Linked Life Data

17894423

Source:http://linkedlifedata.com/resource/pubmed/id/17894423

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-2-25
pubmed:abstractText
The surrounding medium of periodontal pathogen Porphyromonas gingivalis (P. gingivalis) increased cardiomyocyte hypertrophy and apoptosis whereas Actinobaeillus actinomycetemcomitans and Prevotella intermedia had no effects. The purpose of this study is to clarify the role of p38 pathway in P. gingivalis conditioned medium-induced H9c2 myocardial cell hypertrophy and apoptosis. DNA fragmentation, cellular morphology, nuclear condensation, p38 protein products, and mitochondrial-dependent apoptotic related proteins in cultured H9c2 myocardial cell were measured by agarose gel electrophoresis, immunofluorescence, DAPI, and western blotting following P. gingivalis conditioned medium and/or pre-administration of SB203580 (p38 inhibitor). The p38 protein products and associated activities in H9c2 cells were both upregulated by P. gingivalis conditioned medium. P. gingivalis conditioned medium increased cellular sizes, DNA fragmentation, nuclear condensation, mitochondrial Bcl2-associated death promoter (Bad), cytosolic cytochrome c (cyt c), and the activated form of caspase-9 proteins in H9c2 cells. The increased cellular sizes, DNA fragmentation, nuclear condensation, Bad, cyt c, and caspase-9 activities of H9c2 cells treated with P. gingivalis conditioned medium were all significantly reduced after pre-administration of SB203580. Our findings suggest that the activity of p38 signal pathway may be initiated by P. gingivalis conditioned medium and further activate mitochondrial-dependent apoptotic pathways leading to cell death in cultured H9c2 myocardial cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1099-0844
pubmed:author
pubmed:copyrightInfo
Copyright 2007 John Wiley & Sons, Ltd.
pubmed:issnType
Electronic
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
246-55
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17894423-Apoptosis, pubmed-meshheading:17894423-Blotting, Western, pubmed-meshheading:17894423-Caspase 9, pubmed-meshheading:17894423-Cells, Cultured, pubmed-meshheading:17894423-Culture Media, Conditioned, pubmed-meshheading:17894423-Cytochromes c, pubmed-meshheading:17894423-Cytosol, pubmed-meshheading:17894423-DNA Fragmentation, pubmed-meshheading:17894423-Humans, pubmed-meshheading:17894423-Hypertrophy, pubmed-meshheading:17894423-Imidazoles, pubmed-meshheading:17894423-Indoles, pubmed-meshheading:17894423-Myocytes, Cardiac, pubmed-meshheading:17894423-Porphyromonas gingivalis, pubmed-meshheading:17894423-Pyridines, pubmed-meshheading:17894423-Up-Regulation, pubmed-meshheading:17894423-bcl-Associated Death Protein, pubmed-meshheading:17894423-p38 Mitogen-Activated Protein Kinases
pubmed:articleTitle
P38 mitogen-activated protein kinase pathways are involved in the hypertrophy and apoptosis of cardiomyocytes induced by Porphyromonas gingivalis conditioned medium.
pubmed:affiliation
School of medicine, China Medical University and Hospital, Taichung, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't