Linked Life Data

15967869

Source:http://linkedlifedata.com/resource/pubmed/id/15967869

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-7-29
pubmed:abstractText
The antifibrotic effects of the peptide hormone relaxin on cardiac and renal fibrosis were studied in 9- to 10-month-old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Rats (n=8 to 9 per group) were allocated into 3 groups: WKY controls, vehicle-treated SHR (SHR-V), and relaxin-treated SHR (SHR-R). Relaxin (0.5 mg/kg per day) was administered via subcutaneously implanted osmotic mini-pumps over 2 weeks before hearts and kidneys were harvested for analysis. Collagen content was analyzed by hydroxyproline assay, gel electrophoresis, and quantitative histology. Zymography was used to determine matrix metalloproteinase (MMP) expression and Western blotting to determine proliferating cell nuclear antigen (PCNA) expression and alpha-smooth muscle actin (alpha-SMA)/myofibroblast expression, whereas cardiac hypertrophy was assessed by myocyte size and real-time polymerase chain reaction of associated genes. The left ventricular (LV) myocardium of SHR-V contained increased collagen levels (by 25+/-1%, P<0.01 using biochemical analysis and 3-fold; P<0.01 using quantitative histology), enhanced expression of PCNA (by 70+/-8%; P<0.01), alpha-SMA (by 32+/-2%; P<0.05), and the collagen-degrading enzyme MMP-9 (by 70+/-6%; P<0.05) versus respective levels measured in WKY controls. The kidneys of SHR-V also contained increased collagen (25+/-2%, P<0.05 using biochemical analysis and 2.4-fold; P<0.01 using quantitative histology). Relaxin treatment significantly normalized collagen content in the LV (P<0.01) and kidney (P<0.05), completely inhibited cell proliferation (P<0.01) and fibroblast differentiation (P<0.05) in the LV, and increased MMP-2 expression (by 25+/-1%; P<0.05) without affecting MMP-9 in the LV compared with that measured in SHR-V. Thus, relaxin is a potent antifibrotic hormone with a rapid-occurring efficacy that may have therapeutic potential for hypertensive disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
412-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15967869-Animals, pubmed-meshheading:15967869-Atrial Natriuretic Factor, pubmed-meshheading:15967869-Biological Markers, pubmed-meshheading:15967869-Cardiomegaly, pubmed-meshheading:15967869-Collagen, pubmed-meshheading:15967869-Fibroblasts, pubmed-meshheading:15967869-Fibrosis, pubmed-meshheading:15967869-Heart, pubmed-meshheading:15967869-Humans, pubmed-meshheading:15967869-Hypertension, pubmed-meshheading:15967869-Kidney, pubmed-meshheading:15967869-Male, pubmed-meshheading:15967869-Matrix Metalloproteinase 2, pubmed-meshheading:15967869-Matrix Metalloproteinase 9, pubmed-meshheading:15967869-Myocardium, pubmed-meshheading:15967869-Rats, pubmed-meshheading:15967869-Rats, Inbred SHR, pubmed-meshheading:15967869-Rats, Inbred WKY, pubmed-meshheading:15967869-Recombinant Proteins, pubmed-meshheading:15967869-Relaxin
pubmed:year
2005
pubmed:articleTitle
Relaxin reverses cardiac and renal fibrosis in spontaneously hypertensive rats.
pubmed:affiliation
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't