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LL 37 induces VEGF expression in dental pulp cells through ERK signalling
Author(s) -
Khung R.,
Shiba H.,
Kajiya M.,
Kittaka M.,
Ouhara K.,
Takeda K.,
Mizuno N.,
Fujita T.,
Komatsuzawa H.,
Kurihara H.
Publication year - 2015
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.12365
Subject(s) - mapk/erk pathway , vascular endothelial growth factor , pulp (tooth) , chemistry , kinase , microbiology and biotechnology , phosphorylation , protein kinase a , vegf receptors , biology , cancer research , medicine , dentistry
Aim To examine the in vitro effects of LL 37 on the expression of vascular endothelial growth factor ( VEGF ) in human pulp cells and to identify the intracellular signalling pathway involved. Methodology Pulp cells at passage 6 were treated with 10 μg mL −1 synthesized LL 37, and an inhibition assay was performed with MAPK or NF ‐κ B inhibitors to determine the possible signalling pathway. VEGF m RNA , VEGF protein and phosphorylated ERK 1/2 levels were determined by real‐time PCR , ELISA and W estern blot, respectively. Data were analysed using t ‐tests. Results LL 37 significantly increased both the m RNA and protein levels of VEGF in pulp cells ( P < 0.01). However, pre‐treatment with an ERK kinase inhibitor suppressed these increases. Furthermore, the inhibitor blocked LL 37‐induced ERK 1/2 phosphorylation. Conclusions LL 37 activated the ERK pathway to boost VEGF secretion from human pulp cells. Because of this angiogenic effect and its reported induction of pulp cell migration and antimicrobial activity against cariogenic bacteria, LL 37 may be applicable as a pulp capping material.