Linked Life Data

7966347

Source:http://linkedlifedata.com/resource/pubmed/id/7966347

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1994-12-14
pubmed:abstractText
In the present study, we examined whether insulin-like growth factor-II (IGF-II) induces hypertrophy of cultured neonatal rat cardiomyocytes. IGF-II (10(-7) M) increased the cell surface area of, and the protein content in, cardiomyocytes after 48 h-exposure. IGF-II dose-dependently (10(-10)-10(-7) M) stimulated protein synthesis as evaluated by [3H]leucine incorporation; the maximum response was 1.7-fold increase over control at 10(-7) M. Since the response of cardiac hypertrophy is characterized by enhanced expression of muscle specific genes, effects of IGF-II on steady-state levels of mRNA for myosin light chain 2 (MLC2), troponin I and alpha-actin isoforms (skeletal and cardiac isoforms) were evaluated by Northern blot analysis. IGF-II (10(-7) M) increased mRNA levels for MLC2, troponin I and skeletal alpha-actin, as early as 60 min with a maximum response after 6 h, whereas cardiac alpha-actin mRNA levels were unaffected. Calcium channel blocker, nicardipine, inhibited IGF-II-stimulated skeletal alpha-actin mRNA levels, however, inhibitor of protein kinase C, H-7, unaffected. These results suggest that IGF-II plays a potential role in cardiac hypertrophy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
789-95
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Insulin-like growth factor-II induces hypertrophy with increased expression of muscle specific genes in cultured rat cardiomyocytes.
pubmed:affiliation
Second Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't