Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-9-30
pubmed:abstractText
Cultured endothelial cells characteristically form a monolayer and become quiescent at saturation density. This study shows that microtubule destabilization in confluent cultures of bovine aortic endothelial cells stimulates fibroblast growth factor 2 (FGF-2, bFGF)-dependent DNA synthesis. Twenty-four hours after addition of the microtubule-disrupting drug colchicine, tritiated thymidine incorporation increases up to fivefold when compared to control cultures. Significant stimulation is seen with doses from 0.05 to 1.0 microgram/ml. The effect of colchicine is quantitatively similar to stimulation of the same cultures with 5 ng/ml FGF-2. Furthermore, the stimulation of DNA synthesis by colchicine can be completely blocked by the addition of a neutralizing antibody to FGF-2. This suggests that colchicine may stimulate bovine aortic endothelial cells by modulating endogenous FGF-2/receptor interactions or that colchicine acts by a different mechanism that requires the growth factor for mitogenicity. The combined effects of colchicine and FGF-2 are more than additive, which supports the idea that microtubule disruption may facilitate cellular response to FGF-2. Cytochalasin B, preventing actin polymerization, inhibits the mitogenic response to FGF-2 but not the response to colchicine. These results are best interpreted as evidence that colchicine stimulates endothelial cell DNA synthesis by a pathway that requires endogenous FGF-2 and may be facilitating cellular responsiveness to the growth factor by disrupting the monolayer via the cytoskeleton.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1061164, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1309784, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1594631, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1657293, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1724246, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1764263, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1860889, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1868547, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1918064, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-1990021, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2023924, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2085440, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2153562, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2298295, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2318909, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2333303, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2347923, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2425435, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2433585, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2438264, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2474036, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2479375, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2738102, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2760113, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-293731, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-2996359, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-3126193, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-315067, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-3417781, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-3470794, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-3997978, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-468908, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-6111398, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-6244563, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-6429159, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-6862514, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-7096451, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-7263771, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-805204, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-830992, http://linkedlifedata.com/resource/pubmed/commentcorrection/8362986-895874
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0002-9440
pubmed:author
pubmed:issnType
Print
pubmed:volume
143
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
937-48
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Microtubule disruption stimulates DNA synthesis in bovine endothelial cells and potentiates cellular response to basic fibroblast growth factor.
pubmed:affiliation
Department of Pathology, University of Washington, Seattle 98195.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.