Glucose Protection from MPP+-Induced Apoptosis Depends on Mitochondrial Membrane Potential and ATP Synthase

Chalmers-Redman, R. M. E.; Fraser, Andrew; Carlile, Graeme W.; Pong, Amanda; Tatton, W. G.

doi:10.1006/bbrc.1999.0487

Cited by 56 publications

(37 citation statements)

References 71 publications

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“…Complex I inhibition would disrupt the mitochondrial membrane potential, which is required for mitochondrial protein import (45). In fact, it has been shown that MPP ϩ reduces the mitochondrial membrane potential, which ultimately causes cell death (46,47). Although we could not demonstrate this conclusively, several indirect lines of evidence suggest that the mitochondrial import system is an intermediate between complex I inhibition and proteasome activation.…”

Section: Discussioncontrasting

confidence: 55%

Commitment of 1-Methyl-4-phenylpyrinidinium Ion-induced Neuronal Cell Death by Proteasome-mediated Degradation of p35 Cyclin-dependent Kinase 5 Activator

Endo

Saito

Asada

et al. 2009

Journal of Biological Chemistry

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Section: Discussioncontrasting

confidence: 55%

Commitment of 1-Methyl-4-phenylpyrinidinium Ion-induced Neuronal Cell Death by Proteasome-mediated Degradation of p35 Cyclin-dependent Kinase 5 Activator

Endo

Saito

Asada

et al. 2009

Journal of Biological Chemistry

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“…In contrast, IL-1␤ greatly decreased ATP synthase regulatory subunit A (match number 176), an effect that was NO mediated. A role for ATP synthase in glucose protection against apoptosis in neurons has been proposed (80). Previous extensive research on ATP synthase, which uses a transmembrane proton gradient to drive synthesis of cellular ATP, has been reviewed (81).…”

Section: Discussionmentioning

confidence: 99%

Cytokine- or chemically derived nitric oxide alters the expression of proteins detected by two-dimensional gel electrophoresis in neonatal rat islets of Langerhans.

et al. 2000

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Interleukin-1␤ (IL-1␤) treatment of neonatal rat islets19 of a total of 1,600 detectable proteins in GSNOtreated islets (P < 0.01). We conclude 1) that the expression of up to 42 proteins is altered by cytokineinduced or chemically generated NO in the precise experimental conditions chosen and 2) that the majority of proteins altered by prior treatment with IL-1␤ may be the result of NO-independent IL-1␤-mediated regulation of gene expression. This study demonstrates that the combination of 2D gel electrophoresis and mass spectrometry is a powerful tool in the identification of ␤-cell proteins involved in the response to toxic mediators.

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“…We [34][35][36][37][38] and others [39][40][41] have used rhodamine derivatives, which contain a chloromethyl moiety that binds to matrix thiols like CMXRos and chloromethyltetramethylrosamine (CMTMR or Mitotracker orange) to measure ¢ae M . These derivatives offer the advantage that fixation binds them to matrix proteins allowing immunocytochemistry to be subsequently carried out in the same cells.…”

Section: Using Potentiometric Dye Fluorescence To Measure ¢Ae Mmentioning

confidence: 99%

“…We have employed similar calibrations to those of Metivier et al [33] using varying concentrations of FCCP, a protonophore, and atractyloside, which opens the PTPC, to dissi-pate the proton gradient and reduce ¢ae M [38]. We have jointly examined CMTMR, JC-1 and TMRM.…”

Section: Using Potentiometric Dye Fluorescence To Measure ¢Ae Mmentioning

confidence: 99%

Mitochondrial Membrane Potential in Aging Cells

Sugrue

Tatton

2001

Neurosignals

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Decreased mitochondrial membrane potential (ΔΨ_M) has been found in a variety of aging cell types from several mammalian species. The physiological significance and mechanisms of the decreased ΔΨ_M in aging are not well understood. This review considers the generation of ΔΨ_M and its role in ATP generation together with factors that modify ΔΨ_M with emphasis on mitochondrial membrane permeability, particularly the role of a multiprotein membrane megapore, the mitochondrial permeability transition pore complex (PTPC). Previous data showing decreased ΔΨ_M in aged cells is considered in relation to the methods available to estimate ΔΨ_M. In the past the majority of studies used whole cell rhodamine 123 fluorescence to estimate ΔΨ_M in lymphocytes from mice or rats. Imaging of ΔΨ_M in living, in situ mitochondria using laser confocal scanning microscopy offers advantages over whole cell measurements or those from isolated mitochondria, particularly if several different potentiometric dyes are employed. Furthermore, high resolution imaging of the newer fixable potentiometric dyes allows immunocytochemistry for specific proteins and ΔΨ_M to be examined in the same cells or even the same mitochondria. We found that decreased ΔΨ_M in p53 overexpression-induced or naturally occurring senescence is associated with decreased responsiveness of the PTPC to agents that induce either its opening or closing. The decreased PTPC responsiveness seems to reflect, at least in part, decreased levels of a key PTPC protein, the adenine nucleotide translocase. We also consider the possible basis for decreased ΔΨ_M in fibroblasts from patients with Parkinson’s disease, an age-related neurodegenerative disease. Finally, we speculate on the mechanisms and functional significance of decreased ΔΨ_M in aging.

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Glucose Protection from MPP+-Induced Apoptosis Depends on Mitochondrial Membrane Potential and ATP Synthase

Cited by 56 publications

References 71 publications

Commitment of 1-Methyl-4-phenylpyrinidinium Ion-induced Neuronal Cell Death by Proteasome-mediated Degradation of p35 Cyclin-dependent Kinase 5 Activator

Commitment of 1-Methyl-4-phenylpyrinidinium Ion-induced Neuronal Cell Death by Proteasome-mediated Degradation of p35 Cyclin-dependent Kinase 5 Activator

Cytokine- or chemically derived nitric oxide alters the expression of proteins detected by two-dimensional gel electrophoresis in neonatal rat islets of Langerhans.

Mitochondrial Membrane Potential in Aging Cells

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