| pubmed-article:1860893 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1860893 | lifeskim:mentions | umls-concept:C0026844 | lld:lifeskim |
| pubmed-article:1860893 | lifeskim:mentions | umls-concept:C1135918 | lld:lifeskim |
| pubmed-article:1860893 | lifeskim:mentions | umls-concept:C0033371 | lld:lifeskim |
| pubmed-article:1860893 | lifeskim:mentions | umls-concept:C0033640 | lld:lifeskim |
| pubmed-article:1860893 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:1860893 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:1860893 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
| pubmed-article:1860893 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1860893 | pubmed:dateCreated | 1991-9-5 | lld:pubmed |
| pubmed-article:1860893 | pubmed:abstractText | The effects of prolactin (PRL) on A10 (aortic smooth muscle) cell proliferation were examined by measuring both [3H]thymidine incorporation and increases in cell number. PRL induced a significant proliferative response from 10(-11) to 10(-7) M, with optimal activity at 10(-10) M. PRL also enhanced platelet-derived growth factor (PDGF)-induced proliferation. The possibility that PRL induces proliferation through a protein kinase C (PKC)-mediated mechanism was also examined. PRL caused activation of PKC from 10(-12) to 10(-8) M. Antiserum to PRL, a monoclonal antibody directed against the PRL receptor and the immunosuppressive agent cyclosporine A, were able to inhibit PRL-induced proliferation and activation of PKC. The PKC inhibitors, staurosporine, sphingosine, and 1-(-5-iso-quinoline-sulfonyl)-2-methylpiperazine (H-7) also antagonized both proliferation and PKC activation. These data strongly suggest that PRL-induced A10 cell proliferation is mediated through the PKC pathway and that this may play a role in vascular smooth muscle cell hyperplasia, characteristic of the pathogenesis of cardiovascular diseases such as hypertension and atherosclerosis. | lld:pubmed |
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| pubmed-article:1860893 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1860893 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1860893 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1860893 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1860893 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:1860893 | pubmed:issn | 0021-9541 | lld:pubmed |
| pubmed-article:1860893 | pubmed:author | pubmed-author:SauroM DMD | lld:pubmed |
| pubmed-article:1860893 | pubmed:author | pubmed-author:ZornN ENE | lld:pubmed |
| pubmed-article:1860893 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1860893 | pubmed:volume | 148 | lld:pubmed |
| pubmed-article:1860893 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1860893 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1860893 | pubmed:pagination | 133-8 | lld:pubmed |
| pubmed-article:1860893 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:1860893 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1860893 | pubmed:articleTitle | Prolactin induces proliferation of vascular smooth muscle cells through a protein kinase C-dependent mechanism. | lld:pubmed |
| pubmed-article:1860893 | pubmed:affiliation | Department of Pharmacology and Therapeutics, University of South Florida College of Medicine, Tampa. | lld:pubmed |
| pubmed-article:1860893 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1860893 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1860893 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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