scholarly journals Prostaglandin E 2 Signaling via EP4 Receptor is Important for Cell Cycle Progression and the Regulation of Reactive Oxygen Species Production in Primary Myoblast

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Chenglin Mo ◽  
Lori Wetmore ◽  
Ruonan Zhao ◽  
Lynda Bonewald ◽  
Marco Brotto
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Reactive Oxygen Species Production ◽  
Cell Cycle Progression ◽  
Prostaglandin E ◽  
Oxygen Species ◽  
Cycle Progression ◽  
Ep4 Receptor ◽  
Primary Myoblast ◽  
Species Production

scholarly journals Regulation of Late G1/S Phase Transition and APCCdh1 by Reactive Oxygen Species

2006 ◽  
Vol 26 (12) ◽  
pp. 4701-4711 ◽  
Author(s):  
Courtney G. Havens ◽  
Alan Ho ◽  
Naohisa Yoshioka ◽  
Steven F. Dowdy
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Cell Size ◽  
Cell Cycle Progression ◽  
Reactive Oxygen ◽  
Cyclin A ◽  
S Phase ◽  
Oxygen Species ◽  
Cycle Progression ◽  
Mitochondrial Mass

ABSTRACT Proliferating cells have a higher metabolic rate than quiescent cells. To investigate the role of metabolism in cell cycle progression, we examined cell size, mitochondrial mass, and reactive oxygen species (ROS) levels in highly synchronized cell populations progressing from early G1 to S phase. We found that ROS steadily increased, compared to cell size and mitochondrial mass, through the cell cycle. Since ROS has been shown to influence cell proliferation and transformation, we hypothesized that ROS could contribute to cell cycle progression. Antioxidant treatment of cells induced a late-G1-phase cell cycle arrest characterized by continued cellular growth, active cyclin D-Cdk4/6 and active cyclin E-Cdk2 kinases, and inactive hyperphosphorylated pRb. However, antioxidant-treated cells failed to accumulate cyclin A protein, a requisite step for initiation of DNA synthesis. Further examination revealed that cyclin A continued to be ubiquitinated by the anaphase promoting complex (APC) and to be degraded by the proteasome. This antioxidant arrest could be rescued by overexpression of Emi1, an APC inhibitor. These observations reveal an intrinsic late-G1-phase checkpoint, after transition across the growth factor-dependent G1 restriction point, that links increased steady-state levels of endogenous ROS and cell cycle progression through continued activity of APC in association with Cdh1.

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