Document Detail

The susceptibility of granulosa cells to apoptosis is influenced by oestradiol and the cell cycle.
MedLine Citation:
PMID:  16731776     Owner:  NLM     Status:  MEDLINE    
Experiments were conducted to test whether oestradiol (E2) protects granulosa cells from Fas ligand (FasL)-induced apoptosis and whether protection involves modulation of the cell cycle of proliferation. Treatment of cultured bovine granulosa cells with E2 decreased susceptibility to FasL-induced apoptosis. The effects of E2 were mediated through oestrogen receptor and were not mediated by stimulation of IGF production. E2 also increased the percentage of cells progressing from G1 to S phase of the cell cycle, and increased expression of cyclin D2 protein and the cell proliferation marker Ki67. Progression from G1 to S phase of the cell cycle was necessary for the protective effect of E2; blocking progression from G1 to S phase with the cdk2 inhibitor roscovitine, or blocking cells in S phase with hydroxyurea, prevented protection by E2. The stages of the cell cycle during which granulosa cells are susceptible to apoptosis were assessed. First, treatment with the G1 phase blocker, mimosine, protected cells from FasL-induced apoptosis, indicating that cells in G0 or early- to mid-G1 phase are relatively resistant to apoptosis. Secondly, examination of recent DNA synthesis by cells that became apoptotic indicated that apoptosis did not occur in S, G2 or M phases. Taken together, the experiments indicate that cells may be most susceptible to apoptosis at the transition from G1 to S phase. E2 stimulates transition from G1 to S phase and protects against apoptosis only when cell cycle progression is unperturbed.
Susan M Quirk; Robert G Cowan; Rebecca M Harman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  The Journal of endocrinology     Volume:  189     ISSN:  0022-0795     ISO Abbreviation:  J. Endocrinol.     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-05-29     Completed Date:  2006-08-07     Revised Date:  2013-06-11    
Medline Journal Info:
Nlm Unique ID:  0375363     Medline TA:  J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  441-53     Citation Subset:  IM    
Department of Animal Science, Cornell University, Ithaca, New York 14850, USA.
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MeSH Terms
Apoptosis / drug effects
Biological Markers / analysis
Bromodeoxyuridine / metabolism
Cell Proliferation / drug effects
Cells, Cultured
Cyclins / analysis
Estradiol / analogs & derivatives,  pharmacology*
Estrogen Antagonists / pharmacology
Fas Ligand Protein
Flow Cytometry
G1 Phase
Granulosa Cells / cytology*,  drug effects,  metabolism
Hydroxyurea / pharmacology
Immunohistochemistry / methods
Ki-67 Antigen / analysis
Membrane Glycoproteins / pharmacology
Nucleic Acid Synthesis Inhibitors / pharmacology
Protein Kinase Inhibitors / pharmacology
Purines / pharmacology
Random Allocation
S Phase
Tumor Necrosis Factors / pharmacology
Grant Support
Reg. No./Substance:
0/Biological Markers; 0/Cyclins; 0/Estrogen Antagonists; 0/Fas Ligand Protein; 0/Ki-67 Antigen; 0/Membrane Glycoproteins; 0/Nucleic Acid Synthesis Inhibitors; 0/Protein Kinase Inhibitors; 0/Purines; 0/Tumor Necrosis Factors; 0/roscovitine; 127-07-1/Hydroxyurea; 22X328QOC4/fulvestrant; 50-28-2/Estradiol; 59-14-3/Bromodeoxyuridine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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