Linked Life Data

8014198

Source:http://linkedlifedata.com/resource/pubmed/id/8014198

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-7-26
pubmed:abstractText
We previously reported that pertussis toxin-sensitive GTP-binding protein is involved in prostaglandin F2 alpha (PGF2 alpha)-induced phosphoinositide (PI) hydrolysis in osteoblast-like MC3T3-E1 cells [Miwa et al. (1990): Biochem Biophys Res Commun 171:1229-1235]. In the present study, we investigated the mechanism of PGF2 alpha-induced Ca2+ influx in MC3T3-E1 cells. PGF2 alpha-induced formation of total inositol phosphates (IPs) was markedly reduced by the depletion of extracellular Ca2+ with EGTA. On the other hand, the depletion of extracellular Ca2+ had little effect on PGF2 alpha-induced inositol 1,4,5-trisphosphate formation. PGF2 alpha stimulated 45Ca2+ influx dose dependently, attaining a maximum effect at 10 nM. Dose of PGF2 alpha above 10 nM caused less than maximal stimulation. Genistein, an inhibitor of protein tyrosine kinase, which by itself had little effect on 45Ca2+ influx, significantly suppressed the PGF2 alpha-induced 45Ca2+ influx in a dose-dependent manner in the range between 1 micrograms/ml and 0.1 mg/ml. Sodium orthovanadate, an inhibitor of protein tyrosine phosphatases, enhanced the PGF2 alpha-induced 45Ca2+ influx. Genistein also suppressed the PGF2 alpha-induced total IPs formation dose dependently in the range between 1 micrograms/ml and 0.1 mg/ml. However, it had little effect on the PGF2 alpha-induced inositol 1,4,5-trisphosphate formation. The pretreatment with pertussis toxin had little effect on the PGF2 alpha-induced 45Ca2+ influx. These results strongly suggest that PGF2 alpha stimulates Ca2+ mobilization from extracellular space and PI hydrolysis via independent pathways in osteoblast-like cells, and the PGF2 alpha-induced Ca2+ influx is regulated by protein tyrosine kinase, resulting in the promotion of PI hydrolysis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Dinoprost, http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Genistein, http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate, http://linkedlifedata.com/resource/pubmed/chemical/Inositol Phosphates, http://linkedlifedata.com/resource/pubmed/chemical/Isoflavones, http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin, http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatases, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Vanadates, http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors, Bordetella
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0730-2312
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
487-93
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Effect of prostaglandin F2 alpha on Ca2+ influx in osteoblast-like cells: function of tyrosine kinase.
pubmed:affiliation
First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't