The Antimicrobial Peptide LL37 Induces the Migration of Human Pulp Cells: A Possible Adjunct for Regenerative Endodontics
The Antimicrobial Peptide LL37 Induces the Migration of Human Pulp Cells: A Possible Adjunct for Regenerative Endodontics
复制标题
DOI：
10.1016/j.joen.2010.02.028
复制
发表时间：
2010-06-01
影响因子：
4.2
通讯作者：
Kurihara, Hidemi
中科院分区：
文献类型：
--
作者：
Kajiya, Mikihito;Shiba, Hideki;Kurihara, Hidemi
前言：抗菌肽LL 37具有多种功能，如诱导血管生成和迁移。牙髓细胞迁移是牙髓-牙本质复合体再生早期的关键现象。在这项研究中，我们研究了LL 37对人牙髓（HP）细胞迁移的影响。方法：将第6代HP细胞暴露于LL 37。HP细胞的迁移通过伤口愈合测定来评估。通过免疫印迹分析表皮生长因子受体（EGFR）和c-Jun N-末端激酶（JNK）的磷酸化。结果：LL 37和肝素结合（HB）-EGF（EGFR的激动剂）诱导HP细胞迁移。LL 37增加磷酸化EGFR的水平。抗EGFR抗体、EGFR酪氨酸激酶抑制剂和JNK抑制剂消除了LL 37和HB-EGF诱导的迁移。此外，两种肽增加磷酸化JNK的水平。结论：LL 37通过激活EGFR和JNK诱导HP细胞迁移，可能有助于促进牙髓-牙本质复合体的再生。（J Endod 2010;36：1009-1013）
Introduction: The antimicrobial peptide LL37 has multiple functions, such as the induction of angiogenesis and migration. Pulp cell migration is a key phenomenon in the early stage of pulp-dentin complex regeneration. In this study, we examined the effect of LL37 on the migration of human pulp (HP) cells. Methods: HP cells at the sixth passage were exposed to LL37. The migration of HP cells was assessed by a wound-healing assay. The phosphorylation of epidermal growth factor receptor (EGFR) and c-Jun N-terminal kinase (JNK) was analyzed by immunoblotting. Results: LL37 as well as heparin binding (HB)-EGF, which is an agonist of EGFR, induced HP cell migration. LL37 increased the level of phosphorylated EGFR. An anti-EGFR antibody, an EGFR tyrosine kinase inhibitor, and a JNK inhibitor abolished the migration induced by both LL37 and HB-EGF. Furthermore, the two peptides increased the levels of phosphorylated JNK. Conclusions: LL37 activates EGFR and JNK to induce HP cell migration, and it may contribute to enhancing the regeneration of pulp-dentin complexes. (J Endod 2010;36:1009-1013)