首页> 外文期刊>International Orthopaedics >Periprosthetic strain magnitude-dependent upregulation of type I collagen synthesis in human osteoblasts through an ERK1/2 pathway.
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Periprosthetic strain magnitude-dependent upregulation of type I collagen synthesis in human osteoblasts through an ERK1/2 pathway.

机译:通过ERK1 / 2途径,人成骨细胞中I型胶原合成的假体周围应变幅度依赖性上调。

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摘要

Human osteoblasts sense mechanical stimulation and synthesise type I collagen in periprosthetic osseointegration following total hip arthroplasty. However, the regulation of type I collagen synthesis by periprosthetic strain is unclear because the cellular-level strain magnitude remains unknown to date. Fortunately, the tissue-level strain in implanted femurs is measurable. According to the mechanism of strain amplification, the tissue-level strain was amplified 20 times to stretch human osteoblasts in this study. Elongation of 0.8-3.2% enhanced the mRNA level of type I collagen, whereas the release of procollagen type I C propeptide only increased at 2.4% and 3.2% elongation. Type I collagen expression increased with the activation of ERK1/2 phosphorylation in a strain-magnitude-dependent manner, whereas JNK and P38 were unaffected. The responses were completely inhibited by blocking the ERK1/2 pathway with U0126. The results indicate that type I collagen synthesis in human osteoblasts depends on the level of periprosthetic strain and ERK1/2 activation.
机译:人成骨细胞在全髋关节置换术后感觉到假体周围骨整合中的机械刺激并合成I型胶原。然而,目前尚不清楚假体周围应变对I型胶原蛋白合成的调控,因为细胞水平的应变幅度仍然未知。幸运的是,植入股骨的组织水平应变是可以测量的。根据应变放大的机理,本研究将组织水平的应变放大了20倍,以拉伸人类成骨细胞。伸长率为0.8-3.2%增强了I型胶原的mRNA水平,而I型胶原原胶原的释放仅在伸长2.4%和3.2%时增加。 I型胶原蛋白表达随应变幅度依赖的ERK1 / 2磷酸化的激活而增加,而JNK和P38不受影响。通过用U0126阻断ERK1 / 2途径,反应被完全抑制。结果表明,人类成骨细胞中的I型胶原蛋白合成取决于假体周围应变水平和ERK1 / 2激活。

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