Glucose deprivation induces mitochondrial dysfunction and oxidative stress in PC12 cell line

Liu, Yan; Song, Xiaodong; Liu, Wen; Zhang, Tianyi; Zuo, Jiane

doi:10.1111/j.1582-4934.2003.tb00202.x

Cited by 118 publications

(89 citation statements)

References 25 publications

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“…When severe, membrane ionic gradients cannot be maintained, intracellular Ca 2+ levels increase (Harris et al, 1984) the intracellular redox state shifts towards oxidation (Auer and Siesjö, 1988), and oxidative stress develops (Liu et al, 2003). All of these events may eventually cause the mPT.…”

Section: Hypoglycemiamentioning

confidence: 99%

The mitochondrial permeability transition in neurologic disease

Norenberg

Rao

2007

Neurochemistry International

144

107

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Mitochondria, being the principal source of cellular energy, are vital for cell life. Yet, ironically, they are also major mediators of cell death, either by necrosis or apoptosis. One means by which these adverse effects occur is through the mitochondrial permeability transition (mPT) whereby the inner mitochondrial membrane suddenly becomes excessively permeable to ions and other solutes, resulting in a collapse of the inner membrane potential, ultimately leading to energy failure and cell necrosis. The mPT may also bring about the release of various factors known to cause apoptotic cell death. The principal factors leading to the mPT are elevated levels of intracellular Ca 2+ and oxidative stress. Characteristically, the mPT is inhibited by cyclosporin A. This article will briefly discuss the concept of the mPT, its molecular composition, its inducers and regulators, agents that influence its activity and describe the consequences of its induction. Lastly, we will review its potential contribution to acute neurological disorders, including ischemia, trauma, and toxic-metabolic conditions, as well as its role in chronic neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis.

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Section: Hypoglycemiamentioning

confidence: 99%

The mitochondrial permeability transition in neurologic disease

Norenberg

Rao

2007

Neurochemistry International

144

107

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“…8b), the loosely attached cells were removed by several washes, and the number of surviving cells were counted. Glucose deprivation was the apoptotic stimulus of choice because it affects the energetic metabolism of the cell (Almeida et al, 2002;Y. Liu et al, 2003;Majewski et al, 2004), thus mimicking the environment encountered by oligodendrocytes in pathological conditions such as MS (Roelcke et al, 1997;Bakshi et al, 1998).…”

Section: Elevated Stathmin Levels In Differentiated Oligodendrocytes mentioning

confidence: 99%

Expression of Stathmin, a Developmentally Controlled Cytoskeleton-Regulating Molecule, in Demyelinating Disorders

Liu

Stadelmann²,

Moscarello³

et al. 2005

J. Neurosci.

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Understanding the biological relevance of reexpression of developmental molecules in pathological conditions is crucial for the development of new therapies. In this study, we report the increased expression of stathmin, a developmentally regulated tubulin-binding protein, in the brains of patients with multiple sclerosis (MS). In physiological conditions, stathmin immunoreactivity was observed in polysialic acid-neural cell adhesion molecule-positive migratory progenitors in the subventricular zone, and its expression progressively decreased as the cells matured into oligodendrocytes (OLs). In MS patients, however, stathmin levels were elevated in 2Ј,3Ј-cyclic nucleotide 3Ј-phosphodiesterase-positive OLs, in 10 of 10 bioptic samples analyzed. Increased levels of stathmin were confirmed by Western blot analysis of normal-appearing white matter samples from MS brains. In addition, using mass spectrometry, stathmin was identified as the main component of a specific myelin protein fraction consistently increased in MS preparations compared with controls.To test the biological relevance of increased stathmin levels, primary OL progenitors were transfected using a myc-tagged stathmin cDNA and were allowed to differentiate. Consistent with a distinct role played by this molecule in cells of the OL lineage at different developmental stages, transient transfection in progenitors favored the bipolar migratory phenotype but did not affect survival. However, sustained stathmin levels in differentiating OLs, because of overexpression, resulted in enhanced apoptotic susceptibility.We conclude that stathmin expression in demyelinating disorders could have a dual role. On one hand, by favoring the migratory phenotype of progenitors, it may promote myelin repair. On the other hand, stathmin in mature OLs may indicate cell stress and possibly affect survival.

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“…Alternatively, oxidative stress due to mitochondrial oxygen free radicals can mediate glucose withdrawalinduced cell death (15)(16)(17). A combination of oxidative stress and ATP depletion has also been reported to precede cell death after glucose withdrawal (18).…”

Section: Introductionmentioning

confidence: 99%

Glucose Withdrawal Induces Oxidative Stress followed by Apoptosis in Glioblastoma Cells but not in Normal Human Astrocytes

Jelluma¹,

Yang²,

Stokoe³

et al. 2006

Molecular Cancer Research

136

103

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Tumor cells rely preferentially on anaerobic glycolysis rather than on respiration for ATP generation, a phenomenon known as the Warburg effect. We explored the effects of glucose withdrawal on glioblastoma multiforme -derived cell lines and their nontransformed counterparts, normal human astrocytes. We found that glucose withdrawal induces extensive apoptosis in glioblastoma multiforme cells but not in normal astrocytes. In all cells examined, ATP levels are sustained on glucose withdrawal due to elevation of fatty acid oxidation and ensuing respiration; however, we show that oxidative stress generated in the mitochondrial respiratory chain is the direct cause of cell death in glioblastoma multiforme cells. Oxidative stress that only occurs in glioblastoma multiforme cells underlies the selective susceptibility to glucose withdrawal -induced apoptosis documented in the malignant cells. This study implicates glycolysis as a potentially efficient and selective target for glioblastoma multiforme treatment. (Mol Cancer Res 2006;4(5):319 -30)

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Glucose deprivation induces mitochondrial dysfunction and oxidative stress in PC12 cell line

Cited by 118 publications

References 25 publications

The mitochondrial permeability transition in neurologic disease

The mitochondrial permeability transition in neurologic disease

Expression of Stathmin, a Developmentally Controlled Cytoskeleton-Regulating Molecule, in Demyelinating Disorders

Glucose Withdrawal Induces Oxidative Stress followed by Apoptosis in Glioblastoma Cells but not in Normal Human Astrocytes

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