Abnormalities of extracellular matrices and transforming growth factor beta1 localization in the kidney of the hereditary nephrotic mice (ICGN strain).
Abnormalities of extracellular matrices and transforming growth factor beta1 localization in the kidney of the hereditary nephrotic mice (ICGN strain).
复制标题
遗传性肾病小鼠（ICGN品系）肾脏细胞外基质异常和转化生长因子β1定位。
DOI：
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发表时间：
1999
影响因子：
1.2
通讯作者：
Hajime Miyamoto
中科院分区：
文献类型：
--
作者：
K. Uchio;Noboru Manabe;Akiko Kinoshita;Kotaro Tamura;Makoto Miyamoto;Atsuo Ogura;Yoshie Yamamoto;Hajime Miyamoto
ICR 衍生的肾小球肾炎品系 (ICGN) 是一种患有遗传性肾病综合征的小鼠品系，其原因不明。基于组织病理学和生化数据，ICGN小鼠被认为是人类特发性肾病综合征的良好实验模型。在本研究中，我们通过组织化学研究了细胞外基质（ECM）成分和转化生长因子β1（TGF-β1）定位的变化。与用作正常健康对照的性别和年龄匹配的 ICR 小鼠相比，ICGN 小鼠的肾小球和肾小管间质中显示出基底膜 ECM 成分（IV 型胶原和层粘连蛋白）和间质 ECM 成分（III 型胶原和纤连蛋白）的强免疫组织化学染色。在ICGN小鼠的肾小球中观察到了在ICR小鼠的肾小球中未检测到的标记的I型胶原和腱蛋白沉积。仅在 ICGN 小鼠的肾小球中检测到活性 TGF-β1 显着增加，而在 ICR 小鼠的肾小球中未检测到。此外，在 ICGN 小鼠的肾小球（主要是系膜细胞）中，α-平滑肌肌动蛋白（激活的肾小球系膜细胞的标志物）显着增加。这些发现表明ICGN小鼠的肾小球和肾小管间质中的ECM成分增加，并且活性TGF-β1诱导ECM成分的这种增加。目前的发现可能有助于阐明 ICGN 小鼠遗传性肾病综合征以及未来人类特发性肾病综合征的致病机制。
ICR-derived strain with glomerulonephritis (ICGN) is a strain of mice with hereditary nephrotic syndrome with an unidentified cause. Based on histopathological and biochemical data, ICGN mice are considered to be a good experimental model for human idiopathic nephrotic syndrome. In the present study, we histochemically investigated the changes in localization of extracellular matrix (ECM) components and transforming growth factor beta1 (TGF-beta1). Strong immunohistochemical staining of basal membrane ECM components (collagen IV and laminin) and interstitial ECM components (type III collagen and fibronectin) were demonstrated in glomeruli and tubulointerstitum of ICGN mice as compared with those of sex and age-matched ICR mice, used as normal healthy controls. Marked type I collagen and tenascin deposition, which were not detected in the glomeruli of ICR mice, were seen in the glomeruli of ICGN mice. A remarkable increase in active-TGF-beta1 was also detected only in glomeruli of ICGN mice, but not in those of ICR mice. Furthermore, strikingly increased alpha-smooth muscle actin, a marker of activated glomerular mesangial cells, was demonstrated in the glomeruli, mainly in the mesangial cells, of ICGN mice. These findings indicated that ECM components are increased in the glomerulus and tubulointerstitum of ICGN mice, and that active-TGF-beta1 induces such increases in ECM components. The present findings may contribute to elucidation of the pathogenic mechanisms of hereditary nephrotic syndrome in ICGN mice and, in future, human idiopathic nephrotic syndrome.
影响因子：
19.6
作者：
S. Tomooka;W. A. Border;B. C. Marshall;N. Noble
通讯作者：
S. Tomooka;W. A. Border;B. C. Marshall;N. Noble
影响因子：
3.3
作者：
MEREDITH, JE;FAZELI, B;SCHWARTZ, MA
通讯作者：
SCHWARTZ, MA
肾小球系膜细胞连续传代后，细胞外基质蛋白的表达增加，基质蛋白酶的表达减少。
影响因子：
4
作者：
Schnaper,HW;Kopp,JB;Poncelet,AC;Hubchak,SC;Stetler-Stevenson,WG;Klotman,PE;Kleinman,HK
通讯作者：
Kleinman,HK