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超声刺激肌腱细胞I型和III型胶原蛋白表达及转化生长因子β上调。

Ultrasound stimulation of types I and III collagen expression of tendon cell and upregulation of transforming growth factor beta.

作者信息

Tsai Wen-Chung, Pang Jong-Hwei S, Hsu Chih-Chin, Chu Ngok-Kiu, Lin Miao-Sui, Hu Ching-Fang

机构信息

Department of Physical Medicine and Rehabilitation, Chang Gung Memorial Hospital, 5, Fu-Shin Street, Kweishan, Taoyuan 333, Taiwan.

出版信息

J Orthop Res. 2006 Jun;24(6):1310-6. doi: 10.1002/jor.20130.

Abstract

Traumatic tendon injuries are commonly treated with ultrasound. However, previous research has not examined the molecular mechanism of this therapeutic effect on collagen synthesis of tendon cells. This study was designed to determine the effect of ultrasound on the expression of type I and type III collagen of tendon cells intrinsic to rat Achilles tendon. Whether a correlation exits between this effect and the expression of transforming growth factor beta (TGF-beta), which enhances collagen synthesis, was also investigated. Tendon cells after ultrasound treatment and protein expression of types I and III collagen were determined by immunocytochemistry. The mRNA expressions of alpha1(I) procollagen, alpha1(III) procollagen, and TGF-beta were determined by reverse transcription-polymerase chain reaction (RT-PCR). Furthermore, the concentration of TGF-beta in conditioned medium was evaluated by enzyme-linked immunosorbent assay (ELISA). Immunocytochemical staining revealed that ultrasound-treated tendon cells were stained more strongly for types I and III collagen than were control cells. Upregulation of procollagen alpha1(I) gene, procollagen alpha1(III) gene, and TGF-beta at the mRNA level was confirmed by RT-PCR. A dose-dependent increase in the concentration of TGF-beta in conditioned medium obtained from cells treated with ultrasound was demonstrated by ELISA assay (p = 0.043). In conclusion, ultrasound stimulates the expression of type I and type III collagen in a process that is likely mediated by the upregulation of TGF-beta.

摘要

创伤性肌腱损伤通常采用超声治疗。然而,先前的研究尚未探讨这种治疗作用对肌腱细胞胶原蛋白合成的分子机制。本研究旨在确定超声对大鼠跟腱固有肌腱细胞I型和III型胶原蛋白表达的影响。还研究了这种作用与增强胶原蛋白合成的转化生长因子β(TGF-β)表达之间是否存在相关性。通过免疫细胞化学测定超声处理后的肌腱细胞以及I型和III型胶原蛋白的蛋白表达。通过逆转录-聚合酶链反应(RT-PCR)测定α1(I)前胶原、α1(III)前胶原和TGF-β的mRNA表达。此外,通过酶联免疫吸附测定(ELISA)评估条件培养基中TGF-β的浓度。免疫细胞化学染色显示,超声处理的肌腱细胞I型和III型胶原蛋白染色比对照细胞更强。RT-PCR证实了前胶原α1(I)基因、前胶原α1(III)基因和TGF-β在mRNA水平上的上调。ELISA分析表明,用超声处理的细胞获得的条件培养基中TGF-β浓度呈剂量依赖性增加(p = 0.043)。总之,超声在一个可能由TGF-β上调介导的过程中刺激I型和III型胶原蛋白的表达。

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