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首页> 外文期刊>Kidney Research and Clinical Practice >Diabetic conditions modulate the adenosine monophosphate-activated protein kinase of podocytes
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Diabetic conditions modulate the adenosine monophosphate-activated protein kinase of podocytes

机译：糖尿病条件调节足细胞腺苷一磷酸激活的蛋白激酶

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Background: Adenosine monophosphate-activated protein kinases (AMPKs), as a sensor of cellular energy status, have been known to play an important role in the pathophysiology of diabetes and its complications. Because AMPKs are known to be expressed in podocytes, it is possible that podocyte AMPKs could be an important contributing factor in the development of diabetic proteinuria. We investigated the roles of AMPKs in the pathological changes in podocytes induced by high-glucose (HG) and advanced glycosylation end products (AGEs) in diabetic proteinuria. Methods: We prepared streptozotocin-induced diabetic renal tissues and cultured rat and mouse podocytes under diabetic conditions with AMPK-modulating agents. The changes in AMPK@a were analyzed with confocal imaging and Western blotting under the following conditions: (1) normal glucose (5mM, =control); (2) HG (30mM); (3) AGE-added; or (4) HG plus AGE-added. Results: The density of glomerularphospho-AMPK@a in experimental diabetic nephropathy decreased as a function of the diabetic duration. Diabetic conditions including HG and AGE changed the localization of phospho-AMPK@a from peripheral cytoplasm to internal cytoplasm and peri- and intranuclear areas in podocytes. HG reduced the AMPK@a (Thr172) phosphorylation of rat podocytes, and similarly, AGEs reduced the AMPK@a (Thr172) phosphorylation of mouse podocytes. The distributional and quantitative changes in phospho-AMPK@a caused by diabetic conditions were preventable using AMPK activators, metformin, and 5-aminoimidazole-4-carboxamide-1@b-riboside. Conclusion: We suggest that diabetic conditions induce the relocation and suppression of podocyte AMPK@a, which would be a suggestive mechanism in diabetic podocyte injury.
机译：背景：腺苷一磷酸激活的蛋白激酶（AMPK）作为细胞能量状态的传感器，在糖尿病及其并发症的病理生理中起着重要的作用。因为已知AMPK在足细胞中表达，所以足细胞AMPK可能是糖尿病蛋白尿发展的重要促成因素。我们调查了AMPKs在糖尿病蛋白尿症中由高糖（HG）和高级糖基化终产物（AGEs）诱导的足细胞病理变化中的作用。方法：我们制备了链脲佐菌素诱导的糖尿病肾组织，并在糖尿病条件下用AMPK调节剂培养大鼠和小鼠足细胞。在以下条件下通过共聚焦成像和蛋白质印迹分析了AMPK @ a的变化：（1）正常葡萄糖（5mM，＝对照）; （2）HG（30毫米）; （3）增加年龄;或（4）HG加AGE。结果：实验性糖尿病肾病中肾小球磷酸化-AMPK @ a的密度随着糖尿病持续时间的延长而降低。包括HG和AGE在内的糖尿病疾病将磷酸化AMPK @ a的位置从外周细胞质转移到内部细胞质以及足细胞的核周和核内区域。 HG降低了大鼠足细胞的AMPK @ a（Thr172）磷酸化，类似地，AGEs降低了小鼠足细胞的AMPK @ a（Thr172）磷酸化。使用AMPK激活剂，二甲双胍和5-氨基咪唑-4-甲酰胺-1 @ b-核糖苷可预防由糖尿病引起的磷酸-AMPK @ a的分布和定量变化。结论：我们认为糖尿病可引起足细胞AMPK @ a的重新定位和抑制，这可能是糖尿病足细胞损伤的暗示机制。

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