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首页> 外文期刊>Toxicology and Applied Pharmacology >Cadmium- and mercury-induced intercellular adhesion molecule-1 expression in immortalized proximal tubule cells: evidence for a role of decreased transforming growth factor-beta1.
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Cadmium- and mercury-induced intercellular adhesion molecule-1 expression in immortalized proximal tubule cells: evidence for a role of decreased transforming growth factor-beta1.

机译：镉和汞诱导的永生化近端小管细胞中的细胞间粘附分子-1表达：证明转化生长因子-beta1减少的作用。

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A definitive association between the aberrant expression of cytokines and adhesion molecules in renal failure has been established. In this regard a relationship between cytokine and adhesion molecule expression is suggested but has not been shown in models of proximal tubular cell injury. To investigate the impact of acute injury on the relationship between transforming growth factor-beta 1 (TGF-beta1) and intercellular adhesion molecule-1 (ICAM-1) expression, two immortalized mouse proximal tubular epithelial cell lines were exposed to cadmium chloride or mercuric chloride (0-50 microM) for 0-8 h. ELISA and Western blot measured expression of secreted and intercellular TGF-beta1, respectively. Direct cellular ELISA or Western blot was used to assess ICAM-1 expression. Challenge with cadmium caused a greater loss of cell viability than did mercury. Interestingly, cadmium significantly decreased the amount of TGF-beta1 in the conditioned media. Although a similar trend was seen in mercury-challenged cells, no significant differences were observed. The decrease in TGF-beta1 in the culture media was not due to decreased expression of this cytokine, as intercellular levels were not affected by metal-induced injury. Significant increases in ICAM-1 protein expression were observed following cadmium and mercury challenge. The increase in ICAM-1 appears to be due to increased mRNA, as Northern blot analysis demonstrated increased message expression following a 4-h cadmium or mercury challenge. Supplementation of the culture media with exogenous TGF-beta1 decreased basal ICAM-1 expression and attenuated the cadmium-induced increase. These data suggest that metal-induced injury is associated with increased ICAM-1 expression. The mechanism of this induction may involve the decreased TGF-beta1 in the conditioned media following metal challenge. Taken together, these studies suggest a link between cytokine and adhesion molecule expression in renal injury.
机译：在肾衰竭中，细胞因子的异常表达与粘附分子之间已建立了明确的联系。在这方面，暗示了细胞因子和粘附分子表达之间的关系，但是在近端肾小管细胞损伤的模型中尚未显示。为了研究急性损伤对转化生长因子-β1（TGF-β1）和细胞间粘附分子-1（ICAM-1）表达之间关系的影响，将两种永生化的小鼠近端肾小管上皮细胞系暴露于氯化镉或汞氯化物（0-50 microM）进行0-8小时。 ELISA和Western blot分别测定了分泌型和细胞间TGF-beta1的表达。直接细胞ELISA或蛋白质印迹用于评估ICAM-1表达。镉的挑战比汞引起的细胞活力损失更大。有趣的是，镉显着降低了条件培养基中TGF-β1的含量。尽管在汞激发的细胞中发现了类似的趋势，但未观察到显着差异。培养基中TGF-β1的降低不是由于这种细胞因子的表达降低，因为细胞间水平不受金属诱导的损伤的影响。镉和汞激发后，ICAM-1蛋白表达显着增加。 ICAM-1的增加似乎是由于mRNA的增加所致，因为Northern印迹分析表明在4 h镉或汞激发后消息表达增加。补充外源性TGF-beta1的培养基会降低基础ICAM-1的表达，并减弱镉诱导的增加。这些数据表明金属诱导的损伤与ICAM-1表达增加有关。这种诱导的机制可能涉及金属攻击后条件培养基中TGF-β1的降低。综上所述，这些研究表明肾损伤中细胞因子与粘附分子表达之间存在联系。

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