Carrizo Liliana C, Ruete Celeste M, Manucha Walter A, Ciocca Daniel R, Vallés Patricia G
Area de Fisiopatología, Departamento de Patología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza, Argentina.
Cell Stress Chaperones. 2006 Winter;11(4):309-24. doi: 10.1379/csc-199.1.
The cellular stress response can mediate cellular protection through expression of heat shock protein (Hsp70), which can interfere with the process of apoptotic cell death. Factors regulating renal epithelial cell apoptosis include angiotensin II. In the present study, we have examined the relationship between the Hsp70 expression and the apoptotic pathway in the kidneys from low-protein-fed rats (8% protein). The possible cytoprotective role of Hsp70 has been evaluated during low-protein feeding and after reincorporation of 24% protein in the diet. The effect of angiotensin II AT1 receptor inhibition has also been studied. Rats were fed with a low-protein (LP) diet (8% protein) for 14 days, and then the animals were recovered by means of a normal protein diet (24% protein) (RP) for 14, 21, and 30 days, and control rats received 24% protein (NP) in the diet. LP and NP rats treated with Losartan (10 mg/kg) were also evaluated. The following methods were performed on the kidneys: terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling assay for apoptosis, reverse transcriptase-polymerase chain reaction assay for AT1, Bax, and Bcl-2 messenger ribonucleic acid (mRNA) expression, and immunohistochemical and Western blot for Hsp70 and caspase 3 protein expression and activity. In the LP group, the cells of the medullary ducts (MDs) showed increased apoptosis associated with weak immunoreaction for Hsp70 and decreased Hsp70 protein levels. In these animals, enhanced proapoptotic ratio Bax/Bcl-2 linked to decreased procaspase 3 protein levels with increased caspase 3 activation were demonstrated. A cytoprotection attributed to Hsp70 could be noted in the RP rats after 21 days of reincorporation of the normal diet, and in the LP-fed group treated with Losartan. In these cases, the MD cells displayed decreased apoptosis and increased Hsp70 expression in colocalization staining, and high Hsp70 levels in cytosolic fraction. A decreased proapoptotic ratio Bax/Bcl-2, associated with increased Bcl-2 mRNA, was also observed. Our results provide evidence for an antiapoptotic, cytoprotective effect of Hsp70 in kidney MD cells of rats with LP intake, when the animals were recovered with 24% protein in diet and after angiotensin II AT1 receptor inhibition. Angiotensin II seems to play a role in the pathogenesis of tubule epithelial cell apoptosis during LP feeding.
细胞应激反应可通过热休克蛋白(Hsp70)的表达介导细胞保护作用,Hsp70可干扰细胞凋亡性死亡过程。调节肾上皮细胞凋亡的因素包括血管紧张素II。在本研究中,我们检测了低蛋白饮食(8%蛋白质)大鼠肾脏中Hsp70表达与凋亡途径之间的关系。已评估了Hsp70在低蛋白饮食期间及饮食中重新添加24%蛋白质后可能的细胞保护作用。还研究了血管紧张素II AT1受体抑制的作用。大鼠喂食低蛋白(LP)饮食(8%蛋白质)14天,然后通过正常蛋白饮食(24%蛋白质)(RP)恢复14、21和30天,对照大鼠饮食中摄入24%蛋白质(NP)。还评估了用氯沙坦(10 mg/kg)处理的LP和NP大鼠。对肾脏进行了以下检测:采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法检测细胞凋亡,采用逆转录-聚合酶链反应法检测AT1、Bax和Bcl-2信使核糖核酸(mRNA)表达,采用免疫组织化学和蛋白质免疫印迹法检测Hsp70和半胱天冬酶3蛋白表达及活性。在LP组中,髓质集合管(MD)细胞凋亡增加,同时Hsp70免疫反应较弱,Hsp70蛋白水平降低。在这些动物中,促凋亡比值Bax/Bcl-2升高,与procaspase 3蛋白水平降低及caspase 3活化增加相关。正常饮食重新添加21天后的RP大鼠以及用氯沙坦处理的LP喂养组中,可观察到Hsp70的细胞保护作用。在这些情况下,MD细胞在共定位染色中凋亡减少,Hsp70表达增加,胞质部分Hsp70水平升高。还观察到促凋亡比值Bax/Bcl-2降低,与Bcl-2 mRNA增加相关。我们的结果为Hsp70在低蛋白摄入大鼠肾脏MD细胞中的抗凋亡、细胞保护作用提供了证据,这种作用在动物饮食中重新添加24%蛋白质后以及血管紧张素II AT1受体抑制后出现。血管紧张素II似乎在低蛋白喂养期间肾小管上皮细胞凋亡的发病机制中起作用。