Linked Life Data

7895691

Source:http://linkedlifedata.com/resource/pubmed/id/7895691

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1995-4-25
pubmed:abstractText
PTH-related protein (PTHrP) is induced in aortic vascular smooth muscle cells (VSMC) in association with mitogen-stimulated proliferation. In this study we examined the role of the cell cycle in the control of PTHrP gene expression. In asynchronously cycling cells grown in serum-containing medium, PTHrP-immunoreactive cells were enriched in G2+M, as revealed by fluorescence-activated cell sorting using a specific monoclonal antibody. PTHrP messenger RNA (mRNA) increased transiently in cells after release from chemically induced cell cycle blockade; levels increased by 10-fold at 2 h, coincident with expression of histone-4 mRNA and enrichment of VSMC in the early S phase. However, PTHrP mRNA levels then declined abruptly while the proportion of cells in the S phase and histone-4 mRNA levels remained constant for 8 h. When cell cycle-arrested cells were exposed to fresh serum-containing medium, angiotensin-II, or phorbol ester without removing the cell cycle blocking agents, PTHrP mRNA levels were induced over a time course identical to that observed in cells released from the blockade. This suggests that progression through the cycle per se is not necessary for mitogen-induced PTHrP mRNA expression, and that conventional chemical synchronization is not adequate to examine the cell cycle dependency of PTHrP mRNA abundance in VSMC. By contrast, in two different PTHrP-producing carcinoma cell lines, PTHrP and its mRNA were not altered as a function of cell cycle, demonstrating that different mechanisms control PTHrP expression in these cancer cells. In conclusion, constitutive immunoreactive levels of PTHrP are low in normally cycling VSMC (but not cancer cells) and accumulate during the latter stages of the cell cycle, suggesting a role for this protein in the process of smooth muscle cell division. However, separate mechanisms, which are independent of cell cycle, operate through a protein kinase-C-dependent pathway(s) to mediate the stimulation of PTHrP gene expression by vasoconstrictors such as angiotensin-II.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
136
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1782-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Involvement of cell cycle and mitogen-activated pathways in induction of parathyroid hormone-related protein gene expression in rat aortic smooth muscle cells.
pubmed:affiliation
Department of Medicine, Cedars-Sinai Research Institute, Cedars-Sinai Medical Center, University of California-Los Angeles School of Medicine 90048.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't