Linked Life Data

7538370

Source:http://linkedlifedata.com/resource/pubmed/id/7538370

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-6-22
pubmed:abstractText
The aim of the present investigation was to study the role of the IGF system in the development of smooth muscle hypertrophy. Hypertrophy was initiated by partial ligation of the urethra in female Sprague-Dawley rats. The solution hybridization assay was used to analyse the mRNA levels. Ligation of the urethra induced a sustained increase in bladder wet weight during the following 6-week period studied. IGF-I mRNA increased from 1 to 3 amol/micrograms DNA 1-day after ligation, peaked at 3-days (4-fold), and normalized 6-weeks after ligation. In hypertrophying bladder, IGFBP-2 and -4 mRNA increased sharply during the first 10 days (5-fold) and remained elevated during the 6-week period. The IGF-I receptor mRNA did not change significantly. Removal of the obstruction 10 days after ligation caused a regression of bladder wet weight, and resulted in normalization of IGF-I, IGFBP-2 and -4 mRNA. The results show a close correlation between progression or regression of smooth muscle hypertrophy and differential regulation of IGF-I, IGFBP-2 and -4 mRNA, indicating that the IGF system may play a role in smooth muscle hypertrophy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0956-523X
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
45-52
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Development of smooth muscle hypertrophy is closely associated with increased gene expression of insulin-like growth factor binding protein-2 and -4.
pubmed:affiliation
Department of Cellbiology, Faculty of Health Sciences, University of Linköping, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't