García-López S, González OBD, Wing AH, Villanueva AR

Idioma: Español
Referencias bibliográficas: 27
Paginas: 200-205
Archivo PDF: 140.71 Kb.

RESUMEN

Objetivo: El LPS es un estimulador de la resorción ósea en las enfermedades inflamatorias como la periodontitis, la osteomielitis y algunos tipos de artritis. El propósito del presente estudio fue de evaluar el efecto de 1 µg/mL de LPS adicionado a cultivos de osteoblastos murinos con el fin de evaluar si la PGE₂ induce la producción de RANKL. Material y métodos: Los osteoblastos fueron obtenidos de cráneos de ratón recién nacido Balb/c fueron removidos y sometidos a digestión enzimática con 1 mg/mL de tripsina. Las células desprendidas fueron cultivadas a una densidad de 10⁴ en una caja de pozos de 1.0 cm 1 µg/mL de LPS fue adicionado a cada pozo del grupo experimental (n = 5). Se tomó sobrenadante a las 1, 8, 24, 48, y 72 horas respectivamente y almacenado y ensayado para determinar la producción de RANKL y PGE₂ por medio de la técnica de ELISAs (enzyme-linked immunosorbent assays). Resultados: Los resultados demostraron sobrerregulación de la producción de PGE₂ y RANKL de las 24 a las 48 horas comparadas con el grupo control. La adición de 1 µ/mL de LPS a cultivos de osteoblastos murinos induce la producción de RANKL por diferentes mecanismos incluyendo la PGE₂ en la inducción del proceso de resorción ósea.

REFERENCIAS (EN ESTE ARTÍCULO)

1. Baron R, Net L, Louvard D, Courtoy PJ. Cell-mediated extracellular acidification and bone resorption: evidence for a low pH in resorbing lacunae and localization of a 100-KD lysosomal membrane protein at the osteoclast ruffled border. Cell Biology 1985; 101: 2210-2222.

2. Suda T, Takahashi N, Udagawa N, Jimi E, Gillespie MT, Martin J. Modulation of osteoclasts differentiation and function by the new members of the tumor necrosis factor receptor and ligand family. Endocrine Rev 1999; 20: 345-357.

3. Anderson DM, Maraskovsky E, Billingsley WL, Dougall WC, Tomestko ME, Roux ER, Teepe MC, BDuBose RF, Cosman D, Galibert L. A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic-cell function. Nature 1997; 390: 175-179.

4. Fuller K, Owens JM, Jagger CJ, Wilson A, Moss R, Chambers TJ. Macrophage colony-stimulating factor stimulates surgical and chemotactic behavior in isolated osteoclasts. J Exp Med 1993; 178: 1733-1744.

5. Jimi E, Shoto T, Koga T. Macrophage colony-stimulating factor and interleukin-1a maintain the survival of osteoclast-like cells. Endocrinology 1995; 136: 808-811.

6. Feldman M, Brenman FM, Maini RN. Role of cytokines in rheumatoid arthritis. A Rev Immunol 1996; 14: 397-440.

7. García-López S, Meikle MC, Villanueva RE, Montaño L, Massó F, Ramírez-Amador V, Bojalil R. Mechanical deformation inhibits IL-10 and stimulates IL-12 production by mouse calvarial osteoblasts in vitro. Arch Oral Biol 2005; 50: 449-452.

8. Nair SP, Meghji S, Wilson M, Reddi K, White P, Henderson B. Bacterially induced bone destruction: mechanism and misconceptions. Infec Immun 1996; 64: 2371-2375.

9. Abu-Amer Y, Ross FP, Edwards J, Teitelbaum SL. Lipopolysaccharide-stimulated osteoclastogenesis is mediated by tumor necrosis factor via its p55 receptor. J Clin Invest 1997; 100: 1557-1562.

10. Schletter J, Heme H, Ulmer AJ, Rietschel ET. Molecular mechanism of endotoxin activity. Arch Microbiol 1995; 164: 383-387.

