Time-course effect of high-glucose-induced reactive oxygen species on mitochondrial biogenesis and function in human renal mesangial cells

2015 ◽  
Vol 40 (1) ◽  
pp. 36-48 ◽  
Author(s):  
Ghada Al-Kafaji ◽  
Mohamed Abdalla Sabry ◽  
Cristina Skrypnyk
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Biogenesis ◽  
High Glucose ◽  
Time Course ◽  
Mesangial Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
And Function

scholarly journals TSC–mTOR maintains quiescence and function of hematopoietic stem cells by repressing mitochondrial biogenesis and reactive oxygen species

2008 ◽  
Vol 205 (10) ◽  
pp. 2397-2408 ◽  
Author(s):  
Chong Chen ◽  
Yu Liu ◽  
Runhua Liu ◽  
Tsuneo Ikenoue ◽  
Kun-Liang Guan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Mitochondrial Biogenesis ◽  
Reactive Oxygen ◽  
Mtor Pathway ◽  
Oxygen Species ◽  
Hematopoietic Stem ◽  
And Function

The tuberous sclerosis complex (TSC)–mammalian target of rapamycin (mTOR) pathway is a key regulator of cellular metabolism. We used conditional deletion of Tsc1 to address how quiescence is associated with the function of hematopoietic stem cells (HSCs). We demonstrate that Tsc1 deletion in the HSCs drives them from quiescence into rapid cycling, with increased mitochondrial biogenesis and elevated levels of reactive oxygen species (ROS). Importantly, this deletion dramatically reduced both hematopoiesis and self-renewal of HSCs, as revealed by serial and competitive bone marrow transplantation. In vivo treatment with an ROS antagonist restored HSC numbers and functions. These data demonstrated that the TSC–mTOR pathway maintains the quiescence and function of HSCs by repressing ROS production. The detrimental effect of up-regulated ROS in metabolically active HSCs may explain the well-documented association between quiescence and the “stemness” of HSCs.

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