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在臀肌挛缩症中,胶原、转化生长因子-β1 和-β3 的表达增加。

Increased expression of collagens, transforming growth factor-beta1, and -beta3 in gluteal muscle contracture.

机构信息

Department of Orthopedic Surgery, The 2nd Affiliated Hospital of Medical College, Xi'an JiaoTong University, Xi'an, Shaanxi, PR China.

出版信息

BMC Musculoskelet Disord. 2010 Jan 25;11:15. doi: 10.1186/1471-2474-11-15.

DOI:10.1186/1471-2474-11-15
PMID:20100316
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2828420/
Abstract

BACKGROUND

Gluteal muscle contracture (GMC) is a multi-factor human chronic fibrotic disease of the gluteal muscle. Fibrotic tissue is characterized by excessive accumulation of collagen in the muscle's extracellular matrix. Transforming growth factor (TGF)-beta1 and -beta2 are thought to play an important role in fibrogenesis, while TGF-beta3 is believed to have an anti-fibrotic function. We hypothesize that the expression of collagen and TGF-betas would be up-regulated in GMC patients.

METHODS

The expression of collagen type I, type III and TGF-betas were studied in 23 fibrotic samples and 23 normal/control samples in GMC patients using immunohistochemistry, reverse transcription and polymerase chain reaction (RT-PCR) and western bolt analysis.

RESULTS

Compared to the unaffected adjacent muscle, increased expression of TGF-beta1 and -beta3 was associated with deposition of collagen type I and type III in the fibrotic muscle of the GMC patients at the mRNA level. Strong up-regulation of these proteins in fibrotic muscle was confirmed by immunohistochemical staining and western blot analysis. TGF-beta2 was not up-regulated in relation to GMC.

CONCLUSION

This study confirmed our hypothesis that collagen types I, III, TGF-beta1 and TGF-beta3 were up-regulated in biopsy specimens obtained from patients with GMC. Complex interaction of TGF-beta1 with profibrotic function and TGF-beta3 with antifibrotic function may increase synthesis of collagens and thereby significantly contribute to the process of gluteal muscle scarring in patients with GMC.

摘要

背景

臀肌挛缩症(GMC)是一种多因素的人类慢性臀肌纤维性疾病。纤维组织的特征是肌肉细胞外基质中胶原过度积累。转化生长因子(TGF)-β1 和 -β2 被认为在纤维化发生中起重要作用,而 TGF-β3 被认为具有抗纤维化功能。我们假设 GMC 患者的胶原和 TGF-βs 的表达会上调。

方法

采用免疫组织化学、逆转录和聚合酶链反应(RT-PCR)和 Western blot 分析检测 23 例纤维性样本和 23 例 GMC 患者正常/对照样本中胶原 I 型、胶原 III 型和 TGF-βs 的表达。

结果

与未受影响的相邻肌肉相比,TGF-β1 和 -β3 的表达增加与 GMC 患者纤维性肌肉中胶原 I 型和胶原 III 型的沉积有关。免疫组织化学染色和 Western blot 分析证实了这些蛋白在纤维性肌肉中的强烈上调。TGF-β2 与 GMC 无关。

结论

本研究证实了我们的假设,即 I 型、III 型胶原、TGF-β1 和 TGF-β3 在 GMC 患者活检标本中上调。TGF-β1 与促纤维化功能的复杂相互作用和 TGF-β3 与抗纤维化功能的复杂相互作用可能会增加胶原的合成,从而显著促进 GMC 患者臀肌瘢痕形成过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/0fd898df1677/1471-2474-11-15-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/45995b1712a0/1471-2474-11-15-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/6d45285aea7d/1471-2474-11-15-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/b06c6639823b/1471-2474-11-15-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/0fd898df1677/1471-2474-11-15-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/45995b1712a0/1471-2474-11-15-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/6d45285aea7d/1471-2474-11-15-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/b06c6639823b/1471-2474-11-15-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d5f/2828420/0fd898df1677/1471-2474-11-15-4.jpg

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