哺乳动物细胞在糖尿病、缺血再灌注和疟疾引起的氧化应激下会使总 RNA 加倍。
Mammal cells double their total RNAs against diabetes, ischemia reperfusion and malaria-induced oxidative stress.
机构信息
College of Resources and Environmental Sciences, Sichuan Agriculture University, Chengdu, China.
出版信息
Mol Med. 2011 May-Jun;17(5-6):533-41. doi: 10.2119/molmed.2010.00155. Epub 2010 Dec 8.
Total cellular RNA level is stable usually, although it may increase gradually during growth or decrease gradually under certain stressors. However, we found that mammal cell RNAs could be doubled within 24 h in response to free heme accumulation (ischemia reperfusion and malaria infection) or a high level of glucose treatment (diabetes). Clinical investigations in rats showed that pretreatment with heme (24 h for doubling total RNAs) alleviated oxidative damages caused by diabetes, and pretreatment with glucose (24 h for trebling total RNAs) alleviated oxidative damages caused by ischemia reperfusion or malaria infection. Therefore, this rapid RNA amplification may play an important role in mammal adaptation to diabetes, ischemia reperfusion and malaria infection-derived oxidative stress. This rapid RNA amplification is derived from glucose and heme, but not from their accompanying reactive oxygen species. Hexokinases endure glucose-derived reactive oxygen species accumulation but are not related glucose-derived RNA amplification. In contrast, the TATA box-binding protein (TBP) mediates all glucose- and heme-induced RNA amplification in mammal cells.
总的来说，细胞内的 RNA 水平通常是稳定的，尽管在生长过程中可能会逐渐增加，或者在某些应激条件下逐渐减少。然而，我们发现哺乳动物细胞的 RNA 可以在 24 小时内增加一倍，以响应游离血红素的积累（缺血再灌注和疟疾感染）或高水平的葡萄糖处理（糖尿病）。对大鼠的临床研究表明，血红素预处理（24 小时使总 RNA 加倍）可以减轻糖尿病引起的氧化损伤，而葡萄糖预处理（24 小时使总 RNA 增加三倍）可以减轻缺血再灌注或疟疾感染引起的氧化损伤。因此，这种快速的 RNA 扩增可能在哺乳动物适应糖尿病、缺血再灌注和疟疾感染引起的氧化应激中发挥重要作用。这种快速的 RNA 扩增来源于葡萄糖和血红素，但不是来源于它们伴随的活性氧。己糖激酶能忍受葡萄糖产生的活性氧的积累，但与葡萄糖产生的 RNA 扩增无关。相比之下，TATA 框结合蛋白（TBP）介导了哺乳动物细胞中所有由葡萄糖和血红素诱导的 RNA 扩增。
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