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LL37 induces VEGF expression in dental pulp cells through ERK signalling
1Department of Periodontal Medicine, Applied Life Sciences, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
International Endodontic Journal
|August 8, 2014
Summary
LL37 significantly boosts vascular endothelial growth factor (VEGF) in human pulp cells by activating the ERK pathway. This suggests LL37
Area of Science:
- Biomaterials Science
- Cell Biology
- Molecular Biology
Background:
- Vascular Endothelial Growth Factor (VEGF) is crucial for angiogenesis.
- Human pulp cells are vital for dental pulp health and regeneration.
- LL37 is an antimicrobial peptide with potential therapeutic applications.
Purpose of the Study:
- To investigate the effect of LL37 on VEGF expression in human pulp cells.
- To elucidate the intracellular signaling pathway mediating LL37's effects.
- To explore LL37's potential as a pulp capping agent.
Main Methods:
- Human pulp cells were treated with LL37 in vitro.
- VEGF mRNA and protein levels were quantified using real-time PCR and ELISA.
- The involvement of MAPK/ERK and NF-κB pathways was assessed using specific inhibitors and Western blotting for phosphorylated ERK1/2.
Main Results:
- LL37 significantly upregulated both VEGF mRNA and protein expression in human pulp cells (P < 0.01).
- Inhibition of the ERK pathway suppressed LL37-induced VEGF increases.
- LL37 treatment led to increased phosphorylation of ERK1/2, indicating ERK pathway activation.
Conclusions:
- LL37 activates the ERK signaling pathway, leading to enhanced VEGF secretion from human pulp cells.
- The angiogenic properties of LL37, coupled with its antimicrobial effects, suggest its potential as a novel pulp capping material for dental applications.
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