Efficacy of MitoTracker Green™ and CMXrosamine to measure changes in mitochondrial membrane potentials in living cells and tissues

Pendergrass, William R.; Wolf, Norman S.; Poot, Martin

doi:10.1002/cyto.a.20033

Cited by 428 publications

(348 citation statements)

References 19 publications

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“…7). For these studies, striatal cells were incubated with 20 M rosiglitazone for 24 h, in the absence or presence of 40 M GW9662 prior to being loaded with MitoGreen, which is used for mitochondrial mass determinations (42,44,45). Confocal images were taken from striatal cells treated with the indicated conditions (Fig.…”

Section: Rosiglitazone Treatment Results In An Increase In Mitochondrialmentioning

confidence: 99%

Rosiglitazone Treatment Prevents Mitochondrial Dysfunction in Mutant Huntingtin-expressing Cells

Quintanilla

Jin

Fuenzalida

et al. 2008

Journal of Biological Chemistry

118

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Peroxisome proliferator-activated receptor-␥ (PPAR␥) is a member of the PPAR family of transcription factors. Synthetic PPAR␥ agonists are used as oral anti-hyperglycemic drugs for the treatment of non-insulin-dependent diabetes. However, emerging evidence indicates that PPAR␥ activators can also prevent or attenuate neurodegeneration. Given these previous findings, the focus of this report is on the potential neuroprotective role of PPAR␥ activation in preventing the loss of mitochondrial function in Huntington disease (HD). For these studies we used striatal cells that express wild-type (STHdh Q7/Q7 ) or mutant (STHdh Q111/Q111 ) huntingtin protein at physiological levels. Treatment of mutant cells with thapsigargin resulted in a significant decrease in mitochondrial calcium uptake, an increase in reactive oxygen species production, and a significant decrease in mitochondrial membrane potential. PPAR␥ activation by rosiglitazone prevented the mitochondrial dysfunction and oxidative stress that occurred when mutant striatal cells were challenged with pathological increases in calcium. The beneficial effects of rosiglitazone were likely mediated by activation of PPAR␥, as all protective effects were prevented by the PPAR␥ antagonist GW9662. Additionally, the PPAR␥ signaling pathway was significantly impaired in the mutant striatal cells with decreases in PPAR␥ expression and reduced PPAR␥ transcriptional activity. Treatment with rosiglitazone increased mitochondrial mass levels, suggesting a role for the PPAR␥ pathway in mitochondrial function in striatal cells. Altogether, this evidence indicates that PPAR␥ activation by rosiglitazone attenuates mitochondrial dysfunction in mutant huntingtin-expressing striatal cells, and this could be an important therapeutic avenue to ameliorate the mitochondrial dysfunction that occurs in HD.

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Section: Rosiglitazone Treatment Results In An Increase In Mitochondrialmentioning

confidence: 99%

Rosiglitazone Treatment Prevents Mitochondrial Dysfunction in Mutant Huntingtin-expressing Cells

Quintanilla

Jin

Fuenzalida

et al. 2008

Journal of Biological Chemistry

118

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“…To further characterize that the vacuolated organelle was mitochondria, a plasmid with the mitochondrial targeting sequence from subunit VIII of human cytochrome c oxidase was This process was also studied using MitoTracker Red CMXRos, a fluorescent dye whose accumulation depends on mitochondrial membrane potential [24], to track mitochondria ( Figure 6). Control cells showed typical filamentous mitochondria, but in treated cells mitochondria gradually swelled to a larger size structure and finally lost fluorescence.…”

Section: Mitochondrial Swellingmentioning

confidence: 99%

Synthetic tambjamine analogues induce mitochondrial swelling and lysosomal dysfunction leading to autophagy blockade and necrotic cell death in lung cancer

Rodilla

Korrodi‐Gregório

Hernando

et al. 2017

Biochemical Pharmacology

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Current pharmacological treatments for lung cancer show very poor clinical outcomes, therefore, the development of novel anticancer agents with different mechanisms of action is urgently needed. Cancer cells have a reversed pH gradient compared to normal cells, which favors cancer progression by promoting proliferation, metabolic adaptation and evasion of apoptosis. In this regard, the use of ionophores to modulate intracellular pH appears as a promising new therapeutic strategy. Indeed, there is a growing body of evidence supporting ionophores as a novel antitumor drugs. Despite this, little is known about the implications of pH deregulation and homeostasis imbalance triggered by ionophores at the cellular level. In this work, we deeply analyze for the first time the anticancer effects of tambjamine analogues, a group of highly effective anion selective ionophores, at the cellular and molecular level. First, their effects on cell viability were determined in several lung cancer cell lines and patient-derived cancer stem cells, demonstrating their potent cytotoxic effects. Then, we have characterized the induced lysosomal deacidification, as well as, the massive cytoplasmic vacuolization observed after treatment with these compounds, which is consistent with mitochondrial swelling. Finally, the activation of several proteins involved in stress response, autophagy and apoptosis was also detected, although necrosis was the main mechanism of cell death induced.Altogether, these evidences suggest that tambjamine analogues provoke an imbalance in cellular ion homeostasis that triggers mitochondrial dysfunction and lysosomal deacidification leading to a potent cytotoxic effect through necrosis in lung cancer cell lines and cancer stem cells.

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“…Quantification was per formed by normalizing voxel count to cell number using the Volocity software (PerkinElmer). Mitochondrial content was additionally investigated using MitoTracker green FM (Invitrogen) as previously described (Pendergrass et al, 2004) with slight modification (n = 3). In brief, 0.75 × 10 6 CS1AN cells expressing WT CSB or empty vector were harvested by trypsin, washed, and resuspended in DME without phenol indicator (Invitrogen).…”

Section: Isolation Of Mdfsmentioning

confidence: 99%

Cockayne syndrome group B protein prevents the accumulation of damaged mitochondria by promoting mitochondrial autophagy

Scheibye‐Knudsen¹,

Ramamoorthy²,

Sýkora³

et al. 2012

J Cell Biol

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Efficacy of MitoTracker Green™ and CMXrosamine to measure changes in mitochondrial membrane potentials in living cells and tissues

Cited by 428 publications

References 19 publications

Rosiglitazone Treatment Prevents Mitochondrial Dysfunction in Mutant Huntingtin-expressing Cells

Rosiglitazone Treatment Prevents Mitochondrial Dysfunction in Mutant Huntingtin-expressing Cells

Synthetic tambjamine analogues induce mitochondrial swelling and lysosomal dysfunction leading to autophagy blockade and necrotic cell death in lung cancer

Cockayne syndrome group B protein prevents the accumulation of damaged mitochondria by promoting mitochondrial autophagy

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