Mitochondrial Translocation of TFEB Regulates Complex I and Inflammation

2021 ◽  
Author(s):  
Chiara Calabrese ◽  
Hendrik Nolte ◽  
Melissa Pitman ◽  
Philipp Lampe ◽  
Raymond Laboy ◽  
...  
Keyword(s):  
Complex I ◽  
Mitochondrial Translocation

scholarly journals Molecular Mechanism Underlying Hypoxic Preconditioning-Promoted Mitochondrial Translocation of DJ-1 in Hypoxia/Reoxygenation H9c2 Cells

Molecules ◽  
2019 ◽  
Vol 25 (1) ◽  
pp. 71 ◽  
Author(s):  
Yi-Zhang Deng ◽  
Lin Xiao ◽  
Le Zhao ◽  
Le-Jia Qiu ◽  
Zhao-Xia Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanism ◽  
Complex I ◽  
Hypoxic Preconditioning ◽  
Mitochondrial Complex I ◽  
H9c2 Cells ◽  
Mitochondrial Complex ◽  
Mitochondrial Translocation ◽  
Stress Damage ◽  
Complex I Activity

DJ-1 was recently reported to be involved in the cardioprotection of hypoxic preconditioning (HPC) against hypoxia/reoxygenation (H/R)-induced oxidative stress damage, by preserving mitochondrial complex I activity and, subsequently, inhibiting mitochondrial reactive oxygen species (ROS) generation. However, the molecular mechanism by which HPC enables mitochondrial translocation of DJ-1, which has no mitochondria-targeting sequence, to preserve mitochondrial complex I, is largely unknown. In this study, co-immunoprecipitation data showed that DJ-1 was associated with glucose-regulated protein 75 (Grp75), and this association was significantly enhanced after HPC. Immunofluorescence imaging and Western blot analysis showed that HPC substantially enhanced the translocation of DJ-1 from cytosol to mitochondria in H9c2 cells subjected to H/R, which was mimicked by DJ-1 overexpression induced by pFlag-DJ-1 transfection. Importantly, knockdown of Grp75 markedly reduced the mitochondrial translocation of DJ-1 induced by HPC and pFlag-DJ-1 transfection. Moreover, HPC promoted the association of DJ-1 with mitochondrial complex I subunits ND1 and NDUFA4, improved complex I activity, and inhibited mitochondria-derived ROS production and subsequent oxidative stress damage after H/R, which was also mimicked by pFlag-DJ-1 transfection. Intriguingly, these effects of HPC and pFlag-DJ-1 transfection were also prevented by Grp75 knockdown. In conclusion, these results indicated that HPC promotes the translocation of DJ-1 from cytosol to mitochondria in a Grp75-dependent manner and Grp75 is required for DJ-1-mediated protection of HPC on H/R-induced mitochondrial complex I defect and subsequent oxidative stress damage.

Pressure overload induced heart failure may be due to impaired respiratory capacity and a defect in complex I

2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
M Schwarzer ◽  
M Osterholt ◽  
A Schrepper ◽  
PA Amorim ◽  
T Doenst
Keyword(s):  
Heart Failure ◽  
Complex I ◽  
Pressure Overload ◽  
Respiratory Capacity

197-OR: IL-6 Protects Pancreatic ß Cells from Oxidative Stress via NRF2 Mitochondrial Translocation and Mitophagy

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 197-OR
Author(s):  
MICHELLE MARASCO ◽  
ABASS M. CONTEH ◽  
CHARANYA MURALIDHARAN ◽  
ELIZABETH PFEIFER ◽  
AMELIA K. LINNEMANN
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Translocation
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