Linked Life Data

17012346

Source:http://linkedlifedata.com/resource/pubmed/id/17012346

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-2-8
pubmed:abstractText
The Otsuka Long-Evans Tokushima fatty rat is an animal model of Type 2 diabetes mellitus (DM), which is characterized by diastolic dysfunction associated with decreased sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a). The aim of this study was to examine whether gene transfer of SERCA2a can influence coronary blood flow and cardiomyocyte diameter in this model. DM rats were injected with adenovirus carrying SERCA2a (DM+SERCA) or beta-galactosidase gene (DM+betaGal). Coronary blood flow was measured in cross-circulated excised hearts 3 days after infection. Although in all groups coronary blood flow remained unchanged even if left ventricular (LV) volume or intracoronary Ca(2+) infusion was increased, the DM+SERCA group showed a sustained increase in coronary blood flow compared with the other groups. This result suggests that the sustained high coronary blood flow is a specific response in SERCA2a-overexpressed hearts. Although the LV weight-to-body weight ratio (LV/BW) and cardiomyocyte diameter were higher in the DM and DM+betaGal groups than in the non-DM group, in the DM+SERCA group, these measurements were restored to non-DM size. The percentages of collagen area in the three DM groups was significantly higher than results shown in non-DM rats, and there were no significant differences in collagen area percentage among the three DM groups. These results suggest that a lowered LV/BW by SERCA2a overexpression is due mainly to reduced size of cardiomyocytes without any changes in collagen area percentage. In conclusion, in DM failing hearts, SERCA2a gene transfer can increase coronary blood flow and reduce cardiomyocyte size without reduction in collagen production.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
292
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1204-7
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed-meshheading:17012346-Adenoviridae, pubmed-meshheading:17012346-Animals, pubmed-meshheading:17012346-Cardiomegaly, pubmed-meshheading:17012346-Cell Size, pubmed-meshheading:17012346-Collagen, pubmed-meshheading:17012346-Coronary Circulation, pubmed-meshheading:17012346-Diabetes Mellitus, Type 2, pubmed-meshheading:17012346-Disease Models, Animal, pubmed-meshheading:17012346-Gene Transfer Techniques, pubmed-meshheading:17012346-Genetic Vectors, pubmed-meshheading:17012346-Male, pubmed-meshheading:17012346-Myocardial Contraction, pubmed-meshheading:17012346-Myocytes, Cardiac, pubmed-meshheading:17012346-Random Allocation, pubmed-meshheading:17012346-Rats, pubmed-meshheading:17012346-Rats, Inbred OLETF, pubmed-meshheading:17012346-Rats, Long-Evans, pubmed-meshheading:17012346-Sarcoplasmic Reticulum Calcium-Transporting ATPases
pubmed:year
2007
pubmed:articleTitle
Transcoronary gene transfer of SERCA2a increases coronary blood flow and decreases cardiomyocyte size in a type 2 diabetic rat model.
pubmed:affiliation
Cardiovascular Research Center, Massachusetts General Hospital, 149 13th St., CNY-4, Charlestown, MA 02129, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural