RESUMO
Secretory leuckocyte protease inhibitor (SLPI) is thought as a regulating protein on the synthesis and degradation of matrix proteins. But there was no report of expression and function of SLPI on the tooth development, especially on the odontoblasts. As observed by in-situ hybridization and immunohistochemical analysis, SLPI was expressed in odontoblasts and predentin on post-natal day 4 (PN4). On PN10, SLPI was observed under the dentin and apical region including odontoblasts processes. Further, on PN15, expression of SLPI was the same pattern compared to PN10. SLPI was expressed under layer of the odontoblasts and in odontoblasts on PN20. Matrix metalloproteinase-2 (MMP-2) and -9 levels in SLPI/MDPC-23 cells were higher than that of the MDPC-23 cells. The gene expression of SLPI, bone sialoprotein (BSP), osteocalcin (OCN), osteonectin (ON), and collagen type I (Col I) was higher in SLPI/MDPC-23 than that of MDPC-23 cells and the expression of dentin sialophosphoprotein (DSPP) was lower in SLPI/MDPC-23. Taken together, our results suggest that SLPI may be a MMP-2 and -9 regulating molecule in odontoblasts during dentin matrix formation and acts as a signaling molecule for dentin matrix related proteins during odontoblasts differentiation and mineralization.
Assuntos
Odontoblastos/metabolismo , Inibidor Secretado de Peptidases Leucocitárias/metabolismo , Dente/embriologia , Animais , Calcificação Fisiológica/fisiologia , Diferenciação Celular/fisiologia , Linhagem Celular , Embrião de Mamíferos , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Camundongos , Camundongos Endogâmicos ICR , Odontoblastos/química , Ratos , Inibidor Secretado de Peptidases Leucocitárias/químicaRESUMO
SLPI acts as a modulator of the innate immune responses of macrophages, neutrophils and odontoblasts, and LPS-inducible anti-inflammatory cytokine to suppress the production of pro-inflammatory products by macrophages. Many studies have revealed the effects of light emitting diodes (LEDs) on the tissue repair and inflammatory responses. Although the anti-inflammatory mechanisms of irradiation with LEDs in gingival fibroblasts are known, the effects of 660 nm red LEDs on the inflammation remain unclear. Moreover, there is no report regarding the molecular mechanism for the relationship between SLPI and biological effects of LEDs. The effects of 660 nm red LEDs on inflammation with SLPI were investigated by examining the effects of 660 nm LED on the SLPI expression of RAW264.7 cells after LPS stimulation. This paper reports that the 660 nm red LED induced SLPI expression or reduced the LPS response, and inhibited NF-κB activation directly, leading to the suppression of pro-inflammatory cytokines, such as TNF-α and IL-1ß, suggesting that it might be a useful wavelength LED for inflammation therapy.
Assuntos
Inflamação/imunologia , Ativação de Macrófagos/imunologia , Ativação de Macrófagos/efeitos da radiação , Macrófagos/imunologia , Macrófagos/efeitos da radiação , Inibidor Secretado de Peptidases Leucocitárias/imunologia , Animais , Linhagem Celular , Cor , Relação Dose-Resposta à Radiação , Inflamação/induzido quimicamente , Inflamação/prevenção & controle , Luz , Iluminação , Lipopolissacarídeos , Camundongos , Doses de Radiação , SemicondutoresRESUMO
Titanium (Ti) is the most widely used implant material in dentistry and orthopedics but the release of metal ions from Ti implants results in increased bone resorption by enhancing the production of inflammatory cytokines from the macrophages and facilitating osteoclast differentiation. Thymosin ß4 (Tß4) has several biological activities, such as promoting wound healing, angiogenesis, cell proliferation and migration in mammalian cells. This study examined the role of Tß4 in osteoblasts via focal adhesions (FAs) and ERK1/2 signaling related to cell adhesion and proliferation for cell survival on the Ti surface. As a result, cell adhesion and proliferation increased in the Tß4 treated cells (Tß4/MC3T3-E1) but was significantly lower in the Tß4 knock-down cells by Tß4-siRNA (si-Tß4/MC3T3-E1) than that of the untreated cells. The levels of FAK phosphorylation, paxillin expression, and paxillin localization were higher in the Tß4/IMC3T3-E1 cells than that of the untreated cells but lower in the si-Tß4/MC3T3-E1 cells. In addition, the levels of cell proliferation, Grb2 and Ras protein expression and phosphorylation of ERK1/2 were higher in the Tß4/MC3T3-E1 cells than in the untreated cells but lower in the si-Tß4/IMC3T3-E1 cells. These results suggest that Tß4 might be a good nanomolecule that promotes osteoblast survival by facilitating adhesion and proliferation on the Ti surface.