Source:http://linkedlifedata.com/resource/pubmed/id/19199341
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rdf:type | |
lifeskim:mentions |
umls-concept:C0003695,
umls-concept:C0020281,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0030685,
umls-concept:C0033634,
umls-concept:C0040624,
umls-concept:C0127400,
umls-concept:C0391871,
umls-concept:C0596235,
umls-concept:C0596508,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1314939,
umls-concept:C1414313,
umls-concept:C1514485,
umls-concept:C1963578
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pubmed:issue |
5
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pubmed:dateCreated |
2009-3-25
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pubmed:abstractText |
Reactive oxygen species (ROS) generated by a variety of endogenous factors and roles in embryonic stem (ES) cells has yet to be identified. Thus, we examined role of arachidonic acid (AA) in H(2)O(2)-induced proliferation of mouse ES cells and its related signaling molecules. AA release was maximally increased in response to 10(-4) M H(2)O(2) for 1 h. In addition, H(2)O(2) increased intracellular Ca(2+) concentration ([Ca(2+)](i)) and the phosphorylation of protein kinase C (PKC), p44/42, p38 mitogen-activated protein kinase (MAPK), and JNK/SAPK. Moreover, H(2)O(2) induced an increase in the phosphorylation of epidermal growth factor receptor (EGFR), which was blocked by the inhibition of p44/42 or p38 MAPKs. The inhibition of each signal molecule with specific inhibitors blocked H(2)O(2)-induced cytosolic phospholipase A(2) (cPLA(2)) activation and AA release. H(2)O(2) increased NF-kappaB phosphorylation to induce an increase in the levels of cyclooxygenase (COX)-2 proteins. Subsequently, H(2)O(2) stimulated PGE(2) synthesis, which was reduced by the inhibition of NF-kappaB activation. Moreover, each H(2)O(2) or PGE(2) increased DNA synthesis and the number of cells. However, H(2)O(2)-induced increase in DNA synthesis was inhibited by the suppression of cPLA(2) pathway. In conclusion, H(2)O(2) increased AA release and PGE(2) production by the upregulation of cPLA(2) and COX-2 via Ca(2+)/PKC/MAPKs and EGFR transactivation, subsequently proliferation of mouse ES cells.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrogen Peroxide,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipases A2,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1097-4644
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
106
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
787-97
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:19199341-Animals,
pubmed-meshheading:19199341-Arachidonic Acid,
pubmed-meshheading:19199341-Calcium,
pubmed-meshheading:19199341-Cell Proliferation,
pubmed-meshheading:19199341-Cyclooxygenase 2,
pubmed-meshheading:19199341-Dinoprostone,
pubmed-meshheading:19199341-Embryonic Stem Cells,
pubmed-meshheading:19199341-Hydrogen Peroxide,
pubmed-meshheading:19199341-Mice,
pubmed-meshheading:19199341-Mitogen-Activated Protein Kinases,
pubmed-meshheading:19199341-Phospholipases A2,
pubmed-meshheading:19199341-Protein Kinase C,
pubmed-meshheading:19199341-Receptor, Epidermal Growth Factor,
pubmed-meshheading:19199341-Transcriptional Activation
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pubmed:year |
2009
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pubmed:articleTitle |
Arachidonic acid release by H2O2 mediated proliferation of mouse embryonic stem cells: involvement of Ca2+/PKC and MAPKs-induced EGFR transactivation.
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pubmed:affiliation |
Department of Veterinary Physiology, Biotherapy Human Resources Center (BK 21), College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, South Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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