Bcl-2 increases emptying of endoplasmic reticulum Ca2+ stores during photodynamic therapy-induced apoptosis

Granville, David J.; Ruehlmann, Dietrich O.; Choy, Jonathan C.; Cassidy, Brighid A.; Hunt, David W. C.; Breemen, Cornelis van; McManus, Bruce M.

doi:10.1054/ceca.2001.0243

Cited by 51 publications

(33 citation statements)

References 29 publications

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“…However, in some cell types it was observed that elevation of the [Ca 2 + ] i following photosensitization promotes cell survival and buffering of the intracellular Ca 2 + enhanced cell death [104,108,119]. The [Ca 2 + ] i rise upon photosensitization may originate from the influx of Ca 2 + through ion channels [108,116], release of Ca 2 + sequestered in internal stores, including the ER and possibly the mitochondria [104,106,107,112,120], and/or activation of ion exchange mechanisms [111] (Fig. 2).…”

Section: Effect Of Pdt On the [Ca 2+ ] I Homeostasismentioning

confidence: 99%

“…In contrast, D609, which inhibits the phosphatidylcholine-specific phospholipase C, had no effect on the [Ca 2 + ] i response in sensitized rat pancreatic acini [107]. The [Ca 2 + ] i oscillations induced by photosensitization of pancreatic acinar cells with sulfonated aluminum phthalocyanine were inhibited by an antagonist of the cholecystokinin receptors [117], indicating that the photodynamic In human adenocarcinoma HeLa cells photosensitized with verteporfin the release of Ca 2 + from internal stores, mainly from the ER, was associated with a rapid caspaseindependent depletion of sarco/endoplasmic reticulum Ca 2 + ATPase (SERCA2) [112]. Also, in vitro studies using subcellular fractions isolated from the rat liver showed that microsomal Ca 2 + -uptake mechanisms were more sensitive to photosensitization with haematoporphyrin or protoporphyrin than the influx of Ca 2 + into isolated mitochondria [121].…”

Section: Effect Of Pdt On the [Ca 2+ ] I Homeostasismentioning

confidence: 99%

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Intracellular signaling mechanisms in photodynamic therapy

Almeida

Manadas

Carvalho

et al. 2004

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

242

292

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In photodynamic therapy (PDT) a sensitizer, light and oxygen are used to induce death of tumor cells and in the treatment of certain noncancerous conditions. Cell death in PDT may occur by apoptosis or by necrosis, depending on the sensitizer, on the PDT dose and on the cell genotype. Some sensitizers that have been used in PDT are accumulated in the mitochondria, and this may explain their efficiency in inducing apoptotic cell death, both in vitro and in vivo. In this review we will focus on the events that characterize apoptotic death in PDT and on the intracellular signaling events that are set in motion in photosensitized cells. Activation of phospholipases, changes in ceramide metabolism, a rise in the cytosolic free Ca 2 + concentration, stimulation of nitric oxide synthase (NOS), changes in protein phosphorylation and alterations in the activity of transcription factors and on gene expression have all been observed in PDT-treated cells. Although many of these metabolic reactions contribute to the demise process, some of them may antagonize cell death. Understanding the signaling mechanisms in PDT may provide means to modulate the PDT effects at the molecular level and potentiate its antitumor effectiveness. D

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Section: Effect Of Pdt On the [Ca 2+ ] I Homeostasismentioning

confidence: 99%

Section: Effect Of Pdt On the [Ca 2+ ] I Homeostasismentioning

confidence: 99%

Intracellular signaling mechanisms in photodynamic therapy

Almeida

Manadas

Carvalho

et al. 2004

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

242

292

View full text Add to dashboard Cite

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“…This localization suggests that wolframin may play an as yet undefined role in membrane trafficking, secretion, processing, and/or regulation of ER calcium homeostasis. Rapid but controlled redistribution of intracellular calcium is central in signaling, secretion, and apoptosis in all eukaryotic cells (15)(16)(17)(18)(19)(20)(21)(22). The unfolded protein response and calcium regulation are well defined ER functions that have been shown to play prominent roles in cellular apoptosis (23)(24)(25).…”

mentioning

confidence: 99%

Wolframin Expression Induces Novel Ion Channel Activity in Endoplasmic Reticulum Membranes and Increases Intracellular Calcium

