PMID- 21565185
OWN - NLM
STAT- MEDLINE
DCOM- 20110913
LR  - 20131121
IS  - 1096-0945 (Electronic)
IS  - 0014-4800 (Linking)
VI  - 91
IP  - 1
DP  - 2011 Aug
TI  - Hyperhomocysteinemia inhibited cardiac stem cell homing into the peri-infarcted 
      area post myocardial infarction in rats.
PG  - 411-8
LID - 10.1016/j.yexmp.2011.04.010 [doi]
AB  - BACKGROUND: Hyperhomocysteinemia (HHcy) has been reported as an independent risk 
      factor for coronary artery disease; however it is not clear regarding the action 
      of HHcy on the homing of cardiac stem cells (CSCs) to the damaged myocardium and 
      the consequent CSCs-mediated cardiac repair post myocardial infarction. METHODS: 
      Sprague-Dawley (SD) rats were divided into 4 groups. HHcy was induced in the rats 
      by a 6-week high-methionine diet. Rat heart MI model was developed by left 
      coronary artery ligation. Immunofluorescence was used to examine the CSCs 
      migration in vivo via injecting BrdU-labeled CSCs into AV-groove followed by a 
      coronary ligation. Immunohistochemistry, western blot and ELISA analysis were 
      carried out to detect the expression of stem cell factor (SCF) protein, and 
      RT-PCR was conducted for the expression of SCF mRNA. RESULTS: On day 5 of MI 
      model creation, accumulation of CSCs was significantly increased in the 
      peri-infarcted area by the non-hyperhomocysteinemic rats, which led to an 
      improvement of cardiac function at 3 weeks after MI. however, the accumulation of 
      CSCs was markedly decreased by the hyperhomocysteinemic rats followed with the 
      decline of cardiac function. SCF expression was also significantly decreased in 
      the peri-infarcted area by the hyperhomocysteinemic rats compared to the 
      non-hyperhomocysteinemic rats. The experiments in vitro confirmed that 
      homocysteine (Hcy) decreased SCF expression via inhibition of TNF-alpha-induced 
      activity of NF-kappaB, further reduced the migration of CSCs. CONCLUSION: It 
      demonstrated that hyperhomocysteinemia may significantly contribute to restrain 
      CSCs-mediated cardiac repair by reducing SCF-induced homing of CSCs.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Wan, Jie
AU  - Wan J
AD  - Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan 430030, PR China.
FAU - Deng, Yunte
AU  - Deng Y
FAU - Guo, Junli
AU  - Guo J
FAU - Xiao, Guixiang
AU  - Xiao G
FAU - Kuang, Dong
AU  - Kuang D
FAU - Zhu, Yuanli
AU  - Zhu Y
FAU - Duan, Yaqi
AU  - Duan Y
FAU - Wang, Guoping
AU  - Wang G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110501
PL  - Netherlands
TA  - Exp Mol Pathol
JT  - Experimental and molecular pathology
JID - 0370711
RN  - 0 (Stem Cell Factor)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - AE28F7PNPL (Methionine)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Blotting, Western
MH  - Cell Movement/*physiology
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Homocysteine/pharmacology
MH  - Hyperhomocysteinemia/chemically induced/*physiopathology
MH  - Immunohistochemistry
MH  - Male
MH  - Methionine/administration & dosage
MH  - Myocardial Infarction/drug therapy/metabolism/*pathology
MH  - Myocardium/*cytology
MH  - Myocytes, Cardiac/drug effects/metabolism/*pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Stem Cell Factor/metabolism
MH  - Stem Cells/*cytology
EDAT- 2011/05/14 06:00
MHDA- 2011/09/14 06:00
CRDT- 2011/05/14 06:00
PHST- 2011/01/28 00:00 [received]
PHST- 2011/04/19 00:00 [accepted]
PHST- 2011/05/14 06:00 [entrez]
PHST- 2011/05/14 06:00 [pubmed]
PHST- 2011/09/14 06:00 [medline]
AID - S0014-4800(11)00050-5 [pii]
AID - 10.1016/j.yexmp.2011.04.010 [doi]
PST - ppublish
SO  - Exp Mol Pathol. 2011 Aug;91(1):411-8. doi: 10.1016/j.yexmp.2011.04.010. Epub 2011 
      May 1.