title: Increased expression of collagens, transforming growth factor-beta1, and -beta3 in gluteal muscle contracture.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Orthopedic Surgery, The 2nd Affiliated Hospital of Medical College, Xi'an JiaoTong University, Xi'an, Shaanxi, PR China.
authors.forename: Chen-Guang
authors.initials: CG
authors.lastname: Zhao
authors.forename: Xi-Jing
authors.initials: XJ
authors.lastname: He
authors.forename: Bin
authors.initials: B
authors.lastname: Lu
authors.forename: Hao-Peng
authors.initials: HP
authors.lastname: Li
authors.forename: An-Jing
authors.initials: AJ
authors.lastname: Kang
mesh_terms: D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D002081:Buttocks / Q000473:pathology / Q000503:physiopathology*; D002648:Child; D003094:Collagen / Q000235:genetics* / Q000378:metabolism; D024042:Collagen Type I / Q000235:genetics / Q000378:metabolism; D024061:Collagen Type III / Q000235:genetics / Q000378:metabolism; D003286:Contracture / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D005355:Fibrosis / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D008297:Male; D018482:Muscle, Skeletal / Q000473:pathology / Q000503:physiopathology*; D012333:RNA, Messenger / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000235:genetics* / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism; D053782:Transforming Growth Factor beta3 / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation / Q000235:genetics; D055815:Young Adult
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D024061:Collagen Type III; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D053782:Transforming Growth Factor beta3; D003094:Collagen