Origin of extracellular matrix synthesis during coronary repair.
Origin of extracellular matrix synthesis during coronary repair.
复制标题
冠状动脉修复过程中细胞外基质合成的起源。
DOI:
10.1161/01.cir.95.4.997
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发表时间:
1997
期刊:
影响因子:
37.8
通讯作者:
Zalewski,A
中科院分区:
文献类型:
--
作者:
Shi,Y;O'BrienJr,JE;Ala-Kokko,L;Chung,W;Mannion,JD;Zalewski,A
BackgroundCoronary injury triggers differentiation of activated adventitial fibroblasts to myofibroblasts, which may contribute to neointimal formation and vascular remodeling. Accordingly, the purpose of this study was to examine the cellular origin of the enhanced synthesis of extracellular matrix proteins during coronary repair.Methods and ResultsThe time course and localization of collagen and elastin expression were examined by in situ hybridization and immunohistochemistry in porcine coronary arteries after balloon-induced injury. Procollagen-α1(I) transcripts and intracellular type I procollagen protein increased in the adventitia within 2 days after injury. This was followed by a sustained synthesis of type I procollagen in neointima beginning at 7 days and the extracellular accumulation of type I collagen in both layers. The origin of synthetic cells was further examined by colocalization of type I procollagen and bromodeoxyuridine labeling to activated adventitial cells, which translocated to neointima. Neointimal cells exhibited sustained synthetic activity manifested by the presence of type I procollagen and elastin at 3 months after injury. In contrast, the media showed only minor changes in the synthesis of collagen or elastin throughout coronary repair.ConclusionsActivated adventitial fibroblasts are endowed with synthetic capabilities after coronary injury. They express type I procollagen, with some of them translocating to the intima, where they continue to synthesize procollagen. The accumulation of type I collagen is evident in the adventitia and neointima, whereas elastin accumulates mainly in neointima. These findings support the involvement of adventitial fibroblasts in coronary repair and remodeling after endoluminal injury.
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影响因子:
37.8
作者:
Yi Shi;A. Fard;Anthony Galeo;H. Hutchinson;Pawan Vermani;G. R. Dodge;D. Hall;F. Shaheen;A. Zalewski
通讯作者:
A. Zalewski
DOI:
--
发表时间:
1992
期刊:
The American journal of pathology
影响因子:
--
作者:
Botney,MD;Kaiser,LR;Cooper,JD;Mecham,RP;Parghi,D;Roby,J;Parks,WC
通讯作者:
Parks,WC
影响因子:
20.1
作者:
BENDECK, MP;ZEMPO, N;REIDY, MA
通讯作者:
REIDY, MA
影响因子:
37.8
作者:
Henning Rud Andersen;Michael Maeng;M. Thorwest;Erling Falk
通讯作者:
Erling Falk
DOI:
--
发表时间:
1993
期刊:
Laboratory investigation; a journal of technical methods and pathology
影响因子:
--
作者:
Wiggins,R;Goyal,M;Merritt,S;Killen,PD
通讯作者:
Killen,PD