PMID- 16617122
OWN - NLM
STAT- MEDLINE
DCOM- 20060926
LR  - 20211020
IS  - 0363-6135 (Print)
IS  - 1522-1539 (Electronic)
IS  - 0363-6135 (Linking)
VI  - 291
IP  - 3
DP  - 2006 Sep
TI  - Activation of endoplasmic reticulum stress response during the development of 
      ischemic heart disease.
PG  - H1411-20
AB  - Endoplasmic reticulum (ER) stress has been found to be associated with 
      neurodegenerative diseases and diabetes mellitus. Whether ER stress is involved 
      in the development of heart disease is not known. Cardiac-specific expression of 
      monocyte chemoattractant protein-1 (MCP-1) in mice causes the development of 
      ischemic heart disease. Here we report that microarray analysis of gene 
      expression changes in the heart of these transgenic mice revealed that a cluster 
      of ER stress-related genes was transcriptionally activated in the heart during 
      the development of ischemic heart disease. The gene array results were verified 
      by quantitative real-time PCR that showed highly elevated transcript levels of 
      genes involved in unfolded protein response such as ER and cytoplasmic 
      chaperones, oxidoreductases, protein disulfide isomerase (PDI) family, and 
      ER-associated degradation system such as ubiquitin. Immunoblot analysis confirmed 
      the expression of chaperones, PDI, and ubiquitin. Immunohistochemical analyses 
      showed that ER stress proteins were associated mainly with the degenerating 
      cardiomyocytes. A novel ubiquitin fold modifier (Ufm1) that has not been 
      previously associated with ER stress and not found to be induced under any 
      condition was also found to be upregulated in the hearts of MCP mice (transgenic 
      mice that express MCP-1 specifically in the heart). The present results strongly 
      suggest that activation of ER stress response is involved in the development of 
      ischemic heart disease in this murine model.
FAU - Azfer, Asim
AU  - Azfer A
AD  - Biomolecular Science Center, Burnett College of Biomedical Sciences, University 
      of Central Florida, Bldg. 20, Rm. 136, Orlando, FL 32816-2364, USA.
FAU - Niu, Jianli
AU  - Niu J
FAU - Rogers, Linda M
AU  - Rogers LM
FAU - Adamski, Frances M
AU  - Adamski FM
FAU - Kolattukudy, Pappachan E
AU  - Kolattukudy PE
LA  - eng
GR  - R01 HL069458/HL/NHLBI NIH HHS/United States
GR  - R56 HL069458/HL/NHLBI NIH HHS/United States
GR  - HL-69458/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20060414
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Molecular Chaperones)
RN  - 0 (Proteins)
RN  - 0 (Ubiquitin)
RN  - 0 (Ufm1 protein, mouse)
RN  - 9007-49-2 (DNA)
RN  - EC 1.- (Oxidoreductases)
RN  - EC 5.3.4.1 (Protein Disulfide-Isomerases)
SB  - IM
MH  - Animals
MH  - Apoptosis/physiology
MH  - Chemokine CCL2/genetics/metabolism
MH  - DNA/genetics
MH  - Endoplasmic Reticulum/*physiology
MH  - Gene Expression Profiling
MH  - Gene Expression Regulation/genetics/*physiology
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Molecular Chaperones/genetics/metabolism
MH  - Myocardial Ischemia/*genetics/pathology/*physiopathology
MH  - Myocardium/metabolism/pathology
MH  - Oligonucleotide Array Sequence Analysis
MH  - Oxidoreductases/genetics/metabolism
MH  - Protein Disulfide-Isomerases/genetics/metabolism
MH  - Proteins/genetics/metabolism
MH  - Stress, Physiological/*physiopathology
MH  - Ubiquitin/genetics/metabolism
PMC - PMC1575464
MID - NIHMS11971
EDAT- 2006/04/18 09:00
MHDA- 2006/09/27 09:00
PMCR- 2008/02/01
CRDT- 2006/04/18 09:00
PHST- 2006/04/18 09:00 [pubmed]
PHST- 2006/09/27 09:00 [medline]
PHST- 2006/04/18 09:00 [entrez]
PHST- 2008/02/01 00:00 [pmc-release]
AID - 01378.2005 [pii]
AID - 10.1152/ajpheart.01378.2005 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2006 Sep;291(3):H1411-20. doi: 
      10.1152/ajpheart.01378.2005. Epub 2006 Apr 14.