Linked Life Data

7885058

Source:http://linkedlifedata.com/resource/pubmed/id/7885058

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1995-4-7
pubmed:abstractText
The proliferative response of IMR-90 fibroblasts at low and high population doubling level (PDL) to protein kinase C activation has been investigated to clarify whether the reduced mitogenic responsiveness of senescent cells can be ascribed to an alteration in protein kinase C signal transduction pathway. The results show that the signaling pathway leading to DNA synthesis through protein kinase C activation, appears to be modified in senescent IMR-90 human fibroblasts. High PDL fibroblasts exhibit a different sensitivity to phorbol 12-myristate 13-acetate (PMA) and dioctanoylglycerol (diC8); high glucose reduced responsiveness to PMA only in these cells. In addition, high PDL fibroblasts are characterized by an increase in diacylglycerol (DAG) cellular mass that could contribute to the different regulatory properties of the signaling pathway. On the other hand, the ability of the cyclooxygenase inhibitor indomethacin to strikingly improve the proliferative response of high PDL cells to PMA indicates that an altered overall metabolism of arachidonate may represent a crucial step in the reduced mitogenic response involving protein kinase C activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0047-6374
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-11
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Involvement of protein kinase C and arachidonate signaling pathways in the alteration of proliferative response of senescent IMR-90 human fibroblasts.
pubmed:affiliation
Department of Biochemical Sciences, University of Florence, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't