Osman

Saito

Makepeace

et al. 2003

Journal of Biological Chemistry

179

134

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Wolfram syndrome is an autosomal recessive neurodegenerative disorder associated with juvenile onset non-autoimmune diabetes mellitus and progressive optic atrophy. The disease has been attributed to mutations in the WFS1 gene, which codes for a protein predicted to possess 9 -10 transmembrane segments. Little is known concerning the function of the WFS1 protein (wolframin). Endoglycosidase H digestion, immunocytochemistry, and subcellular fractionation studies all indicated that wolframin is localized to the endoplasmic reticulum in rat brain hippocampus and rat pancreatic islet ␤-cells, and after ectopic expression in Xenopus oocytes. Reconstitution of wolframin from oocyte membranes into planar lipid bilayers demonstrated that the protein induced a large cation-selective ion channel that was blocked by Mg 2؉ or Ca 2؉ . Inositol triphosphate was capable of activating channels in the fused bilayers that were similar to channel components induced by wolframin expression. Expression of wolframin also increased cytosolic calcium levels in oocytes. Wolframin thus appears to be important in the regulation of intracellular Ca 2؉ homeostasis. Disruption of this function may place cells at risk to suffer inappropriate death decisions, thus accounting for the progressive ␤-cell loss and neuronal degeneration associated with the disease.

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“…11 The increase of free calcium ion was responsible for necrosis or apoptosis induced by photodynamic therapy. 11,18 In the present experiment with Fluo-3-AM, the concentration of intracellular calcium increased after ultrasound radiation and HMME-ultrasound treatment. The increase of Ca 2+ in the UMR-106 cells was more significant after the treatment of ultrasound and HMME together than after ultrasound radiation alone, demonstrating that HMME clearly enhanced the intracellular Ca 2+ level induced by ultrasound radiation.…”

Section: Discussionmentioning

confidence: 57%

Hematoporphyrin Monomethyl Ether Enhances the Killing of Ultrasound on Osteosarcoma Cells Involving Intracellular Reactive Oxygen Species and Calcium Ion Elevation

et al. 2010

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Objective: The present study aims to investigate the possible mechanisms of hematoporphyrin monomethyl ether (HMME) enhancing the cytotoxicity of ultrasound in osteosarcoma cells. Methods: Osteosarcoma cell line UMR-106 was treated by HMME and ultrasound radiation, with the HMME concentration kept at 20 mg/mL and ultrasound radiation for 10 seconds at the intensity of 0.5 W/cm 2 . Cell proliferation was investigated at 12, 24, 36, and 48 hours using MTT assay after ultrasound and HMME treatment. Ultrastructural morphology was observed using transmission electron microscopy (TEM). Intracellular reactive oxygen species (ROS) was measured using a flow cytometry with DCFH-DA staining and intracellular free calcium ion (Ca 2+ ) with Fluo-3-AM staining. Results: The UMR-106 cells proliferated rapidly in the sham radiation and HMME treatment alone group, but ultrasound-treated cells and HMME-ultrasound-treated cells proliferated slowly. There was a significant difference between HMME-ultrasound treatment and the controls, including ultrasound radiation, HMME treatment alone, and sham radiation (P < .05). TEM showed endoplasmic reticulum and mitochondrial swelling in the ultrasound-treated cells, and more cells presented apoptosis and necrosis after treatment with ultrasound and HMME together. Intracellular ROS and Ca 2+ in the cells increased more significantly after both ultrasound and HMME treatment than after ultrasound treatment alone. Conclusions: HMME could effectively enhance the inhibition effect of ultrasound on osteosarcoma cells. Intracellular ROS and Ca 2+ in the UMR-106 cells increased more significantly after the treatment of HMME and ultrasound together, indicating that the enhancement of HMME on ultrasound cytotoxicity to osteosarcoma cells possibly involves both intracellular ROS and Ca 2+ elevation.

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Bcl-2 increases emptying of endoplasmic reticulum Ca2+ stores during photodynamic therapy-induced apoptosis

Cited by 51 publications

References 29 publications

Intracellular signaling mechanisms in photodynamic therapy

Intracellular signaling mechanisms in photodynamic therapy

Wolframin Expression Induces Novel Ion Channel Activity in Endoplasmic Reticulum Membranes and Increases Intracellular Calcium

Hematoporphyrin Monomethyl Ether Enhances the Killing of Ultrasound on Osteosarcoma Cells Involving Intracellular Reactive Oxygen Species and Calcium Ion Elevation

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