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Involvement of SDF ‐1 and monocyte chemoattractant protein‐1 in hydrogen peroxide‐induced extracellular matrix degradation in human dental pulp cells
Author(s) -
Kim D.S.,
Kang S. I.,
Lee S.Y.,
Noh K.T.,
Kim E.C.
Publication year - 2014
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/iej.12147
Subject(s) - microbiology and biotechnology , chemistry , extracellular matrix , fibronectin , chemokine , monocyte , downregulation and upregulation , matrix metalloproteinase , receptor , biology , biochemistry , immunology , gene
Aim To determine whether chemokines such as SDF ‐1 and monocyte chemoattractant protein‐1 ( MCP ‐1) are responsible for hydrogen peroxide ( H 2 O 2 )‐induced extracellular matrix ( ECM ) degradation and to identify the underlying mechanism in human dental pulp cells ( HDPC s). Method Human dental pulp cells were exposed to 0.4 mmol H 2 O 2 for 48 h. m RNA expression and protein expression were examined by RT ‐ PCR and W estern blot analysis, respectively. The m RNA expression of chemokine ( SDF ‐1 and MCP ‐1), their receptors ( CXCR 4 and CXCR 2) and extracellular matrix proteins was evaluated by reverse transcriptase‐polymerase chain reaction. The production of SDF ‐1, MCP ‐1, CXCR 4 and CCR 2 in the culture medium was determined by enzyme‐linked immunosorbent assay. Signal transduction pathway was examined by W estern blotting. Results Hydrogen peroxide provoked the activation of MCP ‐1 and SDF ‐1 m RNA and their respective receptors, CXCR 4 and CXCR 2. H 2 O 2 treatment concomitantly downregulated the expression of ECM molecules, such as type I collagen, elastin and fibronectin, and upregulated the m RNA expression of matrix metalloproteinase‐1 ( MMP ‐1), MMP ‐2, MMP ‐8 and MMP ‐9. Hydrogen peroxide‐induced ECM degradation and MMP upregulation were blocked by neutralizing antibodies and si RNA s directed against SDF ‐1 and MCP ‐1. Inhibition of SDF ‐1 and MCP ‐1 blocked the H 2 O 2 ‐induced activation of Akt, p38, ERK and NF ‐k B . Conclusion Inhibition of SDF and MCP ‐1 is a potent component of reducing release reactive oxygen species‐induced ECM degradation in HDPC s and may play an important role in pulpal and periapical inflammation.