Relevant bibliographies by topics / Calcium channel sensitizers

Academic literature on the topic 'Calcium channel sensitizers'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Calcium channel sensitizers"

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Lai, Tsung-Hsuan, Yuan-Feng Lin, Feng-Chang Wu, and Yu-Hui Tsai. "Follicle-Stimulating Hormone-Induced Gαh/Phospholipase C-δ1 Signaling Mediating a Noncapacitative Ca2+ Influx through T-Type Ca2+ Channels in Rat Sertoli Cells." Endocrinology 149, no. 3 (December 6, 2007): 1031–37. http://dx.doi.org/10.1210/en.2007-1244.

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Our previous study demonstrated that FSH-induced immediate Ca2+ influx in rat Sertoli cells (SCs) is mediated by the Gαh/phospholipase C-δ1 (PLC-δ1) signaling pathway. As to which Ca2+ channel is responsible for such Ca2+ influx was not understood. In this study, thapsigargin triggered an in-store calcium release and evoked a 1.5-fold elevation of intracellular Ca2+ in Ca2+-free media, whereas FSH exhibited no effect. The readdition of CaCl2 (2.5 mm) to FSH-pretreated or thapsigargin-sensitized SCs in Ca2+-free media immediately elicited a rapid Ca2+ influx or a 2-fold increase of second intracellular Ca2+ elevation, respectively. The addition of Ca2+ chelator EGTA (0.2 mm) reduced the FSH-induced elevation of intracellular Ca2+ in SCs incubated with CaCl2. However, pretreatment with dantrolene (25 μM), which inhibits in-store calcium release, did not affect the FSH-induced elevation of intracellular Ca2+. NiCl2 (10 μM), a T-type calcium channel blocker, abolished the FSH-induced SC Ca2+ influx. Furthermore, mibefradil (10 and 100 μm), another specific blocker for T-type Ca2+ channels, dose-dependently suppressed the FSH-induced Ca2+ influx. In contrast, nifedipine (10 and 50 μm) or ω-conotoxin GVIA (100 and 500 nm), blocker of L- or N-type Ca2+ channels, respectively, did not affect the FSH-induced SC Ca2+ influx. On the other hand, FSH-induced Ca2+ influx was significantly reduced by pretreatment of SCs with myristoylated synthetic peptide (0.1 and 1 μm) of PLC-δ1 fragment TIPWNSLKQGYRHVHLL but not affected by 2′,5′-dideoxyadenosine (3 and 15 μm), a selective inhibitor of adenylate cyclase. In conclusion, the FSH-induced Gαh/PLC-δ1 pathway-dependent Ca2+ influx of rat SCs is mediated by T-type Ca2+ channels and independent of in-store calcium release.
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Varpula, Tero, Janne Rapola, Marko Sallisalmi, and Jouni Kurola. "Treatment of Serious Calcium Channel Blocker Overdose With Levosimendan, a Calcium Sensitizer." Anesthesia & Analgesia 108, no. 3 (March 2009): 790–92. http://dx.doi.org/10.1213/ane.0b013e3181931737.

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Ham, Seok Won, Hee-Young Jeon, and Hyunggee Kim. "Verapamil augments carmustine- and irradiation-induced senescence in glioma cells by reducing intracellular reactive oxygen species and calcium ion levels." Tumor Biology 39, no. 5 (May 2017): 101042831769224. http://dx.doi.org/10.1177/1010428317692244.

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Resistance to conventional therapies and frequent recurrence are the major obstacles to the treatment of high-grade gliomas, including glioblastoma. Thus, the development of new therapeutic strategies to overcome these obstacles is necessary to improve the treatment outcomes. In this study, we found that verapamil, a pan–adenosine triphosphate–binding cassette transporter and L-type voltage-dependent calcium channel inhibitor, sensitized U87MG glioma cells to carmustine- and irradiation-induced senescence. Furthermore, our results indicated that verapamil treatment, in combination with carmustine and irradiation, rendered U87MG glioma cells and several patient-derived glioma stem cells more sensitive to therapy-induced senescence than individual or dual-combination treatments. When investigating the underlying mechanism, we found that verapamil treatment markedly decreased intracellular reactive oxygen species and calcium ion levels. Reactive oxygen species reduction with N-acetylcysteine, a reactive oxygen species scavenger, rendered U87MG glioma cells more sensitive to carmustine and irradiation whereas the protein kinase C agonist, phorbol 12-myristate 13-acetate, mitigated the effects of carmustine and irradiation. Taken together, our results indicate that verapamil may be a potent therapeutic sensitizer for increasing the effectiveness of glioblastoma treatment.
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Zaloga, G. P., P. R. Roberts, K. W. Black, M. Lin, G. Zapata-Sudo, R. T. Sudo, and T. E. Nelson. "Carnosine is a novel peptide modulator of intracellular calcium and contractility in cardiac cells." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 1 (January 1, 1997): H462—H468. http://dx.doi.org/10.1152/ajpheart.1997.272.1.h462.

