PMID- 22829703
OWN - NLM
STAT- MEDLINE
DCOM- 20121026
LR  - 20220318
IS  - 1535-3699 (Electronic)
IS  - 1535-3699 (Linking)
VI  - 237
IP  - 7
DP  - 2012 Jul
TI  - 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.
PG  - 853-9
LID - 10.1258/ebm.2012.012070 [doi]
AB  - 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.
FAU - Xie, Yuping
AU  - Xie Y
AD  - Regenerative Medicine Research Center, West China Hospital, Sichuan University, 
      Chengdu, Sichuan 610041, China.
FAU - Chen, Jianmin
AU  - Chen J
FAU - Han, Pengfei
AU  - Han P
FAU - Yang, Pingliang
AU  - Yang P
FAU - Hou, Jianglong
AU  - Hou J
FAU - Kang, Y James
AU  - Kang YJ
LA  - eng
GR  - HL63760/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120724
PL  - Switzerland
TA  - Exp Biol Med (Maywood)
JT  - Experimental biology and medicine (Maywood, N.J.)
JID - 100973463
RN  - 0 (Tissue Inhibitor of Metalloproteinase-1)
RN  - EC 1.4.3.13 (Protein-Lysine 6-Oxidase)
RN  - EC 3.4.24.7 (Matrix Metalloproteinase 1)
SB  - IM
MH  - Animals
MH  - Chronic Disease
MH  - Disease Models, Animal
MH  - *Down-Regulation
MH  - Immunohistochemistry
MH  - Macaca mulatta
MH  - Male
MH  - Matrix Metalloproteinase 1/*metabolism
MH  - Myocardial Infarction/*enzymology
MH  - Protein-Lysine 6-Oxidase/*metabolism
MH  - Tissue Inhibitor of Metalloproteinase-1/metabolism
MH  - *Up-Regulation
EDAT- 2012/07/26 06:00
MHDA- 2012/10/27 06:00
CRDT- 2012/07/26 06:00
PHST- 2012/07/26 06:00 [entrez]
PHST- 2012/07/26 06:00 [pubmed]
PHST- 2012/10/27 06:00 [medline]
AID - ebm.2012.012070 [pii]
AID - 10.1258/ebm.2012.012070 [doi]
PST - ppublish
SO  - Exp Biol Med (Maywood). 2012 Jul;237(7):853-9. doi: 10.1258/ebm.2012.012070. Epub 
      2012 Jul 24.