PMID- 19641707
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20110714
LR  - 20231105
IS  - 1205-6626 (Print)
IS  - 1205-6626 (Linking)
VI  - 8
IP  - 3
DP  - 2003 Fall
TI  - Molecular pathogenesis of severe cardiomyopathy in the TO-2 hamster.
PG  - 143-6
AB  - BACKGROUND: Cardiomyopathy (CM) is a life-threatening disease with progressive 
      degeneration of cardiac muscle. From a representative animal model of CM, the 
      BIO14.6 hamster, arose the TO-2 strain manifesting a severe, dilated form of CM. 
      Previous studies demonstrated that both strains have an identical genomic 
      deletion disrupting the delta-sarcoglycan gene to cause CM. OBJECTIVE: To 
      elucidate an additional pathogenesis for cardiac dilation in the TO-2 hamster. 
      METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) was used to 
      assess the expression levels of genes for cardiac hypertrophy, such as 
      beta-myosin heavy chain and preproendothelin-1. The involvement of apoptosis in 
      CM was tested using terminal deoxynucleotidyl transferase-mediated dUTP-biotin 
      end-labelling (TUNEL) and DNA ladder assays. The progression of cardiac 
      degeneration was visualized using specific histological staining techniques. 
      Echocardiography was performed to estimate the wall thickness and the movement of 
      a living hamster heart. RESULTS: RT-PCR showed the expression of the genes 
      involved in cardiac hypertrophy to be higher in TO-2 hamsters than in BIO14.6 
      hamsters, contary to what the thin myocardium may suggest. DNA ladder and TUNEL 
      assays showed no significant difference in apoptosis in the hearts of either 
      strain. In contrast, the infiltrate of inflammatory cells was prominent in the 
      myocardium of TO-2 hamsters. In addition to dilation of the cardiac chamber, 
      echocardiography also revealed disharmonized contraction in TO-2 hearts without 
      apparent arrhythmias. CONCLUSIONS: Impairment of compensatory cardiac hypertrophy 
      or involvement of apoptosis is less likely to be an additional pathogenesis in 
      the TO-2 hamster. The present data suggest that augmented necrosis is the 
      principal cause of severe CM in the TO-2 hamster. Further analysis of the 
      molecular pathogenesis of TO-2 would help to disclose the final common pathways 
      for the manifestation of CM.
FAU - Sakamoto, Aiji
AU  - Sakamoto A
AD  - Division of Biotechnology, National Cardiovascular Center Research Institute, 
      Osaka, and Form and Function, PRESTO, Japan Science and Technology Agency, 
      Saitama, Japan.
LA  - eng
PT  - Journal Article
PL  - Canada
TA  - Exp Clin Cardiol
JT  - Experimental and clinical cardiology
JID - 9715903
PMC - PMC2716276
OTO - NOTNLM
OT  - Apoptosis
OT  - Cardiac hypertrophy
OT  - Cardiomyopathy
OT  - Genetic modifier
OT  - Necrosis
OT  - TO-2 hamster
EDAT- 2003/10/01 00:00
MHDA- 2003/10/01 00:01
PMCR- 2003/09/01
CRDT- 2009/07/31 09:00
PHST- 2009/07/31 09:00 [entrez]
PHST- 2003/10/01 00:00 [pubmed]
PHST- 2003/10/01 00:01 [medline]
PHST- 2003/09/01 00:00 [pmc-release]
AID - ecc08143 [pii]
PST - ppublish
SO  - Exp Clin Cardiol. 2003 Fall;8(3):143-6.