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Myocardial contractile failure is a common cause of morbidity and mortality in patients with ischemic heart disease and systemic inflammatory states such as sepsis. Accumulating evidence indicates that contractile failure is associated with dysregulation of myoplasmic calcium levels. In a search for biochemical causes for contractile dysfunction, we found that the dipeptide carnosine improves cardiac contractility and tested the possibility that carnosine plays a role in the regulation of intracellular calcium. Carnosine increased contractility in a dose-dependent manner (1-10 mM) in isolated perfused rat hearts. and it also increased free intracellular calcium levels in isolated myocytes. Carnosine increased myocyte tension via calcium release from the ryanodine receptor calcium release channel in skinned myocardial fibers and increased open-state probability and dwell time of the isolated ryanodine receptor calcium release channel in lipid bilayers. In addition. we report that carnosine sensitizes the contractile proteins so calcium. These results suggest a novel role for carnosine as a modulator of intracellular calcium and contractility in cardiac tissue.
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Babes, Alexandru, Cristian Neacsu, Michael JM Fischer, and Karl Messlinger. "Sumatriptan activates TRPA1." Cephalalgia Reports 2 (January 1, 2019): 251581631984715. http://dx.doi.org/10.1177/2515816319847155.

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Background: Migraine therapy with sumatriptan may cause adverse side effects like pain at the injection site, muscle pain, and transient aggravation of headaches. In animal experiments, sumatriptan excited or sensitized slowly conducting meningeal afferents. We hypothesized that sumatriptan may activate transduction channels of the “irritant receptor,” the transient receptor potential ankyrin type (TRPA1) expressed in nociceptive neurons. Methods: Calcium microfluorometry was performed in HEK293t cells transfected with human TRPA1 (hTRPA1) or a mutated channel (TRPA1-3C) and in dissociated trigeminal ganglion neurons. Membrane currents were recorded in the whole-cell patch clamp configuration. Results: Sumatriptan (10 and 400 µM) evoked calcium transients in hTRPA1-expressing HEK293t cells also activated by the TRPA1 agonist carvacrol (100 µM). In TRPA1-3C-expressing HEK293t cells, sumatriptan had hardly any effect. In rat trigeminal ganglion neurons, sumatriptan, carvacrol, and the transient receptor potential vanillod type 1 agonist capsaicin (1 µM) generated robust calcium signals. All sumatriptan-sensitive neurons (8% of the sample) were also activated by carvacrol (14%) and capsaicin (48%). In HEK293-hTRPA1 cells, sumatriptan (100 µM) evoked outwardly rectifying currents, which were almost completely inhibited by the TRPA1 antagonist HC-030031 (10 µM). Conclusion: Sumatriptan activates TRPA1 channels inducing calcium inflow and membrane currents. TRPA1-dependent activation of primary afferents may explain the painful side effects of sumatriptan.
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Daya, Hiba Abou, Sana Kouba, Hakim Ouled-Haddou, Nazim Benzerdjeb, Marie-Sophie Telliez, Charles Dayen, Henri Sevestre, Loïc Garçon, Frédéric Hague, and Halima Ouadid-Ahidouch. "Orai3-Mediates Cisplatin-Resistance in Non-Small Cell Lung Cancer Cells by Enriching Cancer Stem Cell Population through PI3K/AKT Pathway." Cancers 13, no. 10 (May 12, 2021): 2314. http://dx.doi.org/10.3390/cancers13102314.

