Linked Life Data

20096665

Source:http://linkedlifedata.com/resource/pubmed/id/20096665

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2010-3-9
pubmed:abstractText
Irsogladine maleate (IM) counters Aggregatibacter actinomycetemcomitans-induced reduction of the gap junction intercellular communication and the expression of zonula occludens-1, which is a major tight junction structured protein, in cultured human gingival epithelial cells (HGEC). In addition, IM obviates the A. actinomycetemcomitans-induced increase in interleukin (IL)-8 levels in HGEC. Thus, by regulating the intercellular junctional complex and chemokine secretion in HGEC, IM may be useful to prevent periodontal disease. To clarify the effects and regulatory mechanism of IM in vivo and in vitro, we examined the expression of E-cadherin and neutrophil chemotaxis induced by A. actinomycetemcomitans under IM pretreatment. Immunohistochemical studies revealed that A. actinomycetemcomitans application to the gingival sulcus decreased the number of cells positive for E-cadherin and increased those positive for cytokine-induced neutrophil chemoattractant-2alpha (CINC-2alpha) in rat gingival epithelium. However, in IM-pretreated rats, A. actinomycetemcomitans application had little effect on CINC-2alpha and E-cadherin in gingival epithelium. In cultured HGEC, real-time PCR and Western blotting showed that IM and the ERK inhibitor PD98059 abolished the A. actinomycetemcomitans-induced increase in CXCL-1 and IL-8 in HGEC. On the other hand, IM, PD98059, and the p38 MAP kinase inhibitor SB203580 recovered the decrease in E-cadherin expression. In addition, conditioned medium from A. actinomycetemcomitans-stimulated HGEC enhanced human neutrophil chemotaxis, compared to that from un-stimulated HGEC or that from A. actinomycetemcomitans-stimulated HGEC under IM pretreatment. Furthermore, IM down-regulated the p38 MAP kinase and ERK phosphorylations induced by A. actinomycetemcomitans. In conclusion, IM may control A. actinomycetemcomitans-induced gingival inflammation by regulating neutrophil migration and E-cadherin expression in gingival epithelium.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1873-2968
pubmed:author
pubmed:copyrightInfo
2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
79
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1496-505
pubmed:meshHeading
pubmed-meshheading:20096665-Actinobacillus actinomycetemcomitans, pubmed-meshheading:20096665-Actins, pubmed-meshheading:20096665-Animals, pubmed-meshheading:20096665-Cadherins, pubmed-meshheading:20096665-Chemokine CXCL1, pubmed-meshheading:20096665-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:20096665-Epithelium, pubmed-meshheading:20096665-Gingiva, pubmed-meshheading:20096665-Humans, pubmed-meshheading:20096665-Immunoblotting, pubmed-meshheading:20096665-Interleukin-8, pubmed-meshheading:20096665-Male, pubmed-meshheading:20096665-Neutrophil Infiltration, pubmed-meshheading:20096665-Neutrophils, pubmed-meshheading:20096665-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:20096665-Rats, pubmed-meshheading:20096665-Rats, Inbred F344, pubmed-meshheading:20096665-Triazines, pubmed-meshheading:20096665-p38 Mitogen-Activated Protein Kinases
pubmed:year
2010
pubmed:articleTitle
Irsogladine maleate regulates neutrophil migration and E-cadherin expression in gingival epithelium stimulated by Aggregatibacter actinomycetemcomitans.
pubmed:affiliation
Department of Periodontal Medicine, Hiroshima University Graduate School of Biomedical Sciences, Minami-ku, Japan. tfuji@hiroshima-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't