PMID- 17971502
OWN - NLM
STAT- MEDLINE
DCOM- 20080616
LR  - 20161124
IS  - 1531-2267 (Electronic)
IS  - 1094-8341 (Linking)
VI  - 32
IP  - 2
DP  - 2008 Jan 17
TI  - Identification of Nogo as a novel indicator of heart failure.
PG  - 182-9
AB  - Numerous genetically engineered animal models of heart failure (HF) exhibit 
      multiple characteristics of human HF, including aberrant beta-adrenergic 
      signaling. Several of these HF models can be rescued by cardiac-targeted 
      expression of the Gbetagamma inhibitory carboxy-terminus of the beta-adrenergic 
      receptor kinase (betaARKct). We recently reported microarray analysis of gene 
      expression in multiple animal models of HF and their betaARKct rescue, where we 
      identified gene expression patterns distinct and predictive of HF and rescue. We 
      have further investigated the muscle LIM protein knockout model of HF (MLP-/-), 
      which closely parallels human dilated cardiomyopathy disease progression and 
      aberrant beta-adrenergic signaling, and their betaARKct rescue. A group of known 
      and novel genes was identified and validated by quantitative real-time PCR whose 
      expression levels predicted phenotype in both the larger HF group and in the 
      MLP-/- subset. One of these novel genes is herein identified as Nogo, a protein 
      widely studied in the nervous system, where it plays a role in regeneration. Nogo 
      expression is altered in HF and normalized with rescue, in an isoform-specific 
      manner, using left ventricular tissue harvested from both animal and human 
      subjects. To investigate cell type-specific expression of Nogo in the heart, 
      immunofluorescence and confocal microscopy were utilized. Nogo expression appears 
      to be most clearly associated with cardiac fibroblasts. To our knowledge, this is 
      the first report to demonstrate the relationship between Nogo expression and HF, 
      including cell-type specificity, in both mouse and human HF and phenotypic 
      rescue.
FAU - Bullard, Tara A
AU  - Bullard TA
AD  - Cardiovascular Research Institute, Division of Cardiology, Department of 
      Medicine, University of Rochester Medical Center, Rochester, New York, USA.
FAU - Protack, Tricia L
AU  - Protack TL
FAU - Aguilar, Frederick
AU  - Aguilar F
FAU - Bagwe, Suveer
AU  - Bagwe S
FAU - Massey, H Todd
AU  - Massey HT
FAU - Blaxall, Burns C
AU  - Blaxall BC
LA  - eng
GR  - T32-HL-07949/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 - 20071030
PL  - United States
TA  - Physiol Genomics
JT  - Physiological genomics
JID - 9815683
RN  - 0 (LIM Domain Proteins)
RN  - 0 (Muscle Proteins)
RN  - 0 (Myelin Proteins)
RN  - 0 (Nogo Proteins)
RN  - 0 (RTN4 protein, human)
RN  - 0 (Rtn4 protein, mouse)
RN  - 0 (cysteine and glycine-rich protein 3)
RN  - EC 2.7.11.15 (beta-Adrenergic Receptor Kinases)
SB  - IM
MH  - Animals
MH  - Cardiomyopathy, Dilated/genetics/metabolism/pathology
MH  - Gene Deletion
MH  - Gene Expression Profiling
MH  - Heart Failure/genetics/metabolism/*pathology
MH  - Humans
MH  - Immunohistochemistry
MH  - LIM Domain Proteins
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Muscle Proteins/*genetics/metabolism
MH  - Myelin Proteins/*genetics/metabolism
MH  - Myocardium/metabolism/*pathology
MH  - Nogo Proteins
MH  - Oligonucleotide Array Sequence Analysis
MH  - beta-Adrenergic Receptor Kinases/genetics/metabolism
EDAT- 2007/11/01 09:00
MHDA- 2008/06/17 09:00
CRDT- 2007/11/01 09:00
PHST- 2007/11/01 09:00 [pubmed]
PHST- 2008/06/17 09:00 [medline]
PHST- 2007/11/01 09:00 [entrez]
AID - 00200.2007 [pii]
AID - 10.1152/physiolgenomics.00200.2007 [doi]
PST - ppublish
SO  - Physiol Genomics. 2008 Jan 17;32(2):182-9. doi: 
      10.1152/physiolgenomics.00200.2007. Epub 2007 Oct 30.