Document Detail


Cell cycle-dependent calcium oscillations in mouse embryonic stem cells.
MedLine Citation:
PMID:  17092997     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During cell cycle progression, somatic cells exhibit different patterns of intracellular Ca(2+) signals during the G(0) phase, the transition from G(1) to S, and from G(2) to M. Because pluripotent embryonic stem (ES) cells progress through cell cycle without the gap phases G(1) and G(2), we aimed to determine whether mouse ES (mES) cells still exhibit characteristic changes of intracellular Ca(2+) concentration during cell cycle progression. With confocal imaging of the Ca(2+)-sensitive dye fluo-4 AM, we identified that undifferentiated mES cells exhibit spontaneous Ca(2+) oscillations. In control cultures where 50.4% of the cells reside in the S phase of the cell cycle, oscillations appeared in 36% of the cells within a colony. Oscillations were not initiated by Ca(2+) influx but depended on inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) release and the refilling of intracellular stores by a store-operated Ca(2+) influx (SOC) mechanism. Using cell cycle synchronization, we determined that Ca(2+) oscillations were confined to the G(1)/S phase ( approximately 70% oscillating cells vs. G(2)/M with approximately 15% oscillating cells) of the cell cycle. ATP induced Ca(2+) oscillations, and activation of SOC could be induced in G(1)/S and G(2)/M synchronized cells. Intracellular Ca(2+) stores were not depleted, and all three IP(3) receptor isoforms were present throughout the cell cycle. Cell cycle analysis after EGTA, BAPTA-AM, 2-aminoethoxydiphenyl borate, thapsigargin, or U-73122 treatment emphasized that IP(3)-mediated Ca(2+) release is necessary for cell cycle progression through G(1)/S. Because the IP(3) receptor sensitizer thimerosal induced Ca(2+) oscillations only in G(1)/S, we propose that changes in IP(3) receptor sensitivity or basal levels of IP(3) could be the basis for the G(1)/S-confined Ca(2+) oscillations.
Authors:
Nidhi Kapur; Gregory A Mignery; Kathrin Banach
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-11-08
Journal Detail:
Title:  American journal of physiology. Cell physiology     Volume:  292     ISSN:  0363-6143     ISO Abbreviation:  Am. J. Physiol., Cell Physiol.     Publication Date:  2007 Apr 
Date Detail:
Created Date:  2007-04-12     Completed Date:  2007-06-07     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  100901225     Medline TA:  Am J Physiol Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  C1510-8     Citation Subset:  IM    
Affiliation:
Department of Physiology, Stritch School of Medicine, Loyola University Chicago, 2160 South First Ave., Maywood, IL 60153, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphatases / antagonists & inhibitors
Animals
Boron Compounds / pharmacology
Calcium / metabolism*
Calcium Signaling*
Cell Cycle / drug effects,  physiology*
Cells, Cultured
Chelating Agents / pharmacology
Egtazic Acid / analogs & derivatives,  pharmacology
Embryonic Stem Cells / drug effects,  physiology*
Estrenes / pharmacology
Inositol 1,4,5-Trisphosphate / physiology
Inositol 1,4,5-Trisphosphate Receptors / antagonists & inhibitors,  metabolism
Mice
Protein Isoforms / antagonists & inhibitors,  metabolism
Pyrrolidinones / pharmacology
Thapsigargin / pharmacology
Type C Phospholipases / antagonists & inhibitors
Grant Support
ID/Acronym/Agency:
MH-53367/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/2-aminoethoxydiphenyl borate; 0/Boron Compounds; 0/Chelating Agents; 0/Estrenes; 0/Inositol 1,4,5-Trisphosphate Receptors; 0/Protein Isoforms; 0/Pyrrolidinones; 112648-68-7/1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; 139890-68-9/1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; 67-42-5/Egtazic Acid; 67526-95-8/Thapsigargin; 7440-70-2/Calcium; 85166-31-0/Inositol 1,4,5-Trisphosphate; EC 3.1.4.-/Type C Phospholipases; EC 3.6.1.-/Adenosine Triphosphatases

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