2007 Fiscal Year Final Research Report Summary
Regeneration of Pulp-dentin Complex by Antimicrobial Peptides
Project/Area Number |
18592089
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Conservative dentistry
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Research Institution | Hiroshima University |
Principal Investigator |
SHIBA Hideki Hiroshima University, Hospital, Lecturer (60260668)
|
Co-Investigator(Kenkyū-buntansha) |
KOMATSUZAWA Hitoshi Kagoshima University, Graduate School of Medical and Dental Sciences, Professor (90253088)
HASEGAWA Naohiko Kagoshima University, Hospital, Assistant Professor (10346512)
|
Project Period (FY) |
2006 – 2007
|
Keywords | pulp cells / antimicrobial peptide / LL37 / inflammatory cytokine / P2X_7 receptor / migration / JNK / pulu-dentin complex |
Research Abstract |
LL37 is the last 37 amino acid at the C-terminus of 18 kDa cationic antimicrobial protein and shows antimicrobial activity against Gram-positive and -negative bacteria. Elimination of bacteria, inhibition of inflammation and promotion of pulp cell function are necessary for regeneration of pulp-dentin complex in the treatment of reversible pulpitis. In addition to antimicrobial activity, LL37 also may influences cytokine expression and activation of pulp cell function. In the present study, we examined the effects of LL37 on the gene expression of inflammatory cytokines, IL-6 and IL-8 and migration in human pulp cells (HP cells). (1)Expression of inflammatory cytokine expression: 1. HP cells expressed P2X_7 receptor. LL37 as well as Bz-ATP, an agonist of P2X_7 receptor abolished the increase in IL-6 and IL-8 mRNA levels in HP cells stimulated with peptidoglycan. LL37 did not influence mRNA expression of ALPase and osteonectin. Thus, LL37 may possess the ability to inhibit cytokine expression through P2X_7 receptor. (2) Migration: LL37 is suggested to induce migration of HP cells through transactivation of EGF receptor and activation of INK. These findings demonstrated that in addition to antimicrobial activity, LL37 possesses the ability to inhibit cytokine expression and induce migration of pulp cells. LL37 may play a role in regeneration of pulp-dentin complex.
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