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Regeneration of Pulp-dentin Complex by Antimicrobial Peptides

Research Project

Project/Area Number 18592089
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Conservative dentistry
Research InstitutionHiroshima 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
Project Status Completed (Fiscal Year 2007)
Budget Amount *help
¥3,880,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥480,000)
Fiscal Year 2007: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
Keywordspulp cells / antimicrobial peptide / LL37 / inflammatory cytokine / P2X_7 receptor / migration / JNK / pulu-dentin complex / 歯随細胞 / HB-EGF / EGF受容体 / transactivation / IL-6 / IL-8
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.

Report

(3 results)
  • 2007 Annual Research Report   Final Research Report Summary
  • 2006 Annual Research Report
  • Research Products

    (3 results)

All 2007 2006

All Journal Article (1 results) Presentation (2 results)

  • [Journal Article] 抗菌ペプチドLL37がヒト歯髄細胞の炎症性サイトカイン発現およびmigrationに及ぼす影響2006

    • Author(s)
      柴 秀樹
    • Journal Title

      日本歯科保存学雑誌 49 秋季特別

      Pages: 50-50

    • NAID

      10020294834

    • Related Report
      2006 Annual Research Report
  • [Presentation] Effect of LL37 on expressions of inflammatory cytokines and migration in human pulp cells2007

    • Author(s)
      Kajiya Mikihito
    • Organizer
      第28回日本歯内療法学会学術大会(The 5th KAE-JEA Joint-Meeting)
    • Place of Presentation
      広島
    • Year and Date
      2007-05-27
    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2007 Annual Research Report 2007 Final Research Report Summary
  • [Presentation] Effect of LL37 on expressions of inflammatory cytokines and migration in human pulp cells2007

    • Author(s)
      Kajiya, Hikihito
    • Organizer
      The 28th Congress of Japan Endodontic Association
    • Place of Presentation
      Hiroshima
    • Year and Date
      2007-05-27
    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2007 Final Research Report Summary

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Published: 2006-04-01   Modified: 2016-04-21  

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