Linked Life Data

8922680

Source:http://linkedlifedata.com/resource/pubmed/id/8922680

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1997-3-11
pubmed:abstractText
Environmental cues are known to be important in the migration, survival, and differentiation of neural crest cells and their derivatives. Retinoic acid (RA) can increase the number of adrenergic cells that develop in neural crest cultures in a dose dependent manner. These results with RA prompted us to investigate the effects of other retinoids and other related compounds on neural crest cultures. We have investigated the role of thyroid hormone (T3) in the development of adrenergic cells in quail neural crest cultures. T3 produced a significant decrease in the number of catecholamine-positive cells that developed in neural crest cultures after 7 days in vitro, as compared to untreated controls. The decrease in adrenergic cells produced by T3 was paralleled by a decrease in the number of tyrosine hydroxylase-positive cells, but T3 did not reduce either total or melanocyte cell number. Cultures were sensitive to T3 during the first 5 days in culture and T3 was not cytotoxic to adrenergic cells. The decrease in adrenergic cells seen with T3 was partially reversed by RA suggesting that these two compounds may be working through a common pathway.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0165-3806
pubmed:author
pubmed:issnType
Print
pubmed:day
23
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
184-91
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Thyroid hormone decreases the number of adrenergic cells that develop in neural crest cultures and can inhibit the stimulatory action of retinoic acid.
pubmed:affiliation
Neuroscience Program, University of Connecticut Health Center, Farmington 06030-3405, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.