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Specific expression of survivin, SOX9, and CD44 in renal tubules in adaptive and maladaptive repair processes after acute kidney injury in rats
Journal of Applied Toxicology ( IF 3.3 ) Pub Date : 2020-09-23 , DOI: 10.1002/jat.4069
Kohei Matsushita 1 , Takeshi Toyoda 1 , Takanori Yamada 1, 2 , Tomomi Morikawa 1 , Kumiko Ogawa 1
Affiliation  

Acute kidney injury (AKI) is thought to be a reversible condition; however, growing evidence has suggested that AKI may be associated with subsequent development of chronic kidney disease. Although renal tubules have intrinsic regeneration capacity, disruption of the regeneration mechanisms leads to irreversible interstitial fibrosis. In this study, we investigated immunohistochemical markers of renal tubules in adaptive and maladaptive repair processes to predict AKI reversibility. Histopathological analysis demonstrated that regenerative tubules and dilated tubules were observed in the kidneys of AKI model rats after ischemia/reperfusion (I/R). Regenerative tubules gradually redifferentiated after I/R, whereas dilated tubules exhibited no tendency for redifferentiation. In fibrotic areas of the kidney in renal fibrosis model rats subjected to I/R, renal tubules were dilated or atrophied. There results suggested that the histopathological features of renal tubules in the maladaptive repair were dilation or atrophy. From microarray data of regenerative tubules, survivin, SOX9, and CD44 were extracted as candidate markers. Immunohistochemical analysis demonstrated that survivin and SOX9 were expressed in regenerative tubules, whereas SOX9 was also detected in renal tubules in fibrotic areas. These findings indicated that survivin and SOX9 contributed to renal tubular regeneration, whereas sustained SOX9 expression may be associated to fibrosis. CD44 was expressed in dilated tubules in the kidneys of AKI model rats and in the tubules of fibrotic areas of renal fibrosis model rats, suggesting that CD44 was expressed in renal tubules in maladaptive repair. Thus, these factors could be useful markers for detecting disruption of the regenerative mechanisms of renal tubules.

中文翻译:

Survivin、SOX9、CD44在大鼠急性肾损伤后适应性和适应不良修复过程中肾小管的特异性表达

急性肾损伤 (AKI) 被认为是一种可逆的疾病;然而,越来越多的证据表明 AKI 可能与慢性肾病的后续发展有关。尽管肾小管具有内在的再生能力,但再生机制的破坏会导致不可逆的间质纤维化。在这项研究中,我们研究了适应性和适应不良修复过程中肾小管的免疫组织化学标志物,以预测 AKI 的可逆性。组织病理学分析表明,在缺血/再灌注(I/R)后,AKI 模型大鼠的肾脏中观察到再生小管和扩张的小管。再生小管在 I/R 后逐渐再分化,而扩张的小管没有再分化的趋势。在接受 I/R 的肾纤维化模型大鼠的肾脏纤维化区域,肾小管扩张或萎缩。结果表明,适应不良修复中肾小管的组织病理学特征为扩张或萎缩。从再生小管的微阵列数据中,提取存活蛋白、SOX9 和 CD44 作为候选标记。免疫组织化学分析表明,survivin 和 SOX9 在再生小管中表达,而 SOX9 在纤维化区域的肾小管中也检测到。这些发现表明存活蛋白和 SOX9 有助于肾小管再生,而持续的 SOX9 表达可能与纤维化有关。CD44 在 AKI 模型大鼠肾脏的扩张小管和肾纤维化模型大鼠的纤维化区的小管中表达,表明 CD44 在适应不良修复的肾小管中表达。因此,这些因素可能是检测肾小管再生机制破坏的有用标志物。
更新日期:2020-09-23
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