Linked Life Data

16287488

Source:http://linkedlifedata.com/resource/pubmed/id/16287488

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2005-11-18
pubmed:abstractText
It has been repeatedly reported that endothelin-3 (ET-3) is expressed by gastrointestinal mesenchymes, and that paracrine signaling between ET-3 and its receptor plays an essential role in controlling differentiation of the enteric nervous system in the gut, especially in the colon. However it remains to be solved whether ET-3 plays a role in regulating the growth of gastrointestinal epithelial cells. We have previously reported culture systems for forestomach, glandular stomach and duodenal epithelial cells, but a system for colonic epithelial cells has not been established. In the present study, we examined optimal culture conditions for colonic epithelial cells, and examined whether ET-3 affects the growth of gastrointestinal epithelial cells, with special reference to colonic cells. We found that ET-3 dose-dependently and region-specifically stimulated their growth in primary culture: colonic epithelial cells were most responsive, followed by duodenal and glandular stomach epithelial cells. Reverse transcription-polymerase chain reaction analysis showed that ET-3 and a receptor for ET-3 were expressed by both colonic mesenchymes and epithelia, but the levels were much higher in mesenchymes than in epithelia. These results suggest that ET-3 plays an important role in the growth control of colonic epithelial cells, possibly by mediating epithelial-mesenchymal interactions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0012-1592
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
573-80
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Endothelin-3 controls growth of colonic epithelial cells by mediating epithelial-mesenchymal interaction.
pubmed:affiliation
Department of Biological Sciences, Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. hfukama.monc@tmd.ac.jp
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't