Overexpression of Transforming Growth Factor-beta1 in the Valvular Fibrosis of Chronic Rheumatic Heart Disease.
10.3346/jkms.2008.23.1.41
- Author:
Lucia KIM
1
;
Do Kyun KIM
;
Woo Ick YANG
;
Dong Hwan SHIN
;
Ick Mo JUNG
;
Han Ki PARK
;
Byung Chul CHANG
Author Information
1. Department of Pathology, Inha University College of Medicine, Incheon, Korea. luciado@inha.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Rheumatic Heart Disease;
Transforming Growth Factor-beta1;
Heart Valves;
Fibrosis
- MeSH:
Adult;
Aged;
Chronic Disease;
Collagen/metabolism;
Female;
Fibrosis;
Humans;
Immunohistochemistry;
Male;
Middle Aged;
Mitral Valve/*pathology;
Proteoglycans/metabolism;
Rheumatic Heart Disease/*metabolism/pathology;
Transforming Growth Factor beta1/analysis/*physiology
- From:Journal of Korean Medical Science
2008;23(1):41-48
- CountryRepublic of Korea
- Language:English
-
Abstract:
For the purpose of determining the pathogenic role of transforming growth factor-beta1 (TGF-beta1) in the mechanism of chronic rheumatic heart disease, we evaluated the expression of TGF-beta1, 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-beta1 expression was identified in 21 cases (70%) of rheumatic mitral valves, whereas only 3 cases (20%) of the control group showed high TGF-beta1 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-beta1 expression in mitral valves (p=0.040). In conclusion, an ongoing inflammatory process, the expression of TGF-beta1, 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.