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The development of the resistance to platinum salts is a major obstacle in the treatment of non-small cell lung cancer (NSCLC). Among the reasons underlying this resistance is the enrichment of cancer stem cells (CSCs) populations. Several studies have reported the involvement of calcium channels in chemoresistance. The Orai3 channel is overexpressed and constitutes a predictive marker of metastasis in NSCLC tumors. Here, we investigated its role in CSCs populations induced by Cisplatin (CDDP) in two NSCLC cell lines. We found that CDDP treatment increased Orai3 expression, but not Orai1 or STIM1 expression, as well as an enhancement of CSCs markers. Moreover, Orai3 silencing or the reduction of extracellular calcium concentration sensitized the cells to CDDP and led to a reduction in the expression of Nanog and SOX-2. Orai3 contributed to SOCE (Store-operated Calcium entry) in both CDDP-treated and CD133+ subpopulation cells that overexpress Nanog and SOX-2. Interestingly, the ectopic overexpression of Orai3, in the two NSCLC cell lines, lead to an increase of SOCE and expression of CSCs markers. Furthermore, CD133+ cells were unable to overexpress neither Nanog nor SOX-2 when incubated with PI3K inhibitor. Finally, Orai3 silencing reduced Akt phosphorylation. Our work reveals a link between Orai3, CSCs and resistance to CDDP in NSCLC cells.
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Sweet, Wendy E., and Christine S. Moravec. "Direct Measurement of Sarcoplasmic Reticulum Calcium Content Following Isoproterenol or Caffeine Treatment." Microscopy and Microanalysis 3, S2 (August 1997): 919–20. http://dx.doi.org/10.1017/s143192760001148x.

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The major storage site for calcium in cardiac muscle is the sarcoplasmic reticulum (SR). It has been shown using indirect methods that the amount of calcium stored in the SR can be altered by various agonists and anesthetics. The only technique to date which directly quantifies the amount of calcium in the SR is Electron Probe Microanalysis (EPMA). Using EPMA, an accurate measurement of the size of the SR calcium store can be made following treatments with known agonists.Isoproterenol (ISO) causes an increased inotropic response in cardiac muscle via the (3-adrenergic pathway. When ISO binds to the (β-receptor on the plasma membrane, it causes the activation of Protein Kinase A (PKA) through a cascade of events. PKA phosphorylates the sarcolemmal calcium channels causing an increase in the rate of calcium influx. PKA also phosphorylates Tnl, which sensitizes the myofilaments to calcium, thereby increasing the rate of calcium release from the myofilaments.
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FULCERI, Rosella, Jens KNUDSEN, Roberta GIUNTI, Pompeo VOLPE, Alessandra NORI, and Angelo BENEDETTI. "Fatty acyl-CoA–acyl-CoA-binding protein complexes activate the Ca2+ release channel of skeletal muscle sarcoplasmic reticulum." Biochemical Journal 325, no. 2 (July 15, 1997): 423–28. http://dx.doi.org/10.1042/bj3250423.

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We previously reported that fatty acyl-CoA esters activate ryanodine receptor/Ca2+ release channels in a terminal cisternae fraction from rabbit skeletal muscle [Fulceri, Nori, Gamberucci, Volpe, Giunti and Benedetti (1994) Cell Calcium 15, 109–116]. Skeletal muscle cytosol contains a high-affinity fatty acyl-CoA-binding protein (ACBP) [Knudsen, Hojrup, Hansen, H. O., Hansen, H. F. and Roepstorff (1989) Biochem. J. 262, 513–519]. We show here that palmitoyl-CoA (PCoA) in a complex with a molar excess of bovine ACBP causes a discrete Ca2+ efflux or allows Ca2+ release from the Ca2+-preloaded terminal cisternae fraction by sub-optimal caffeine concentrations. Both effects were abolished by elevating the free [Mg2+] in the system, which inhibits the Ca2+ release channel activity. Sensitization towards caffeine was a function of both the concentration of the complex and the [PCoA]-to-[ACBP] ratio. In all experimental conditions the calculated free [PCoA] was no more than 50 nM, and such concentrations by themselves were inactive on Ca2+ release channels. The KD for PCoA binding was approx. 2 nM for bovine and yeast ACBP, and slightly higher (8 nM) for rat ACBP. The PCoA–rat ACBP complex behaved in the same manner as the PCoA–bovine ACBP complex, whereas the ester complexed with yeast ACBP was more active in activating/sensitizing Ca2+ efflux. A non-hydrolysable analogue of PCoA bound to (bovine) ACBP also sensitized the Ca2+ release channel towards caffeine. These findings indicate that fatty acyl-CoA–ACBP complexes either interact directly with one or more components in the terminal cisternae membranes or, through interaction with the component(s), donate the fatty acyl-CoA esters to high-affinity binding sites of the membrane, thus affecting (and possibly regulating) Ca2+ release channel activity.
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Liu, Zhenyu, Youtian Hu, Xiaoyun Yu, Jiefeng Xi, Xiaoming Fan, Chung-Ming Tse, Allen C. Myers, Pankaj J. Pasricha, Xingde Li, and Shaoyong Yu. "Allergen challenge sensitizes TRPA1 in vagal sensory neurons and afferent C-fiber subtypes in guinea pig esophagus." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 6 (March 15, 2015): G482—G488. http://dx.doi.org/10.1152/ajpgi.00374.2014.

