Relation between mitochondrial calcium transport and control of energy metabolism

1985 ◽  
pp. 1-72 ◽  
Author(s):  
Richard G. Hansford
Keyword(s):  
Energy Metabolism ◽  
Calcium Transport ◽  
Mitochondrial Calcium ◽  
And Control

scholarly journals ApoE4 (Δ272–299) induces mitochondrial‐associated membrane formation and mitochondrial impairment by enhancing GRP75-modulated mitochondrial calcium overload in neuron

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tao Liang ◽  
Weijian Hang ◽  
Jiehui Chen ◽  
Yue Wu ◽  
Bin Wen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Calcium Transport ◽  
Calcium Overload ◽  
Mitochondrial Calcium ◽  
Mitochondrial Impairment

Abstract Background Apolipoprotein E4 (apoE4) is a major genetic risk factor of Alzheimer’s disease. Its C-terminal-truncated apoE4 (Δ272–299) has neurotoxicity by affecting mitochondrial respiratory function. However, the molecular mechanism(s) underlying the action of apoE4 (Δ272–299) in mitochondrial function remain poorly understood. Methods The impact of neuronal apoE4 (Δ272–299) expression on ER stress, mitochondrial-associated membrane (MAM) formation, GRP75, calcium transport and mitochondrial impairment was determined in vivo and in vitro. Furthermore, the importance of ER stress or GRP75 activity in the apoE4 (Δ272–299)-promoted mitochondrial dysfunction in neuron was investigated. Results Neuronal apoE4 (Δ272–299) expression induced mitochondrial impairment by inducing ER stress and mitochondrial-associated membrane (MAM) formation in vivo and in vitro. Furthermore, apoE4 (Δ272–299) expression promoted GRP75 expression, mitochondrial dysfunction and calcium transport into the mitochondria in neuron, which were significantly mitigated by treatment with PBA (an inhibitor of ER stress), MKT077 (a specific GRP75 inhibitor) or GRP75 silencing. Conclusions ApoE4 (Δ272–299) significantly impaired neuron mitochondrial function by triggering ER stress, up-regulating GRP75 expression to increase MAM formation, and mitochondrial calcium overload. Our findings may provide new insights into the neurotoxicity of apoE4 (Δ272–299) against mitochondrial function and uncover new therapeutic targets for the intervention of Alzheimer’s disease.

Inhibition of rat brain mitochondrial calcium transport by chlordecone

1979 ◽  
Vol 51 (1) ◽  
pp. 189-196 ◽  
Author(s):  
David W. End ◽  
Richard A. Carchman ◽  
Richard Ameen ◽  
William L. Dewey
Keyword(s):  
Rat Brain ◽  
Calcium Transport ◽  
Mitochondrial Calcium

Mechanisms of Mitochondrial Calcium Transport

1988 ◽  
pp. 1-14 ◽  
Author(s):  
Thomas E. Gunter ◽  
Douglas E. Wingrove ◽  
Srabani Banerjee ◽  
Karlene K. Gunter
Keyword(s):  
Calcium Transport ◽  
Mitochondrial Calcium

scholarly journals A Kinetic Study of Mitochondrial Calcium Transport

1975 ◽  
Vol 55 (3) ◽  
pp. 497-504 ◽  
Author(s):  
Ken C. REED ◽  
Fyfe L. BYGRAVE
Keyword(s):  
Kinetic Study ◽  
Calcium Transport ◽  
Mitochondrial Calcium

scholarly journals Mitochondrial energy metabolism in a model of undernutrition induced by dexamethasone

2003 ◽  
Vol 90 (5) ◽  
pp. 969-977 ◽  
Author(s):  
Jean-François Dumas ◽  
Gilles Simard ◽  
Damien Roussel ◽  
Olivier Douay ◽  
Françoise Foussard ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Treated Group ◽  
Liver Mitochondria ◽  
Proton Leak ◽  
Thermodynamic Efficiency ◽  
Liver Mass ◽  
Mitochondrial Energy Metabolism ◽  
Thermodynamic Coupling ◽  
And Control ◽  
Complex Activities

The present investigation was undertaken to evaluate whether mitochondrial energy metabolism is altered in a model of malnutrition induced by dexamethasone (DEX) treatment (1·5mg/kg per d for 5d). The gastrocnemius and liver mitochondria were isolated from DEX-treated, pair-fed (PF) and control (CON) rats. Body weight was reduced significantly more in the DEX-treated group (−16%) than in the PF group (−9%). DEX treatment increased liver mass (+59% v. PF, +23% v. CON) and decreased gastrocnemius mass. Moreover, in DEX-treated rats, liver mitochondria had an increased rate of non-phosphorylative O2 consumption with all substrates (approximately +42%). There was no difference in enzymatic complex activities in liver mitochondria between rat groups. Collectively, these results suggest an increased proton leak and/or redox slipping in the liver mitochondria of DEX-treated rats. In addition, DEX decreased the thermodynamic coupling and efficiency of oxidative phosphorylation. We therefore suggest that this increase in the proton leak and/or redox slip in the liver is responsible for the decrease in the thermodynamic efficiency of energy conversion. In contrast, none of the variables of energy metabolism determined in gastrocnemius mitochondria was altered by DEX treatment. Therefore, it appears that DEX specifically affects mitochondrial energy metabolism in the liver.

PROTEINS IN MITOCHONDRIAL CALCIUM TRANSPORT

1978 ◽  
pp. 171-186 ◽  
Author(s):  
E. Carafoli ◽  
K. Schwerzmann ◽  
I. Roos ◽  
M. Crompton
Keyword(s):  
Calcium Transport ◽  
Mitochondrial Calcium
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