Linked Life Data

9537440

Source:http://linkedlifedata.com/resource/pubmed/id/9537440

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1998-4-16
pubmed:abstractText
Cultured parenchymal liver cells (PC) were recently recognized to contain (latent) transforming growth factor beta (TGF-beta) while the expression of TGF-beta mRNA remains controversial. This study was designed to analyze PC in different microenvironments (liver in situ, highly purified, isolated, and cultured PC) regarding the qualitative and quantitative content of mature and latent TGF-beta protein (immunostainings, enzyme-linked immunosorbent assay [ELISA], and enzyme-labeled fluorescence [ELF] technique). The results were compared with its gene expression (reverse-transcription polymerase chain reaction [RT-PCR]). In all microenvironments, PC contained latent TGF-beta, which was partially activated after cell isolation and culture. The amount of total TGF-beta (mature plus latent) of latency-associated peptide (LAP) and of latent TGF-beta binding protein (LTBP) were shown to decrease during culture. In contrast, TGF-beta2 and TGF-beta3 mRNA and LTBP-1 and -3 mRNA expression were first detectable after culture. Permeabilization of cell membranes in whole liver and of isolated PC with streptolysin O or carbon tetrachloride, respectively, released TGF-beta, a part of which was integrated in the large latent complex as estimated by analytical gel filtration chromatography. The TGF-beta released by damaged PC induces paracrine effects on hepatic stellate cell cultures. It stimulates hyaluronan synthesis and antagonizes the effect of mitogenic factor(s) of PC on [3H]thymidine incorporation. The results strongly suggest that the main part of hepatocellular TGF-beta is not generated by de novo synthesis but from uptake into the liver in vivo. The immunodetection of preexisting mature TGF-beta after isolation of the cells is probably caused by intracellular activation of latent TGF-beta. The injury-dependent discharge of TGF-beta from PC might be an important mechanism for initiation and perpetuation of various forms of chronic human liver diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1003-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
(Latent) transforming growth factor beta in liver parenchymal cells, its injury-dependent release, and paracrine effects on rat hepatic stellate cells.
pubmed:affiliation
Department of Clinical Chemistry, Philipps University, Marburg, Germany.
pubmed:publicationType
Journal Article