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Overexpression of transforming growth factor-beta 1 in the valvular fibrosis of chronic rheumatic heart disease

Authors
 Lucia Kim  ;  Do Kyun Kim  ;  Woo Ick Yang  ;  Dong Hwan Shin  ;  Ick Mo Jung  ;  Han Ki Park  ;  Byung Chul Chang 
Citation
 JOURNAL OF KOREAN MEDICAL SCIENCE, Vol.23(1) : 41-48, 2008 
Journal Title
 JOURNAL OF KOREAN MEDICAL SCIENCE 
ISSN
 1011-8934 
Issue Date
2008
MeSH
Adult ; Aged ; Chronic Disease ; Collagen/metabolism ; Female ; Fibrosis ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Mitral Valve/pathology* ; Proteoglycans/metabolism ; Rheumatic Heart Disease/metabolism* ; Rheumatic Heart Disease/pathology ; Transforming Growth Factor beta1/analysis ; Transforming Growth Factor beta1/physiology*
Keywords
Rheumatic Heart Disease ; Transforming Growth Factor- 1 ; Heart Valves ; Fibrosis
Abstract
For the purpose of determining the pathogenic role of transforming growth factor-beta1 (TGF-beta 1) in the mechanism of chronic rheumatic heart disease, we evaluated the expression of TGF-beta 1, proliferation of myofibroblasts, and changes in extracellular matrix components including collagen and proteoglycan in 30 rheumatic mitral valves and in 15 control valves. High TGF-beta 1 expression was identified in 21 cases (70%) of rheumatic mitral valves, whereas only 3 cases (20%) of the control group showed high TGF-beta 1 expression (p<0.001). Additionally, increased proliferation of myofibroblasts was observed in the rheumatic valves. High TGF-beta1 expression positively correlated with the proliferation of myofibroblasts (p=0.004), valvular fibrosis (p<0.001), inflammatory cell infiltration (p=0.004), neovascularization (p=0.007), and calcification (p<0.001) in the valvular leaflets. The ratio of proteoglycan to collagen deposition inversely correlated with TGF-beta 1 expression in mitral valves (p=0.040). In conclusion, an ongoing inflammatory process, the expression of TGF-beta 1, and proliferation of myofibroblasts within the valves have a potential role in the valvular fibrosis, calcification, and changes in the extracellular matrix that lead to the scarring sequelae of rheumatic heart disease.
Files in This Item:
T200800979.pdf Download
DOI
10.3346/jkms.2008.23.1.41
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Thoracic and Cardiovascular Surgery (흉부외과학교실) > 1. Journal Papers
Yonsei Authors
Park, Han Ki(박한기) ORCID logo https://orcid.org/0000-0002-7472-7822
Chang, Byung Chul(장병철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/107245
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