Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.

ÁãÀÇ °ñ¼¼Æ÷¿¡¼­ PGE2 ÇÕ¼º°ú plasminogen activator È°¼º Á¶Àý¿¡ ÀÇÇÑ IL-1¡áÀÇ °ñ Èí¼öÀ¯µµ¿Í TGF-¡á¿¡ ÀÇÇÑ °ñ Èí¼ö ¾ïÁ¦ ±âÀü¿¡ °üÇÑ ¿¬±¸

Interleuken-1 ¡á induces bone resorption by regulation of prostaglandin E2 synthesis and plasminogen activator activity, and TGF-¡á inhibits bone resorption of rat bone cells

Korean Journal of Orthodontics 2000³â 30±Ç 6È£ p.713 ~ 721
¼Ò¼Ó »ó¼¼Á¤º¸
±è¿µÈÆ

Abstract


Bone cells produce multiple growth factors and cytokines that have effects on bone metabolism and can be incorporated into the bone matrix. The present study was designed to extend these observations by examining the interactions between transforming growth factor-Il (TGF-p) or interleukin-1)3 (rh1L-111) and bone cells in a rat long bone culture model. IL-1)3 regulates several activities of the osteoblast cells derived from rat long bone explants in vitro. IL-113 stimulated cellular proliferation as well as the synthesis of prostaglandin E2 and plasminogen .activator activity in the cultured cells in a dose-dependent manner. TGF-D is present in the bone matrix and potentially released during bone resorption. TGF-l3 reduced basal bone resorption and inhibited vitamin 1)3 [1,2b(OH)2D31-induced bone resorption in rat long bone cells. These results support the role.of IL-ill in the pathological modulation of bone cell metabolism, with regard to implication in the pathogenesis of osteoporosis by IL-1p, and that TGF-i3 positively inhibits the bone resorptio~L

Å°¿öµå

Interleukin 1-¥â;Tranforming Growth Factor-¥â;osteoblast;osteoclast;Prostaglandin E_(2);Plasminogen activator;bone resorption;IL-1¥â;TGF-¥â;Á¶°ñ¼¼Æ÷;ÇÇ°ñ¼¼Æ÷ PGE_(2);°ñÈí¼ö

¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸

  

µîÀçÀú³Î Á¤º¸

SCI(E)
KCI
KoreaMed