et al.Molecular identification of the apical Ca^2+ channel in 1,25-dihydroxyvitamin D3-responsive epithelia[J].J Biol Chem,1999,274:8375-8378.
  • 5Peng JB,Brown EM,Hediger MA.Apical entry channels in calcium-transporting epithelia[J].News Physiol Sci,2003,18:158-163.
  • 6Voets T,Janssens A,Prenen J,et al.Mg^2+-dependent gating and strong inward rectification of the cation channel TRPV6[J].J Gen Physiol,2003,121:245-260.
  • 7Nilius B,Prenen J,Hoenderop JG,et al.Fast and slow inactivation kinetics of the Ca^2+ channels ECaC1 and ECaC2 (TRPV5 and 6):role of the intracellular loop located between transmembrane segment 2 and 3[J].J Biol Chem,2002,277:30852-30858.
  • 8Vennekens R,Hoenderop JG,Prenen J,et al.Permeation and gating properties of the novel epithelial Ca^2+ channel[J].J Biol Chem,2000,275:3963-3969.
  • 9Loffing J,Loffing-Cueni D,Valderrabano V,et al.Distribution of transcellular calcium and sodium transport pathways along mouse distal nephron[J].Am J Physiol Renal Physiol,2001,281:F1021-F1027.
  • 10Hoenderop JG,Dardenne O,van Abel M,et al.Modulation of renal Ca^2+ transport protein genes by dietary Ca^2+ and 1,25-dihydroxyvitamin D3 in 25-hydroxyvitamin D3-1 -hydroxylase knockout mice[J].FASEB J,2002,16:1398-1406.

共引文献83

同被引文献51

引证文献2

二级引证文献14

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