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首页> 外文期刊>American Journal of Physiology >Temporal expression profile and distribution pattern indicate a role of connective tissue growth factor (CTGF/CCN-2) in diabetic nephropathy in mice.
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Temporal expression profile and distribution pattern indicate a role of connective tissue growth factor (CTGF/CCN-2) in diabetic nephropathy in mice.

机译：时间表达谱和分布模式表明结缔组织生长因子（CTGF / CCN-2）在小鼠糖尿病肾病中的作用。

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摘要

Connective tissue growth factor (CTGF) is overexpressed in diabetic nephropathy (DN) and has therefore been implicated in its pathogenesis. The objective of the present study was to determine the tissue distribution of increased CTGF expression and the relationship of plasma, urinary, and renal CTGF levels to the development and severity of DN. We studied the relationship between CTGF and renal pathology in streptozotocin (STZ)-induced diabetes in C57BL/6J mice. Diabetic and age-matched control mice were killed after 1, 2, 4, and 9 wk of diabetes. In addition, key parameters of diabetes and DN were analyzed in 10-mo-old diabetic ob/ob mice and their ob/+ littermates. STZ-induced diabetic mice showed a significantly increased urinary albumin excretion after 1 wk and increased mesangial matrix score after 2 wk. Increased renal fibronectin, fibronectin ED-A, and collagen IValpha1 expression, as well as elevated plasma creatinine levels, were observed after 9 wk. After 2 wk, CTGF mRNA was upregulated threefold in the renal cortex. By 9 wk, CTGF mRNA was also increased in the heart and liver. In contrast, transforming growth factor-beta1 mRNA content was significantly increased only in the kidney by 9 wk. Renal CTGF expression was mainly localized in podocytes and parietal glomerular epithelial cells, and less prominent in mesangial cells. In addition, plasma CTGF levels and urinary CTGF excretion were increased in diabetic mice. Moreover, albuminuria strongly correlated with urinary CTGF excretion (R = 0.83, P < 0.0001). Increased CTGF expression was also demonstrated in type 2 diabetic ob/ob mice, which points to a causal relationship between diabetes and CTGF and thus argues against a role of STZ in this process. The observed relationship of podocyte and urinary CTGF to markers of DN suggests a pathogenic role of CTGF in the development of DN.
机译：结缔组织生长因子（CTGF）在糖尿病性肾病（DN）中过表达，因此与它的发病机理有关。本研究的目的是确定CTGF表达增加的组织分布以及血浆，尿液和肾脏CTGF水平与DN的发展和严重程度之间的关系。我们研究了C57BL / 6J小鼠链脲佐菌素（STZ）诱导的糖尿病中CTGF与肾脏病理之间的关系。糖尿病，与年龄匹配的对照小鼠在糖尿病1、2、4和9周后被杀死。此外，在10个月大的糖尿病ob / ob小鼠及其ob / +同窝仔中分析了糖尿病和DN的关键参数。 STZ诱导的糖尿病小鼠1周后尿白蛋白排泄显着增加，而2周后肾小球系膜基质评分增加。 9周后观察到肾纤连蛋白，纤连蛋白ED-A和胶原IValpha1表达增加，以及血浆肌酐水平升高。 2周后，CTGF mRNA在肾皮质中上调了三倍。到9周时，心脏和肝脏中的CTGF mRNA也增加了。相反，仅在肾脏中，转化生长因子β1mRNA含量显着增加了9周。肾CTGF表达主要定位于足细胞和顶肾小球上皮细胞中，而肾小球系膜细胞中较少。另外，糖尿病小鼠的血浆CTGF水平和尿CTGF排泄增加。此外，蛋白尿与尿液CTGF排泄密切相关（R = 0.83，P <0.0001）。在2型糖尿病ob / ob小鼠中也证实了CTGF表达的增加，这表明糖尿病与CTGF之间存在因果关系，因此反对STZ在此过程中的作用。观察到的足细胞和尿液CTGF与DN标记的关系表明CTGF在DN的发展中具有致病作用。

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