Mechanisms of cell proliferation and extracellular matrix production in glomeruli

肾小球细胞增殖和细胞外基质产生的机制

• 批准号: 63570155
• 负责人: OITE Takashi
• 金额: $ 1.41万
• 依托单位: Niigata University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1988
• 资助国家: 日本
• 起止时间: 1988 至 1989
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-63570155/
• 关键词: RENAL GLOMERULI; GLOMERULAR SCLEROSIS; EXTRACELLULAR MATRIX; CELL PROLIFERATION; EXPERIMENTAL NEPHRITIS; CULTURE OF GLOMERULI; GROWTH FACTORS; HAPTEN-SPECIFIC INJURY; 腎糸球体硬化; 糸球体細胞培養; 血液単球由来因子; 細胞外基質産生; 糸球体腎炎

With aid of the above grant, we have researched and reported on the mechanisms of cell proliferation and extracellular matrix increment in the renal glomeruli. The following results have been obtained during the period of research project:1).Monocyte-macrophage line cells were detected electron microscopically and immunohistologically within the inflamed glomeruli from human (using renal biopsy) and experimental animals.2).Electrophoretic patterns of urinary proteins corresponded to differences in morphological expression such as proliferative changes in experimental glomerulonephritis (GN) models.3).Using culture of isolated glomeruli, we found a human monocute-derived factors which were able to induce proliferation of glomerular mesangial cells in vitro. One of this factors is similar in nature to platelet- derived growth factor.4).Furthermore, we detected the enhancing activity of extracelluar matrix production in the culture supernatant of human monocytes.5).We reported a new model of experimental GN model in which marked exudative and proliferative changes in glomeruli and cellular influx containing Ia-positive leukocytes. Using this model of hapten-specific glomerular injury, mechanisms responsible for inducing cell infiltration and cell proliferation within glomeruli could be researched at molecular and cellular levels.

在上述基金资助下，我们对肾小球细胞增殖和细胞外基质增加的机制进行了研究和报道。本研究取得了以下成果：1）通过电镜和免疫组织化学方法在人和实验动物的炎症肾小球中检测到单核-巨噬细胞系细胞; 2）在实验性肾小球肾炎（GN）模型中，尿蛋白电泳图谱与形态学表达的差异相对应，如增生性改变; 3）利用离体肾小球培养，我们发现了一种人单核细胞源性因子，其能够在体外诱导肾小球系膜细胞增殖。其中一种因子在性质上与血小板源性生长因子相似。4）此外，我们还检测到人单核细胞培养上清中细胞外基质产生的增强活性。5）我们报道了一种新的实验性GN模型，其中肾小球有明显的渗出和增殖变化，含有Ia阳性白细胞的细胞内流。利用这种半抗原特异性肾小球损伤模型，可以在分子和细胞水平上研究引起肾小球内细胞浸润和细胞增殖的机制。

项目成果

Morioka T et al.: "The electrophoretic pattern of urinary protein in situ immune complex glomerulonephritis." Nephron 50:116-120(1988).

Morioka T 等人：“尿蛋白原位免疫复合物肾小球肾炎的电泳模式。”

Nakamura T et al.: "Monoclonal antibodies to human glomerular antigens." Virchows Archiv A Pathol Anat Histopathol. 412:573-582.

Nakamura T 等人：“针对人肾小球抗原的单克隆抗体。”

Kagami S et al.: "Active in situ immune complex glomerulonephritis using the hapten-carrier system: role of epitope density in cationic antigens." Clin exp Immunol 74:121-125(1988).

Kagami S 等人：“使用半抗原载体系统的活性原位免疫复合物肾小球肾炎：表位密度在阳离子抗原中的作用。”

Oite T et al.: "Glomerular deposition of immune complexes and the role of infiltrating monocytes." "Recent Studies of IgA Nephropathy in Japan", edited by M. Arakawa and F. Gejyo, Nishimura Co Ltd, Niigata, p 3-22(1989).

Oite T 等人：“免疫复合物的肾小球沉积和浸润单核细胞的作用。​​”

Oite,Takashi: "Hapten-specific cellular immune response producing glomerular injury." Clin exp Immounol. 76. 463-468 (1989)

Oite，Takashi：“半抗原特异性细胞免疫反应产生肾小球损伤。”