Rivard Christopher J, Brown Lewis M, Almeida Nestor E, Maunsbach Arvid B, Pihakaski-Maunsbach Kaarina, Andres-Hernando Ana, Capasso Juan M, Berl Tomas
Division of Renal Diseases and Hypertension, School of Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
J Biol Chem. 2007 Mar 2;282(9):6644-52. doi: 10.1074/jbc.M609432200. Epub 2007 Jan 2.
Proteomic analysis of Inner Medullary Collecting Duct (IMCD3) cells adapted to increasing levels of tonicity (300, 600, and 900 mosmol/kg H(2)O) by two-dimensional difference gel electrophoresis and mass spectrometry revealed several proteins as yet unknown to be up-regulated in response to hypertonic stress. Of these proteins, one of the most robustly up-regulated (22-fold) was S100A4. The identity of the protein was verified by high pressure liquid chromatography-mass spectrometry. Western blot analysis confirmed increased expression with increased tonicity, both acute and chronic. S100A4 protein expression was further confirmed by immunocytochemical analysis. Cells grown in isotonic conditions showed complete absence of immunostaining, whereas chronically adapted IMCD3 cells had uniform cytoplasmic localization. The protein is also regulated in vivo as in mouse kidney tissues S100A4 expression was many -fold greater in the papilla as compared with the cortex and increased further in the papilla upon 36 h of thirsting. Increased expression of S100A4 was also observed in the medulla and papilla, but not the cortex of a human kidney. Data from Affymetrix gene chip analysis and quantitative PCR also revealed increased S100A4 message in IMCD3 cells adapted to hypertonicity. The initial expression of message increased at 8-10 h following exposure to acute sublethal hypertonic stress (550 mosmol/kg H(2)O). Protein and message half-life in IMCD3 cells were 85.5 and 6.8 h, respectively. Increasing medium tonicity with NaCl, sucrose, mannitol, and choline chloride stimulated S100A4 expression, whereas urea did not. Silencing of S100A4 expression using a stable siRNA vector (pSM2; Open Biosystems) resulted in a 48-h delay in adaptation of IMCD3 cells under sublethal osmotic stress, suggesting S100A4 is involved in the osmoadaptive response. In summary, we describe the heretofore unrecognized up-regulation of a small calcium-binding protein, both in vitro and in vivo, whose absence profoundly delays osmoadaptation and slows cellular growth under hypertonic conditions.
通过二维差异凝胶电泳和质谱分析,对适应于不同渗透压水平(300、600和900毫摩尔/千克H₂O)的髓质内集合管(IMCD3)细胞进行蛋白质组学分析,发现了几种在高渗应激下上调但此前未知的蛋白质。在这些蛋白质中,上调最为显著(22倍)的一种是S100A4。该蛋白质的身份通过高压液相色谱 - 质谱法得以验证。蛋白质印迹分析证实,无论是急性还是慢性高渗状态下,随着渗透压升高,S100A4的表达均增加。免疫细胞化学分析进一步证实了S100A4蛋白的表达。在等渗条件下生长的细胞未显示免疫染色,而长期适应的IMCD3细胞具有均匀的细胞质定位。该蛋白质在体内也受到调控,例如在小鼠肾组织中,乳头区域的S100A4表达比皮质高许多倍,且在口渴36小时后乳头区域的表达进一步增加。在人类肾脏中也观察到S100A4在髓质和乳头区域表达增加,但皮质中未增加。来自Affymetrix基因芯片分析和定量PCR的数据也显示,适应高渗的IMCD3细胞中S100A4的信使核糖核酸(mRNA)增加。在暴露于急性亚致死性高渗应激(550毫摩尔/千克H₂O)后8 - 10小时,mRNA的初始表达增加。IMCD3细胞中蛋白质和mRNA的半衰期分别为85.5小时和6.8小时。用氯化钠、蔗糖、甘露醇和氯化胆碱提高培养基渗透压可刺激S100A4表达,而尿素则无此作用。使用稳定的小干扰RNA载体(pSM2;Open Biosystems)使S100A4表达沉默,导致IMCD3细胞在亚致死性渗透应激下的适应延迟48小时,这表明S100A4参与了渗透适应反应。总之,我们描述了一种迄今未被认识的小钙结合蛋白在体外和体内的上调情况,其缺失会严重延迟渗透适应并减缓高渗条件下的细胞生长。