11. Hwang D. Modulation of the expression of cyclooxigenasa-2 by fatty acids mediated through Toll-like receptor 4-deried signaling pathways. FASEB J 2001; 15: 2556-2561.

12. Heath JK, Atkinson SJ, Meikle MC. Mouse osteoblasts synthesize collagenase in response to bone resorbing agents. Biochem Biophys Acta 1984; 802: 151-154.

13. Ellies LG, Aubin JE. Temporal sequences of interleukin 1a mediated stimulation and inhibition of bone formation by isolated fetal rat calvaria cells in vitro. Cytokine 1990; 2: 430-437.

14. Sakuma S, Kato Y, Suda M. Impaired bone resorption by lipopolysaccharide in vivo in mice deficient in the prostaglandin E receptor EP4 subtype. Infec Immun 2000; 68: 6819-25.

15. Romaga MA, Yeh WC, Sarosi I, Duncan GS, Furlonger A. TRAF6 deficiency results in osteopetrosis and defective Interleuki-1, CD40, and LPS signaling. Gen Dev 1999; 13: 1015-1019.

16. Baud V, Liu Z, Bennett B. Signaling by proinflammatory cytokines: oligomerization of TRAF” and TRAF6 is sufficient for JNK and IKK activation and target gene induction via an amino-terminal effectors domain. Genes Development 1999; 13: 1297-308.

17. Lynn WA, Golenbock DT. Lipopolysaccharide antagonists. Immunol Today 1992; 13: 271-276.

18. Nair SP, Meghji S, Wilson M, Reddi K, White P, Henderson B. Bacterially induced bone destruction: mechanism and misconceptions. Infect Immun 1996; 64: 2371-2375.

19. Yasuda H, Shima N, Nakagawa N. Identify of osteoclastogenesis inhibitory factor (OCIF) and osteoprotegerin (OPG): a mechanism by which OPG/OCIF inhibits osteoclastogenesis in vitro. Endocrinology 1998; 139: 1329-1337.

20. Yasuda H, Shima N, Nakagawa K, Yamaguchi M, Kinosaki S et al. Osteoclasts differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL. Proc Natl Acad Sci USA 1998; 95: 3597-3601.

21. Suda T, Takahashi N, Udagawa N, IIMI E, Gillespie MT, Martin J. Modulation of osteoclast differentiation and function by new members of the tumor necrosis factor receptor and ligand families. Endocrine Rev 1999; 20: 345-357.

22. Anderson DM, Maraskovsky E, Billingsley WL, Dougall WC et al. A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic-cell function. Nature 1997; 390: 175-180.

23. Feldman M, Brennan FM, Maini RN. Role of cytokines in rheumatoid arthritis. Annu Rev Immunol 1989; 14: 397-440.

24. Tanabe N, Maeno M, Naoto S, Kyosuke F, Tanaka H, Ogiso B, Ito K. IL-1a stimulates the formation of osteoclast-like cells by increasing M-CSF and PGE2 production and decreasing OPG production by osteoblasts. Life Sci 2005; 77: 615-626.

25. Suda K, Udagawa N, Sato N, Takami M, Itoh K, Woo J, Takahashi N, Nagai K. Suppression of osteoprotegerin expression by prostaglandin E2 is crucially involved in lipopolysaccharide-induced osteoclast formation. J Immunol 2004; 172: 2504-2510.

26. Susawa T, Miyaura C, Inanda M, Maruyama T, Sugimoto Y, Ushikubi F, Ichikawa T, Narumiya S, Suda T. The role of prostaglandin E receptor subtypes (EP1, EP2, EP3 and EP4) in bone resorption: an analysis using specific agonist for the respective EPs. Endocrinology 2000; 141: 1554-1561.

27. Kikuchi T, Matsuguchi T, Tsuboi N, Mitani A, Tanaka S, Matsuoka G et al. Gene expression of osteoclast differentiation factor in induced by lipopolysaccharide in mouse osteoblasts via Toll-like receptors. J Immunol 2001; 166: 3574-3581.