Linked Life Data

8639564

Source:http://linkedlifedata.com/resource/pubmed/id/8639564

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
20
pubmed:dateCreated
1996-7-15
pubmed:abstractText
The "selective" cholesterol uptake pathway represents a bulk pathway by which many steroidogenic cells internalize lipoprotein-delivered cholesteryl esters. In the current report, we question whether cholesteryl esters entering cells via this pathway are capable of governing standard cholesterol end product feedback repression mechanisms. Cultured rat ovary granulosa cells which utilize both the "selective" and "endocytic" pathways to internalize lipoprotein-derived cholesteryl esters were used as a model system. ApoE-free hHDL3 was used to deliver cholesteryl esters to the cells exclusively by the selective pathway; hLDL was used as a control ligand which when internalized by the endocytic pathway releases cholesteryl esters which subsequently regulate the expression of the B/E (LDL)-receptor, HMG CoA reductase, and acyl-CoA:cholesterol acyltransferase (ACAT). Whereas trophic hormone (Bt2cAMP) stimulation by itself increased the activity, mRNA, and protein levels of both B/E-receptor and HMG CoA reductase, pretreatment with either lipoprotein (adjusted for equal cholesterol ester content) down-regulated this expression. Linked with these lipoprotein-related changes was an increase in activity (though not gene expression) of ACAT. The level of change in mRNA levels, protein content, and activity for the examined regulatory proteins was essentially equivalent whether the lipoprotein provided to the cells was hLDL or hHDL3. Thus, similar signals appear to have been received by the cells despite differences in the uptake and processing of the ligand-derived cholesteryl esters, and these signals resulted in identical homeostatic responses by the cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-2960
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6243-50
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:8639564-Animals, pubmed-meshheading:8639564-Base Sequence, pubmed-meshheading:8639564-Biological Transport, Active, pubmed-meshheading:8639564-Bucladesine, pubmed-meshheading:8639564-Cells, Cultured, pubmed-meshheading:8639564-Chloramphenicol O-Acetyltransferase, pubmed-meshheading:8639564-Cholesterol, pubmed-meshheading:8639564-Cholesterol Esters, pubmed-meshheading:8639564-DNA Probes, pubmed-meshheading:8639564-Endocytosis, pubmed-meshheading:8639564-Feedback, pubmed-meshheading:8639564-Female, pubmed-meshheading:8639564-Gene Expression Regulation, pubmed-meshheading:8639564-Granulosa Cells, pubmed-meshheading:8639564-Hydroxymethylglutaryl CoA Reductases, pubmed-meshheading:8639564-Lipoproteins, pubmed-meshheading:8639564-Lipoproteins, HDL, pubmed-meshheading:8639564-Lipoproteins, HDL3, pubmed-meshheading:8639564-Molecular Sequence Data, pubmed-meshheading:8639564-RNA, Messenger, pubmed-meshheading:8639564-Rats, pubmed-meshheading:8639564-Receptors, LDL
pubmed:year
1996
pubmed:articleTitle
Regulation of cholesterol responsive genes in ovary cells: impact of cholesterol delivery systems.
pubmed:affiliation
Geriatric Research, Education and Clinical Center, VA Palo Alto Health Care System, California 94304, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.