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首页> 外文期刊>Steroids: An International Journal >The collective influence of 1, 25-dihydroxyvitamin D 3 with physiological fluid shear stress on osteoblasts
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The collective influence of 1, 25-dihydroxyvitamin D 3 with physiological fluid shear stress on osteoblasts

机译:1,25-二羟基苯胺D 3对成骨细胞生理流体剪切应力的集体影响

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摘要

Highlights ? This study reports the collective influences of 1, 25(OH) 2 D 3 and flow shear stress (FSS) on osteoblasts. ? FSS-induced NO release is 1, 25 (OH) 2 D 3 concentration dependent with a pattern of 0-FSS?>?1-FSS?>?10-FSS?>?100-FSS. ? FSS-induced PGE 2 release is 1, 25 (OH) 2 D 3 concentration dependent with a pattern of 100-FSS?>?10-FSS?>?0-FSS?≈?1-FSS. ? ALP release and expressions of OPN, OCN followed the pattern 100-FSS?>?10-FSS?>?1-FSS?≈?0-FSS. ? The potential mechanism is that 1, 25 (OH) 2 D 3 modulates the focal adhesion and cytoskeleton. Abstract 1, 25-dihydroxyvitamin D 3 (1, 25 (OH) 2 D 3 ) and mechanical stimuli in physiological environment contributes greatly to osteoporosis pathogenesis. Wide investigations have been conducted on how 1, 25-dihydroxyvitamin D 3 and mechanical stimuli separately impact osteoblasts. This study reports the collective influences of 1, 25-dihydroxyvitamin D 3 and flow shear stress (FSS) on biological functions of osteoblasts. 1, 25 (OH) 2 D 3 were prepared in various kinds of concentrations (0, 1, 10, 100?nmmol/L), while physiological fluid shear stress (12?dynes/cm 2 ) was produced by using a parallel-plate fluid flow system. 1, 25 (OH) 2 D 3 affects the responses of ROBs to FSS, including the inhibition of NO release and cell proliferation as well as the promotion of PGE 2 release and cell differentiation. These findings provide a possible mechanism by which 1, 25(OH) 2 D 3 influences osteoblasts’ responses to FSS, thus most probably providing guidance for the selection of 1, 25(OH) 2 D 3 concentration and mechanical loading in order to produce functional bone tissues in vitro .
机译:强调 ?本研究报告了成骨细胞上的1,25(OH)2 D 3和流量剪切应力(FSS)的集体影响。还FSS诱导没有释放是1,25(OH)2 D 3浓度与0-FSS的模式依赖于0-FSS?> 1-FSS?>?10-FSS?>?100 FSS。还FSS诱导的PGE 2释放是1,25(OH)2 D 3浓度与100-FSS的图案依赖于100FS?> 10-FSS?>?0-FSS?≈α1-FSS。还ALP释放和OPN的表达,OCN遵循模式100-FSS?>?10-FSS?>?1-FSS?≈α0-FSS。还潜在机制是1,25(OH)2d 3调节局灶性粘附和细胞骨架。摘要1,25-二羟基维胺D 3(1,25(OH)2 d 3)和生理环境中的机械刺激对骨质疏松症发病机构有很大贡献。已经根据1,25-二羟基苯胺D 3和机械刺激分别冲击成骨细胞来进行广泛的调查。本研究报告了1,25-二羟基苯胺D 3和流量剪切应力(FSS)对成骨细胞的生物功能的集体影响。在各种浓度(0,1,100,100·nmmol / L)中制备1,25(OH)2d 3,而通过使用平行产生生理流体剪切应力(12〜达因/ cm 2)板流体流动系统。如图1,25(OH)2 D 3影响ROBS对FSS的反应,包括抑制无释放和细胞增殖以及PGE 2释放和细胞分化的促进。这些发现提供了一种可能的机制,其中1,25(OH)2 D 3对骨灌注物对FSS的反应影响,因此最多可以为选择1,25(OH)2 D 3浓度和机械负载提供指导,以便生产功能性骨组织体外。

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