The Antimicrobial Peptide LL37 Induces the Migration of Human Pulp Cells: A Possible Adjunct for Regenerative Endodontics

Kajiya, Mikihito; Shiba, Hideki; Komatsuzawa, Hitoshi; Ouhara, Kazuhisa; Fujita, Tsuyoshi; Takeda, Katsuhiro; Uchida, Yuushi; Mizuno, Noriyoshi; Kawaguchi, Hiroyuki; Kurihara, Hidemi

doi:10.1016/j.joen.2010.02.028

Cited by 36 publications

(39 citation statements)

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“…Previous studies showed that MAP kinases including p38, Erk and JNK are known to play important roles in cell migration (21, 23,28), and our results suggest that p38 MAP kinase is involved in HEMA-mediated inhibition of DPSC migration (Fig. 3).…”

Section: Discussionsupporting

confidence: 76%

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2-Hydroxyethyl Methacrylate Inhibits Migration of Dental Pulp Stem Cells

Williams¹,

Wu²,

Oh³

et al. 2013

Journal of Endodontics

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Objectives Cell migration is an important step in pulpal wound healing. Although components in the resin-based dental materials are known to have adverse effects on pulp wound healing including proliferation and mineralization, their effects on cell migration have been scarcely examined. Here, we investigated effects of 2-Hydroxyethyl methacrylate (HEMA) on migration of dental pulp stem cells (DPSC) in vitro. Methods Cell viability was assessed using MTT assay, and cell migration was evaluated using wound scratch assay and transwell migration assay at non-cytotoxic doses. Western blotting was used to examine pathways associated with migration such as focal adhesion kinase (FAK), mitogen-activated protein kinase (MAPK), and glycogen synthase kinase 3 (GSK3). Results There were no drastic changes in the cell viability below 3mM HEMA. When DPSC were treated with HEMA at 0.5, 1.0, and 2.5mM, cell migration was diminished. HEMA-treated DPSC exhibited the loss of phosphorylated focal adhesion kinase (FAK) in a dose-dependent manner. The HEMA-mediated inhibition of cell migration was associated with phosphorylation of p38 but not GSK3, ERK or JNK pathways. When we inhibited the p38 signaling pathway using a p38 inhibitor, migration of DPSC was suppressed. Conclusion HEMA inhibits migration of dental pulp cells in vitro, suggesting that poor pulpal wound healing under resin-based dental materials may be due, in part, to inhibition of cell migration by HEMA.

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Section: Discussionsupporting

confidence: 76%

“…Previous reports examining migration of pulp cells showed that cell migration is mediated through different signaling pathways (21,22,23). In particular, recent studies suggest that GSK3 is essential for cell polarization and migration (24).…”

Section: Discussionmentioning

confidence: 99%

2-Hydroxyethyl Methacrylate Inhibits Migration of Dental Pulp Stem Cells

Williams¹,

Wu²,

Oh³

et al. 2013

Journal of Endodontics

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show abstract

“…In particular, JNK regulates cell migration by phosphorylating paxillin, doublecortin X-linked (DCX), Jun and microtubuleassociated proteins. The antimicrobial peptide LL37 promotes the migration of DPSCs via activating the epidermal growth factor receptor (EGFR)-JNK signaling pathway, which may lead to the increased regeneration of pulp-dentin complexes [ 20 ]. MAPK regulates the directional migration of cells via the phosphorylation of MAPK-activated protein kinase 2/3 (MAPKAP 2/3).…”

Section: Mapk Signaling Pathwaymentioning

confidence: 99%

Signaling Pathways in Dental Stem Cells During Their Maintenance and Differentiation

Liu

Zhou

et al. 2016

Stem Cell Biology and Regenerative Medicine

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“…Thus, a dual approach is mandatory to comprehend the task of hosts' immunity in response to, against periodontitis [37]. This involves more comprehensive statistics about HNP and hBD, LL-37, and other oral antimicrobial peptides and proteins, along with their mode of action and clinical significance [38][39][40][41][42][43][44][45][46][47][48][49][50]. These peptides are peculiar in keeping the level of bacteria in control, having distinctive as well as dual roles in maintaining oral health.…”

Section: Discussionmentioning

confidence: 99%