CaM-kinaseII-dependent commitment to microcystin-induced apoptosis is coupled to cell budding, but not to shrinkage or chromatin hypercondensation

Krakstad, Camilla; Herfindal, Lars; Gjertsen, Bjørn Tore; Bøe, Roald; Vintermyr, O K; Fladmark, Kari E.; Døskeland, Stein Ove

doi:10.1038/sj.cdd.4401798

Cited by 48 publications

(45 citation statements)

References 40 publications

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“…Reports of liver cancer due to consumption of microcystins containing drinking water have increased substantially recently (Ouellette and Wilhelm 2003;Codd et al 2005). Krakstad et al (2006) reported that the PPinhibiting toxins induce morphological alteration compatible with apoptosis in different cell types. Ding et al (1999) found that MC-LR has strong mutagenicity and induced DNA damage in rat hepatocytes.…”

Section: Cyclic Peptides (Microcystins and Nodularins)mentioning

confidence: 99%

Sustainability and cyanobacteria (blue-green algae): facts and challenges

Sharma¹,

et al. 2010

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Cyanobacteria (blue-green algae) are widely distributed Gram-negative oxygenic photosynthetic prokaryotes with a long evolutionary history. They have potential applications such as nutrition (food supplements and fine chemicals), in agriculture (as biofertilizer and in reclamation of saline USAR soils) and in wastewater treatment (production of exopolysaccharides and flocculants). In addition, they also produce wide variety of chemicals not needed for their normal growth (secondary metabolites) which show powerful biological activities such as strong antiviral, antibacterial, antifungal, antimalarial, antitumoral and anti-inflammatory activities useful for therapeutic purposes. In recent years, cyanobacteria have gained interest for producing biofuels (both biomass and H 2 production). Because of their simple growth needs, it is potentially cost-effective to exploit cyanobacteria for the production of recombinant compounds of medicinal and commercial value. Recent advances in culture, screening and genetic engineering techniques have opened new ways to exploit the potential of cyanobacteria. This review analyses the sustainability of cyanobacteria to solve global problems such as food, energy and environmental degradation. It emphasizes the need to adopt multidisciplinary approaches and a multi-product production (biorefinery) strategy to harness the maximum benefit of cyanobacteria.

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Section: Cyclic Peptides (Microcystins and Nodularins)mentioning

confidence: 99%

Sustainability and cyanobacteria (blue-green algae): facts and challenges

Sharma¹,

et al. 2010

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“…However, in this study, BAPTA-AM inhibited the decrease of p-CaMKII induced by AlCl 3 , which proves that AlCl 3 increased the phosphorylated CaMKII by increasing [Ca 2+ ]i. In addition, overexpression of p-CaMKII is involved in apoptosis [43,44] and causes oxidative stress response [45]. Odagiri et al [46] found that the activated Ca 2+ / CaMKII signal pathway induce oxidative stress, which leads to myocyte apoptosis in rats.…”

Section: Fig 5 Amentioning

confidence: 47%

Aluminum Chloride Induces Osteoblasts Apoptosis via Disrupting Calcium Homeostasis and Activating Ca2+/CaMKII Signal Pathway

Cao

Liu

Zhang

et al. 2015

Biol Trace Elem Res

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Aluminum promotes osteoblast (OB) apoptosis. Apoptosis is induced by the disordered calcium homeostasis. Therefore, to investigate the relationship between Al-induced OB apoptosis and calcium homeostasis, calvarium OBs from neonatal rats (3-4 days) were cultured and exposed to 0.048-mg/mL Al(3+) or 0.048-mg/mL Al(3+) combined with 5 μM BAPTA-AM (OBs were pretreated with 5 μM BAPTA-AM for 1 h, then added 0.048 mg/mL Al(3+)), respectively. Then OB apoptosis rate, intracellular calcium ions concentration ([Ca(2+)]i), mRNA expression level of calmodulin (CaM), and protein expression levels of CaM and p-CaMKII in OBs were examined. The result showed that AlCl3 increased OB apoptosis rate, and [Ca(2+)]i and p-CaMKII expression levels and decreased CaM expression levels, whereas BAPTA-AM relieved the effects. These results proved that AlCl3 induced OB apoptosis by disrupting the intracellular Ca(2+) homeostasis and activating the Ca(2+)/CaMKII signal pathway. Our findings can provide new insights for revealing the apoptosis mechanism of OBs exposed to AlCl3.

