Linked Life Data

9407494

Source:http://linkedlifedata.com/resource/pubmed/id/9407494

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1998-1-12
pubmed:abstractText
To determine the paracrine interactions involved in the tubulointerstitial response to progressive renal disease, the role of insulin-like growth factor-I (IGF-I) and its binding proteins (IGFBPs) in in vitro interactions between human proximal tubule cells (PTC) and renal cortical fibroblasts (CF) were studied in primary cell culture. PTC growth and transport were increased in the presence of CF-conditioned media (CF-CM), as shown by increased thymidine incorporation, cellular protein content and sodium-hydrogen exchange (NHE) activity, to 185 +/- 31% (P < 0.01), 150 +/- 18% (P < 0.05) and 195 +/- 27% (P < 0.01) of the control values, respectively. IGF-I was produced by cultured CF at a rate of 64.6 +/- 7.5 ng/mg protein/day. Exogenous IGF-I applied to PTC provoked similar enhancement of growth and NHE activity as CF-CM and the stimulatory effect of CF-CM was blocked by specific immunoneutralization of IGF-I receptors. These receptors were threefold more abundant on PTC basolateral versus apical membranes. IGF binding proteins (IGFBP)-2 and IGFBP-3 were secreted by CF at rates of 694 +/- 88 and 1769 +/- 45 ng/mg/day, with the release of IGFBP-3 being enhanced in the presence of PTC-CM (120.0 +/- 9.7% of control, P < 0.01). Moreover, the addition of CF-CM to PTC increased cell-associated IGFBP-3 on PTC surfaces, without changes in IGF-I receptor numbers or affinity and without changes in PTC mRNA for IGFBP-3. Des(1-3)IGF-I, an analog that binds to the IGF-I receptor but not to IGFBPs, provided a less potent stimulus for PTC growth compared with IGF-I, indicating that cell-associated IGFBP-3 facilitates the action of IGF-I on PTC. The results support important paracrine roles for both IGF-I and IGFBPs in the interstitial regulation of proximal tubule growth and transport.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
52
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1486-96
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9407494-Antibodies, pubmed-meshheading:9407494-Binding, Competitive, pubmed-meshheading:9407494-Biological Transport, pubmed-meshheading:9407494-Blotting, Northern, pubmed-meshheading:9407494-Cell Communication, pubmed-meshheading:9407494-Cell Division, pubmed-meshheading:9407494-Cells, Cultured, pubmed-meshheading:9407494-Culture Media, Conditioned, pubmed-meshheading:9407494-Fibroblasts, pubmed-meshheading:9407494-Humans, pubmed-meshheading:9407494-Insulin-Like Growth Factor Binding Protein 2, pubmed-meshheading:9407494-Insulin-Like Growth Factor Binding Protein 3, pubmed-meshheading:9407494-Insulin-Like Growth Factor I, pubmed-meshheading:9407494-Kidney Cortex, pubmed-meshheading:9407494-Kidney Tubules, Proximal, pubmed-meshheading:9407494-Neutralization Tests, pubmed-meshheading:9407494-Paracrine Communication, pubmed-meshheading:9407494-Peptide Fragments, pubmed-meshheading:9407494-RNA, Messenger, pubmed-meshheading:9407494-Receptor, IGF Type 1, pubmed-meshheading:9407494-Sodium-Hydrogen Antiporter
pubmed:year
1997
pubmed:articleTitle
Human renal fibroblasts modulate proximal tubule cell growth and transport via the IGF-I axis.
pubmed:affiliation
Department of Medicine, University of Sydney, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't