Document Detail

Immunohistochemical detection of differentially localized up-regulation of lysyl oxidase and down-regulation of matrix metalloproteinase-1 in rhesus monkey model of chronic myocardial infarction.
MedLine Citation:
PMID:  22829703     Owner:  NLM     Status:  MEDLINE    
Myocardial remodeling after ischemic infarction is characterized by collagen accumulation leading to replacement and interstitial fibrosis. Type I and III collagens are predominant components in cardiac fibrosis. Lysyl oxidase (LOX) facilitates the cross-linking of type I and III fibrils, resulting in the formation of stiff fibers and their subsequent tissue deposition. However, the matrix metalloproteinases (MMPs), a family of zinc-dependent enzymes, function in the degradation of the collagen components of extracellular matrix. Tissue inhibitors for MMPs (TIMPs) manipulate the action of MMPs. To understand the contribution of these molecules to cardiac fibrosis, we developed a rhesus monkey model to determine the changes in LOX, MMP1 and TIMP1 in relation to collagen deposition after myocardial ischemic infarction. Male rhesus monkeys were subjected to left anterior descending artery ligation along with sham-operated controls. Histological examination and immunochemistry were performed eight weeks after the ischemic injury. The results showed that both type I and III collagens were increased in the scar area and in the interstitium, and the ratio of type I/III collagens also increased in the scar area but not in the interstitium. The expression of LOX was up-regulated, but the expression of MMP1 was down-regulated in residual myocytes of the scar area and the border zone. The expression of TIMP1 was not changed. The data thus demonstrated that the collagen deposition in infarcted myocardium is correlated with an enhanced cross-linking capacity and a decreased degradation process.
Yuping Xie; Jianmin Chen; Pengfei Han; Pingliang Yang; Jianglong Hou; Y James Kang
Related Documents :
19120573 - Illness consequences after myocardial infarction: problems with physical functioning an...
2461333 - Comparison of different techniques for the postmortem diagnosis of myocardial infarction.
9316513 - Cause of death analysis in the nhlbi ptca registry: results and considerations for eval...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-07-24
Journal Detail:
Title:  Experimental biology and medicine (Maywood, N.J.)     Volume:  237     ISSN:  1535-3699     ISO Abbreviation:  Exp. Biol. Med. (Maywood)     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-08-09     Completed Date:  2012-10-26     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  100973463     Medline TA:  Exp Biol Med (Maywood)     Country:  England    
Other Details:
Languages:  eng     Pagination:  853-9     Citation Subset:  IM    
Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Chronic Disease
Disease Models, Animal
Macaca mulatta
Matrix Metalloproteinase 1 / metabolism*
Myocardial Infarction / enzymology*
Protein-Lysine 6-Oxidase / metabolism*
Tissue Inhibitor of Metalloproteinase-1 / metabolism
Grant Support
Reg. No./Substance:
0/Tissue Inhibitor of Metalloproteinase-1; EC 6-Oxidase; EC Metalloproteinase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  SERPINB3 expression on B-cell surface in autoimmune diseases and hepatitis C virus-related chronic l...
Next Document:  Extracellular signal-regulated kinase plays a proapoptotic role in podocytes after reactive oxygen s...