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“…For examination of ultrastructure, HL60 cells were fixed and further processed as described previously. 22 …”

Section: Assessment Of Apoptosismentioning

confidence: 99%

“…The pellets were washed in 5% TCA, and then with water-saturated ether before being dissolved in 5 mmol/L Tris buffer, pH 8, containing 8.4 M urea, 2% 3-[(3-cholamidopropyl)dimethylammonio]propanesulfonate (CHAPS), and 100 mmol/L dithioerythritol. Aliquots were diluted in sodium dodecyl sulfate (SDS) loading buffer for SDS-polyacrylamide gel electrophoresis (PAGE) analysis, 22 or the incorporated radioactivity determined by liquid scintillation counting. 24 Isolation of RNA and its use as template for in vitro protein synthesis HL60 cells (10 7 cells) were pelleted, the pellet was lysed in 1 mL of TRIzol (Invitrogen), and RNA was isolated.…”

Section: Metabolic Labeling Of Cellsmentioning

confidence: 99%

Abolition of stress-induced protein synthesis sensitizes leukemia cells to anthracycline-induced death

Gausdal

Gjertsen

McCormack

et al. 2008

Blood

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Anthracycline action has been thought to involve the neosynthesis of proapoptotic gene products and to therefore depend on protein synthesis for optimal effect. We found that inhibition of general, but not rapamycin-sensitive (cap-dependent), protein synthesis in the preapoptotic period enhanced anthracycline-induced acute myelogenous leukemia (AML) cell death, both in vitro and in several animal AML models. Pre-apoptotic anthracyclineexposed AML cells had altered translational specificity, with enhanced synthesis of a subset of proteins, including endoplasmatic reticulum chaperones. The altered translational specificity could be explained by perturbation (protein degradation, truncation, or dephosphorylation) of the cap-dependent translation initiation machinery and of proteins controling translation of specific mRNAs. We propose that judiciously timed inhibition of cap-independent translation is considered for combination therapy with anthracyclines in AML. IntroductionDespite recent achievements, 1,2 progress in therapy is slow for most malignancies, including acute myelogenous leukemia (AML). 3 A more thorough understanding of how the most successful current drugs, such as the anthracyclines, induce cancer cell death can reveal novel therapeutically valuable death mechanisms, which can be targeted more efficiently by specifically tailored compounds than by current drugs. It can also reveal that present drugs activate cancer cell survival pathways in ways that can be overcome by, for example, coadministering complementary agents.The aim of the present study was to undertake a proteomicsbased survey 4 of protein expression and modification in anthracycline-treated AML cells to explain in molecular terms previous observations that inhibitors of translation could protect completely 5 or partially 6-9 against anthracycline-induced cell death. Anthracycline treatment up-regulates the activity of signaling pathways stimulating the transcription factor nuclear factor-B, 10 and we have found that drug-resistant AML cells have up-regulated signal transducers and activators of transcriptions 3 and 5. 11 Because these factors induce genes coding mainly, although not exclusively, for presumed survival promoting proteins, 12-15 the reported dependence on protein synthesis for death implies either that the proapoptotic genes are induced in excess, that anthracycline treatment tips the balance between translation of mRNA coding for proapoptotic and prosurvival proteins in favor of the former, or can convert short-lived prosurvival proteins to prodeath proteins by, for example, dephosphorylation 16 or cleavage. [17][18][19] We found that the first-line AML anthracycline drugs, such as daunorubicin (DNR), modified or altered the expression of several proteins known to alter the translation of specific mRNAs or direct translation from cap dependence to internal ribosome entry site dependence. This might explain that the DNR-treated AML cells in the late preapoptotic phase had enhanced synthesis of a subset of proteins, includ...

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CaM-kinaseII-dependent commitment to microcystin-induced apoptosis is coupled to cell budding, but not to shrinkage or chromatin hypercondensation

Cited by 48 publications

References 40 publications

Sustainability and cyanobacteria (blue-green algae): facts and challenges

Sustainability and cyanobacteria (blue-green algae): facts and challenges

Aluminum Chloride Induces Osteoblasts Apoptosis via Disrupting Calcium Homeostasis and Activating Ca2+/CaMKII Signal Pathway

Abolition of stress-induced protein synthesis sensitizes leukemia cells to anthracycline-induced death

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