Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
2006-8-28
pubmed:abstractText
Glial cells express thromboxane A(2) receptor, but its physiological role remains unknown. The present study was performed to examine thromboxane A(2) receptor-mediated morphological change in 1321N1 human astrocytoma cells. Thromboxane A(2) receptor agonists U46619 and STA(2) caused a rapid morphological change to spindle shape from stellate form of the cells pretreated with dibutyryl cyclic AMP, but neither carbachol nor histamine caused the change, suggesting that G(q) pathway may not mainly contribute to the change. Rho kinase inhibitor Y-27632 inhibited U46619-induced morphological change, and U46619 increased the GTP-bound form of RhoA accompanied with actin stress fiber formation. These responses were reduced by expression of p115-RGS that inhibits G(12)/(13) signaling pathway. U46619 also caused the phosphorylation of extracellular signal-regulated kinase (ERK) and [(3)H]thymidine incorporation mainly through G(12)/(13)-Rho pathway. These results suggest that stimulation of thromboxane A(2) receptor causes the morphological change with proliferation mainly through G(12)/(13) activation in glial cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
545
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
100-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Thromboxane A2 receptor-mediated G12/13-dependent glial morphological change.
pubmed:affiliation
Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't