The antimicrobial peptide LL37 induces the migration of human pulp cells: a possible adjunct for regenerative endodontics.

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.

Irsogladine maleate regulates neutrophil migration and E-cadherin expression in gingival epithelium stimulated by Aggregatibacter actinomycetemcomitans.

Irsogladine maleate (IM) counters Aggregatibacter actinomycetemcomitans-induced reduction of the gap junction intercellular communication and the expression of zonula occludens-1, which is a major tight junction structured protein, in cultured human gingival epithelial cells (HGEC). In addition, IM obviates the A. actinomycetemcomitans-induced increase in interleukin (IL)-8 levels in HGEC.

Brain-derived neurotrophic factor protects cementoblasts from serum starvation-induced cell death.

Our previous studies have shown that brain-derived neurotrophic factor (BDNF) enhances bone/cementum-related protein gene expression through the TrkB-c-Raf-ERK1/2-Elk-1 signaling pathway in cementoblasts, which play a critical role in the establishment of a functional periodontal ligament. To clarify how BDNF regulates survival in cementoblasts, we examined its effects on cell death induced by serum starvation in immortalized human cementoblast-like (HCEM) cells. BDNF inhibited the death of HCEM cells.

Regulation of IL-8 by Irsogladine maleate is involved in abolishment of Actinobacillus actinomycetemcomitans-induced reduction of gap-junctional intercellular communication.

Our previous report has shown that Irsogladine maleate (IM) counters and obviates the reduction in gap junction intercellular communication (GJIC) and the increase in IL-8 levels, respectively, induced by outer membrane protein 29 from Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) in cultured human gingival epithelial cells (HGEC). In addition, IM suppresses the increase in the secretion of IL-8 caused by whole live A.

Irsogladine maleate influences the response of gap junctional intercellular communication and IL-8 of human gingival epithelial cells following periodontopathogenic bacterial challenge.

Gingival epithelial cells first encounter periodontopathogenic bacteria and their metabolic products to produce inflammatory cytokines. Gap junctional intercellular communication (GJIC) is thought to play a critical role in cellular coordination in tissue homeostasis. Gap junctions are structured by connexins (CXs).

Effect of bone morphogenetic proteins-4, -5 and -6 on DNA synthesis and expression of bone-related proteins in cultured human periodontal ligament cells.

Bone morphogenetic proteins (BMPs) have multiple functions in the development and growth of skeletal and extraskeletal tissues. Therefore, BMPs may regulate the regeneration of periodontal tissue. To investigate this issue, we examined the effects of BMP-4, -5 and -6 on DNA synthesis and the expression of bone-related proteins in cultures of human periodontal ligament (HPL) cells.

Outer membrane protein 100, a versatile virulence factor of Actinobacillus actinomycetemcomitans.

Actinobacillus actinomycetemcomitans (Aa) is one of the pathogenic bacteria involved in periodontal diseases. We have previously identified six major outer membrane proteins (Omps) of Aa Y4. Among them is an Omp with high molecular mass, designated Omp100, which has homology to a variety of virulence factors.

Expression of endothelins and their receptors in cells from human periodontal tissues.

Objective: The present study investigated the presence of ET-1 in gingival crevicular fluid (GCF) from patients with periodontitis, and the expression of endothelins (ETs) and their receptors mRNA in cultured cells from human periodontal tissues.

Background: ET was originally discovered as a potent vasoconstrictive peptide from endothelial cells. It has been reported that ETs are produced by various cells besides endothelial cells.

Effects of transforming growth factor-beta 1 and fibronectin on SPARC expression in cultures of human periodontal ligament cells.

Transforming growth factor-beta(1) (TGF-beta(1)) increases synthesis of secreted protein, acidic and rich in cysteine (SPARC), as well as fibronectin (FN) and type I collagen. However, little is known about the regulatory mechanism of SPARC expression. We examined the effect of FN on SPARC expression by TGF-beta(1) in cultures of human periodontal ligament cells (HPL cells).

SPARC stimulates the synthesis of OPG/OCIF, MMP-2 and DNA in human periodontal ligament cells.

Background: Osteonectin/secreted protein, acidic and rich in cysteine (SPARC) is expressed in periodontal ligaments. Therefore, a better understanding of the action of SPARC on periodontal ligament cells could help to elucidate remodelling and repair mechanisms in periodontal tissue. In the present study, we examined the effects of human platelet-derived SPARC (hp-SPARC) on the expressions of SPARC and osteoprotegerin/osteoclastogenesis inhibitory factor (OPG/OCIF), alkaline phosphatase (ALPase) activity, matrix metalloproteinase-2 (MMP-2) production and DNA synthesis in cultures of human periodontal ligament (HPL) cells.

Osteoprotegerin levels increased by interleukin-1beta in human periodontal ligament cells are suppressed through prostaglandin E(2) synthesized de novo.

Osteoprotegerin (OPG) is a novel tumor necrosis factor receptor superfamily that inhibits osteoclast differentiation, activity, and survival. Interleukin-1beta (IL-1beta) increases OPG expression. IL-1beta also increases prostaglandin E(2) (PGE(2)) production and stimulates bone resorption.