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PRODUCTION OF METALLOPROTEINASES AND TIMP1 BY GLOMERULAR CELLS

PRODUCTION OF METALLOPROTEINASES AND TIMP1 BY GLOMERULAR CELLS
肾小球细胞产生金属蛋白酶和 TIMP1
批准号:
3840307
负责人:
L J STRIKER
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
肾小球硬化发生在大量的人类肾脏疾病中, 包括糖尿病肾病。 它包括积累 细胞外基质(ECM)在肾小球内。 硬化症可能是 由ECM合成和降解的失调介导。 一 基质金属蛋白酶大家族以及 金属蛋白酶抑制剂(TIMPs)在降解过程中起作用。 我们 初步工作表明:1)正常小鼠系膜细胞培养 分泌72 kD和92 kD明胶酶(IV型胶原酶)以及 TIMP 1; 2)来源于NOD小鼠和TIMP 1转基因小鼠的系膜细胞 牛生长激素(bGH)仅分泌72 kD明胶酶;和3) TIMP 1 mRNA水平受细胞密度调节。
英文摘要
Glomerulosclerosis occurs in a large number of human kidney diseases, including diabetic nephropathy. It consists of the accumulation of extracellular matrix (ECM) within the glomerulus. Sclerosis may be mediated by dysregulation of both synthesis and degradation of ECM. A large family of matrix metalloproteinases as well as tissue inhibitors of metalloproteinase (TIMPs) play a role in the degradative process. Our preliminary work reveals that: 1) normal mouse mesangial cells in culture secrete a 72 kD and a 92 kD gelatinase (type IV collagenase) as well as TIMP1; 2) mesangial cells derived form NOD mice and mice transgenic for bovine growth hormone (bGH) secrete only the 72 kD gelatinase; and 3) TIMP1 mRNA levels are modulated by cell density.
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PRODUCTION OF METALLOPROTEINASES AND TIMPS BY GLOMERULAR CELLS
GLOMERULAR LESIONS IN NON-OBESE DIABETIC MICE
PRODUCTION OF METALLOPROTEINASES AND TIMPS BY GLOMERULAR CELLS
DEGRADATION OF EXTRACELLULAR MATRIX IN HUMAN GLOMERULI
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