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首页> 外文期刊>American Journal of Physiology >Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury.
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Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury.

机译：缺乏Stathmin的小鼠会发生纤维化，并显示缺血再灌注损伤的恢复延迟。

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摘要

In kidneys subjected to ischemic reperfusion injury (IRI) stathmin, a tubulin-binding protein involved in the regulation of mitosis, is expressed in dedifferentiated and proliferating renal tubule cells during the recovery phase. To ascertain the role of stathmin in the recovery from ischemic kidney injury, stathmin-deficient (OP18-/-) and wild-type (WT) animals were subjected to experimental IRI. At 3, 7, and 14 days after reperfusion serum samples and kidneys were collected for the examination of parameters of renal function, morphology, and recovery. Our studies indicate that on day 14 after reperfusion OP18-/- mice have significant renal failure, whereas the creatinine levels of WT animals have returned to baseline. Compared with WT animals OP18-/- mice had more extensive tubular fibrosis. The examination of proliferating cell nuclear antigen expression indicated that OP18-/- animals have increased proliferative or DNA repair activity for a more prolonged duration. The OP18-/- animals also had an increased number of tubules with apoptotic cells. These results suggest that in stathmin-deficient mice subjected to IRI, the aberrant regulation of cell cycle progression, not observed under normal conditions, impairs or at least delays the process of tubular repair and recovery after acute renal injury.
机译：在遭受缺血性再灌注损伤（IRI）的stathmin的肾脏中，在恢复期的去分化和增殖的肾小管细胞中表达参与有丝分裂调控的微管蛋白结合蛋白。为了确定stathmin在缺血性肾损伤恢复中的作用，对stathmin缺乏症（OP18-/-）和野生型（WT）动物进行了实验性IRI。再灌注后第3、7和14天，收集血清样品和肾脏以检查肾功能，形态和恢复的参数。我们的研究表明，再灌注后第14天，OP18-/-小鼠出现严重的肾衰竭，而野生型动物的肌酐水平已恢复到基线。与野生型动物相比，OP18-/-小鼠的肾小管纤维化更为广泛。增殖细胞核抗原表达的检查表明，OP18-/-动物具有更长时间的增殖或DNA修复活性。 OP18-/-动物的凋亡细胞小管数量也增加。这些结果表明，在接受IRI的有Stathmin缺陷的小鼠中，在正常条件下未观察到异常的细胞周期进程调节会损害或至少延迟急性肾损伤后肾小管修复和恢复的过程。

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