Podocyte specific knock out of selenoproteins does not enhance nephropathy in streptozotocin diabetic C57BL/6 mice.
Podocyte specific knock out of selenoproteins does not enhance nephropathy in streptozotocin diabetic C57BL/6 mice.
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DOI：
10.1186/1471-2369-9-7
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发表时间：
2008-07-22
期刊：
影响因子：
2.3
通讯作者：
Koenig RJ
中科院分区：
文献类型：
--
作者：
Blauwkamp MN;Yu J;Schin MA;Burke KA;Berry MJ;Carlson BA;Brosius FC 3rd;Koenig RJ
硒蛋白含有硒代半胱氨酸（Sec），通常被认为是第21个遗传编码的氨基酸。许多硒蛋白，如谷胱甘肽过氧化物酶和硫氧还蛋白还原酶，通过充当抗氧化剂和/或通过其在维持细胞内氧化还原平衡中的作用来保护细胞免受氧化应激。由于氧化应激与糖尿病肾病的发病机制有关，我们假设硒蛋白可以预防糖尿病的并发症。通过腹膜内注射链脲佐菌素或注射赋形剂使具有足细胞特异性不能将Sec掺入蛋白质的C57 BL/6小鼠（本文中表示为PodoTrsp-/-）和对照小鼠患糖尿病。评估血糖、体重、微量白蛋白尿、肾小球系膜基质扩张和氧化应激的免疫组织化学标记物。糖尿病3个月和6个月后，对照组和PodoTrsp-/-小鼠的血糖水平相似。尿白蛋白/肌酐比值无差异。用于检查系膜基质扩张的过碘酸-希夫染色也表明，在糖尿病6个月后，对照和PodoTrsp-/-小鼠之间没有差异，硝基酪氨酸或NAD（P）H脱氢酶、醌1的免疫组织化学染色也没有差异。链脲佐菌素糖尿病C57 BL/6小鼠足细胞硒蛋白的丢失不会导致氧化应激增加（通过硝基酪氨酸和NAD（P）H脱氢酶，醌1免疫染色评估），也不会导致肾病恶化。
Selenoproteins contain selenocysteine (Sec), commonly considered the 21st genetically encoded amino acid. Many selenoproteins, such as the glutathione peroxidases and thioredoxin reductases, protect cells against oxidative stress by functioning as antioxidants and/or through their roles in the maintenance of intracellular redox balance. Since oxidative stress has been implicated in the pathogenesis of diabetic nephropathy, we hypothesized that selenoproteins protect against this complication of diabetes. C57BL/6 mice that have a podocyte-specific inability to incorporate Sec into proteins (denoted in this paper as PodoTrsp-/-) and control mice were made diabetic by intraperitoneal injection of streptozotocin, or were injected with vehicle. Blood glucose, body weight, microalbuminuria, glomerular mesangial matrix expansion, and immunohistochemical markers of oxidative stress were assessed. After 3 and 6 months of diabetes, control and PodoTrsp-/- mice had similar levels of blood glucose. There were no differences in urinary albumin/creatinine ratios. Periodic acid-Schiff staining to examine mesangial matrix expansion also demonstrated no difference between control and PodoTrsp-/- mice after 6 months of diabetes, and there were no differences in immunohistochemical stainings for nitrotyrosine or NAD(P)H dehydrogenase, quinone 1. Loss of podocyte selenoproteins in streptozotocin diabetic C57BL/6 mice does not lead to increased oxidative stress as assessed by nitrotyrosine and NAD(P)H dehydrogenase, quinone 1 immunostaining, nor does it lead to worsening nephropathy.
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