생쥐의 바이러스성 심근염에서 합병증 동반 유무에 따른 조직 및 혈청내 금속단백효소억제자의 발현 차이
Altered Expression of Tissue Inhibitor of Matrix Metalloproteinase-2 in Complicated Mice Heart Secondary to Experimentally Induced Viral Myocarditis
김성숙, 엄대운, 서재희, 허주령, 홍영미, 최인표,
소속 상세정보
김성숙 ( Kim Sung-Sook )
울산대학교 의과대학 병리학교실
엄대운 ( Eom Dae-Woon )
울산대학교 의과대학 병리학교실
서재희 ( Suh Jae-Hee )
울산대학교 의과대학 병리학교실
허주령 ( Huh Joo-Ryung )
울산대학교 의과대학 병리학교실
홍영미 ( Hong Young-Mi )
이화여자대학교 의과대학 소아과학교실
최인표 ( Choi In-Pyo )
한국생명공학연구원 분자생의학연구실
KMID : 0357920010350030196
Abstract
Background: The pathogenesis of transition from viral myocarditis to dilated cardiomyopathy is elusive, although the incidence of dilated cardiomyopathy in human is increasing.
Methods: To clarify the role of the tissue inhibitor of matrix metaloproteinase-2 (TIMP-2) in this event, we performed immunohistochemistry, immunoblotting and immunoassay of matrix metalloproteinase-9 (MMP-9) and TIMP-2 in the serum and heart tissue of mice, which were inoculated with 4000 plaque-forming units of coxsackie B virus.
Results: The MMP-9 was expressed in damaged cardiomyocytes, and the TIMP-2 was expressed in mainly interstitial connective tissue between cardiac muscle bundles by immunohistochemistry. The level of serum MMP-9 was higher in the complicated than non-complicated group (p<0.001), but the level of TIMP-2 was much lower in complicated than non-complicated group (p<0.05). These findings were similar to the results of immunohistochemistry and immunoblotting in tissues.
Conclusions: These results suggest that an imbalance in the level of MMP-9 and its inhibitor might activate cardiac complication in viral myocarditis.
키워드
Myocarditis;Cardiomyopathy;Gelatinase B;Tissue inhibitor of matrix metalloproteinase-2;Immunohistochemistry
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