ArticleMolecular medicine (Cambridge, Mass.)
Mammal cells double their total RNAs against diabetes, ischemia reperfusion and malaria-induced oxidative stress.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Mitochondrion-Permeable Antioxidants to Treat ROS-Burst-Mediated Acute Diseases.Oxidative medicine and cellular longevity · 2016Review
- The roles of two transcription factors, ABI4 and CBFA, in ABA and plastid signalling and stress responses.Plant molecular biology · 2013Article
- Drugs to cure avian influenza infection--multiple ways to prevent cell death.Cell death & disease · 2013Review
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10 authors at 4 institutions in 1 country.
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Abstract
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.
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