Linked Life Data

7852883

Source:http://linkedlifedata.com/resource/pubmed/id/7852883

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-3-10
pubmed:abstractText
To understand the development of the human pancreas better, we studied the expression and regulation of insulin, insulin-like growth factor-II (IGF-II) and transforming growth factor-alpha (TGF-alpha) genes in the human fetal pancreas and islet-like cell clusters (ICC) from the second trimester human fetuses. Northern blot analysis revealed an abundant expression of IGF-II, insulin and TGF-alpha mRNAs in the intact pancreas and the cultured ICCs. Furthermore, transcripts for insulin receptor, type-1 and -2 IGF receptors, and GH receptor could be amplified by polymerase chain reaction analysis from the pancreas and the ICCs. With in-situ hybridization, IGF-II mRNA was found in abundance in both the exocrine and endocrine pancreas, exceeding the amount of insulin mRNA. In ICCs, insulin mRNA-containing cells were present as small clusters in the periphery and in the centre of the clusters corresponding to the immunolocation of insulin. The ICCs also contained many epidermal growth factor-, insulin- and type-1 IGF receptor- and TGF-alpha-positive cells. When the ICCs were cultured in the presence of various secretagogues, only dibutyryl cyclic AMP was found to up-regulate insulin mRNA (39%; P < 0.05). IGF-II mRNA was also under cyclic AMP-dependent regulation (threefold increase; P = 0.025). Furthermore, blocking the type-1 IGF receptor with a monoclonal receptor antibody drastically reduced insulin expression (87%; P = 0.005) and additionally down-regulated IGF-II mRNA (49%; P = 0.005). IGF-1, IGF-II, TGF-alpha or epidermal growth factor-receptor antibody had no significant effect on either insulin or IGF-II mRNA. Exogenous TGF-alpha inhibited the release of insulin by the ICCs. It was concluded that IGF-II and TGF-alpha may be involved in the regulation of islet growth and differentiation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-0795
pubmed:author
pubmed:issnType
Print
pubmed:volume
138
pubmed:geneSymbol
IGF-II, TGF-&agr;
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
127-36
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:7852883-Base Sequence, pubmed-meshheading:7852883-Blotting, Northern, pubmed-meshheading:7852883-Cells, Cultured, pubmed-meshheading:7852883-Cyclic AMP, pubmed-meshheading:7852883-DNA, pubmed-meshheading:7852883-Fetus, pubmed-meshheading:7852883-Gene Expression Regulation, Developmental, pubmed-meshheading:7852883-Humans, pubmed-meshheading:7852883-Immunohistochemistry, pubmed-meshheading:7852883-In Situ Hybridization, pubmed-meshheading:7852883-Insulin, pubmed-meshheading:7852883-Insulin-Like Growth Factor II, pubmed-meshheading:7852883-Islets of Langerhans, pubmed-meshheading:7852883-Molecular Sequence Data, pubmed-meshheading:7852883-Oligonucleotide Probes, pubmed-meshheading:7852883-Polymerase Chain Reaction, pubmed-meshheading:7852883-RNA, Messenger, pubmed-meshheading:7852883-Receptor, IGF Type 1, pubmed-meshheading:7852883-Receptor, Insulin, pubmed-meshheading:7852883-Receptors, Somatotropin, pubmed-meshheading:7852883-Transforming Growth Factor alpha
pubmed:year
1993
pubmed:articleTitle
Insulin-like growth factor-II and transforming growth factor-alpha in developing human fetal pancreatic islets.
pubmed:affiliation
Department of Pediatrics, University of Helsinki, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't