The effect of TIMP on bone resorption and osteoclast like cell formation induced by juvenile periodontitis related bacteria

TIMP对幼年牙周炎相关菌诱导的骨吸收和破骨细胞样细胞形成的影响

• 批准号: 10671975
• 负责人: ISHIHARA Yuichi
• 金额: $ 1.98万
• 依托单位: Aichi-gakuin University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671975/
• 关键词: osteoclast-like cell; TIMP; Actinobacillus actinomycetemcomitans; IL-1; juvenile periodontitis; マウス骨髄培養系; マウス骨髄細胞培養系

Tissue inhibitor of metallproteinases-1(TIMP-1) and TIMP-2, originally known as intrinsic inhibitors of matrix metalloproteinases (MMPs), are now known as constitutive components in serum and have potent cell growth-promoting activity. In this study, we examined the effects of TIMPs in FCS on osleoclast-like (OCL) cell formation in mouse bone marrow culture. The OCL cell formation is totally dependent not the presence of PGE2 or 1α25(OH)2D3 or IL-1α. The effects of these factors were, however, not completely but greatly suppressed by deleting TIMP-1 and TIMP-2 from FCS in culture. But the suppression was almost fully recovered by the readdilion of the same amount of recombinant(r)TIMPs which were detected in 10% FCS. As low molecular weight MMP inhibitors could not substitute rTIMPs for the recovery. TIMP activity on the OCL cell formation seemed to be independent from their MMP inhibitory activity. These results strongly suggest a secondary but potent stimulating activity of TIMPs on OCL cell formation. In conclusion, TIMPs in serum play an important role in osteogenesis in mouse bone marrow culture.

金属蛋白酶-1（TIMP-1）和TIMP-2的组织抑制剂，最初称为基质金属蛋白酶（MMP）的内在抑制剂（MMP），现在称为血清中的组成型成分，具有潜在的细胞生长促进活性。在这项研究中，我们检查了TIMP对FCS对小鼠骨髓培养物中os骨状细胞形成的影响。 OCL细胞的形成完全取决于PGE2或1α25（OH）2d3或IL-1α的存在。但是，这些因素的影响并非完全，但由于培养中FCS中删除TIMP-1和TIMP-2的抑制作用。但是，通过在10％FC中检测到的相同数量的重组（R）TIMP的读数几乎完全恢复了抑制作用。由于低分子量的MMP抑制剂无法代替rtimps恢复。 TIMP对OCL细胞形成的活性似乎独立于其MMP抑制活性。这些结果强烈表明TIMP对OCL细胞形成的次要但潜在的刺激活性。总之，血清中的TIMP在小鼠骨髓培养中的成骨中起着重要作用。

项目成果

MASANORI KOIDE: "Inhibition of experimental bone and osteoclast formation and survival by 2-aminoethanesulphonic acid"Arch Oral Biol. 44. 711-719 (1999)

MASANORI KOIDE：“2-氨基乙磺酸对实验性骨和破骨细胞形成和存活的抑制”Arch Oral Biol。

NOBUO UEDA: "Involvement of prostaglandin E2 and interleukin-1 α in the differentiation and survival of osteoclasts induced by lipopolysaccharide from Actinobacillus actinomycetemcomitans Y4."J Periodontal Res. 33. 509-516 (1998)

NOBUO UEDA：“前列腺素 E2 和白细胞介素 1 α 在由来自放线杆菌 Y4 的脂多糖诱导的破骨细胞分化和存活中的参与。”J 牙周研究 33. 509-516 (1998)

M.koide: "Inhibition of experimental bone resorption and osteoclast formation and survival by 2-aminoethanesulphonic acid"Arch.Oral Biol. 44. 711-719 (1999)

M.koide：“2-氨基乙磺酸对实验性骨吸收和破骨细胞形成和存活的抑制”Arch.Oral Biol。

MASANORI KOIDE: "Inhibition of experimental bone resorption and osteoclast formation and survival by 2-aminoethanesulphonic acid."Arch Oral Biol. 44. 711-719 (1999)

MASANORI KOIDE：“2-氨基乙磺酸对实验性骨吸收和破骨细胞形成和存活的抑制。”Arch Oral Biol。

N.Ueda: "Involvement of prostaglandin EィイD22ィエD2 and interleukin-la in the differentiation and survival of osteoclasts induced by lipopolysaccharide from Actinobacillus actinomycetemcomitans Y4"J.periodontal Res.. 33. 509-516 (1998)

N.Ueda：“前列腺素 E-D22 和白细胞介素 -1a 在由放线杆菌放线菌 Y4 脂多糖诱导的破骨细胞分化和存活中的参与”J. periodontal Res. 33. 509-516 (1998)