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首页> 外文期刊>Journal of the American Society of Nephrology: JASN >Increased renal angiopoietin-1 expression in folic acid-induced nephrotoxicity in mice.
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Increased renal angiopoietin-1 expression in folic acid-induced nephrotoxicity in mice.

机译：叶酸诱导的小鼠肾毒性中肾血管生成素-1的表达增加。

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摘要

Growth factors affect epithelial regeneration after acute renal injury, but less is known regarding the expression of vascular growth factors in this setting. A mouse model of folic acid (FA)-induced nephrotoxicity was used to study the expression of angiopoietins (Ang), factors that bind the Tie-2 receptor and modulate endothelial growth. Tubular damage was detected 1 d after FA administration; in the next 14 d, most tubules regenerated but patchy atrophy, with interstitial fibrosis, was also observed. Ang-1 immunostaining was detected between cortical tubules and in the vasa rectae of vehicle-treated animals. FA-induced nephropathy was associated with the acquisition of Ang-1 immunostaining in renal arterial walls and in a subset of injured cortical tubules that failed to stain with periodic acid-Schiff stain, which indicated that they were distal tubules. Renal Ang-1 protein levels were significantly increased after FA administration, compared with time-matched control values, as assessed by Western blotting. Capillaries between regenerating tubules expressed both Tie-2 and platelet-endothelial cell adhesion molecule. A subset of these endothelia expressed proliferating cell nuclear antigen, whereas capillary proliferation was absent in control samples. Therefore, FA-induced nephropathy is associated with increased Ang-1 protein expression in renal epithelia and arteries. In addition, Tie-2-expressing capillaries near damaged cortical tubules undergo proliferation. Further experiments are required to establish whether these events are functionally related.
机译：生长因子会影响急性肾损伤后上皮的再生，但对于这种情况下血管生长因子的表达知之甚少。使用叶酸（FA）诱导的肾毒性小鼠模型研究血管生成素（Ang）的表达，血管生成素是与Tie-2受体结合并调节内皮生长的因子。 FA给药1 d后发现肾小管损伤;在接下来的14 d中，大多数肾小管再生了，但是还出现了具有间质纤维化的斑块状萎缩。在皮质小管之间和经媒介物处理的动物的血管直肠中检测到Ang-1免疫染色。 FA诱发的肾病与肾动脉壁和部分受损皮质小管中Ang-1免疫染色的获得有关，这些小管未能用高碘酸Schiff染色染色，表明它们是远端小管。通过Western印迹评估，与时间匹配的对照值相比，FA给药后肾Ang-1蛋白水平显着增加。再生小管之间的毛细血管同时表达Tie-2和血小板-内皮细胞粘附分子。这些内皮细胞的一部分表达增殖的细胞核抗原，而对照样品中没有毛细血管增生。因此，FA诱发的肾病与肾上皮和动脉中Ang-1蛋白表达的增加有关。另外，在受损的皮质小管附近的表达Tie-2的毛细血管会增殖。需要进一步的实验来确定这些事件是否在功能上相关。

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