Ishiguro K, Kadomatsu K, Kojima T, Muramatsu H, Matsuo S, Kusugami K, Saito H, Muramatsu T
Department of Biochemistry, Nagoya University School of Medicine, Nagoya, Japan.
Lab Invest. 2001 Apr;81(4):509-16. doi: 10.1038/labinvest.3780259.
The expression and roles of syndecan-4 in the kidney were investigated. Syndecan-4 expression was detected in the ureteric bud invaginating into the metanephric mesenchyme at 11.5 gestational days, and remained in the collecting ducts, distal renal tubules, glomeruli, and some capillaries between renal tubules until the mature kidney stage. However, organogenesis of the kidney was normal in syndecan-4-deficient (Synd4[-/-]) mice. Although most renal functions of Synd4(-/-) mice were not impaired, a significant increase in susceptibility to kappa-carrageenan-induced renal damage was observed in these mice. kappa-Carrageenan was heavily deposited in the collecting ducts of Synd4(-/-) mice and caused obstructive nephropathy, leading to death of 7 of 24 Synd4(-/-) mice within 7 days after administration, whereas none of 24 Synd4(+/+) mice died. After administration of kappa-carrageenan, blood urea nitrogen of Synd4(-/-) mice was significantly higher than that of Synd4(+/+) mice. Thus, syndecan-4 may function to prevent kappa-carrageenan deposition in the collecting ducts.
研究了syndecan-4在肾脏中的表达及作用。在妊娠第11.5天，syndecan-4表达于侵入后肾间充质的输尿管芽中，并在集合管、远端肾小管、肾小球以及肾小管之间的一些毛细血管中持续存在，直至肾脏成熟阶段。然而，syndecan-4基因缺陷（Synd4[-/-]）小鼠的肾脏器官发生正常。虽然Synd4(-/-)小鼠的大多数肾功能未受损，但观察到这些小鼠对κ-卡拉胶诱导的肾损伤的易感性显著增加。κ-卡拉胶大量沉积在Synd4(-/-)小鼠的集合管中，导致梗阻性肾病，致使24只Synd4(-/-)小鼠中有7只在给药后7天内死亡，而24只Synd4(+/+)小鼠无一死亡。给予κ-卡拉胶后，Synd4(-/-)小鼠的血尿素氮显著高于Synd4(+/+)小鼠。因此，syndecan-4可能具有防止κ-卡拉胶在集合管中沉积的功能。