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Transient receptor potential A1 (TRPA1) is a newly defined cationic ion channel, which selectively expresses in primary sensory afferent nerve, and is essential in mediating inflammatory nociception. Our previous study demonstrated that TRPA1 plays an important role in tissue mast cell activation-induced increase in the excitability of esophageal vagal nodose C fibers. The present study aims to determine whether prolonged antigen exposure in vivo sensitizes TRPA1 in a guinea pig model of eosinophilic esophagitis (EoE). Antigen challenge-induced responses in esophageal mucosa were first assessed by histological stains and Ussing chamber studies. TRPA1 function in vagal sensory neurons was then studied by calcium imaging and by whole cell patch-clamp recordings in 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate (DiI)-labeled esophageal vagal nodose and jugular neurons. Extracellular single-unit recordings were performed in vagal nodose and jugular C-fiber neuron subtypes using ex vivo esophageal-vagal preparations with intact nerve endings in the esophagus. Antigen challenge significantly increased infiltrations of eosinophils and mast cells in the esophagus. TRPA1 agonist allyl isothiocyanate (AITC)-induced calcium influx in nodose and jugular neurons was significantly increased, and current densities in esophageal DiI-labeled nodose and jugular neurons were also significantly increased in antigen-challenged animals. Prolonged antigen challenge decreased esophageal epithelial barrier resistance, which allowed intraesophageal-infused AITC-activating nodose and jugular C fibers at their nerve endings. Collectively, these results demonstrated that prolonged antigen challenge sensitized TRPA1 in esophageal sensory neurons and afferent C fibers. This novel finding will help us to better understand the molecular mechanism underlying esophageal sensory and motor dysfunctions in EoE.
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Takenaka, Tsuneo, Yoichi Ohno, Koichi Hayashi, Takao Saruta, and Hiromichi Suzuki. "Governance of arteriolar oscillation by ryanodine receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 1 (July 2003): R125—R131. http://dx.doi.org/10.1152/ajpregu.00711.2002.

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To investigate the role of ryanodine receptors in glomerular arterioles, experiments were performed using an isolated perfused hydronephrotic kidney model. In the first series of studies, BAYK-8644 (300 nM), a calcium agonist, constricted afferent (19.6 ± 0.6 to 17.6 ± 0.5 μm, n = 6, P < 0.01) but not efferent arterioles. Furthermore, BAYK-8644 elicited afferent arteriolar oscillatory movements. Subsequent administration of nifedipine (1 μM) inhibited both afferent arteriolar oscillation and constriction by BAYK-8644 (to 19.4 ± 0.5 μm). In the second group, although BAYK-8644 constricted afferent arterioles treated with 1 μM of thapsigargin (19.7 ± 0.6 to 16.8 ± 0.6 μm, n = 5, P < 0.05), it failed to induce rhythmic contraction. Removal of extracellular calcium with EGTA (2 mM) reversed BAYK-8644-induced afferent arteriolar constriction (to 20.0 ± 0.5 μm). In the third series of investigations, ryanodine (10 μM) but not 2-aminoethoxyphenyl borate (100 μM) abolished afferent arteriolar vasomotion by BAYK-8644. In the fourth series of experiments, in the presence of caffeine (1 mM), the stronger activation of voltage-dependent calcium channels by higher potassium media resulted in greater afferent arteriolar constriction and faster oscillation. Our results indicate that L-type calcium channels are rich in preglomerular but not postglomerular microvessels. Furthermore, the present findings suggest that either prolonged calcium influx through voltage-dependent calcium channels (BAYK-8644) or sensitized ryanodine receptors (caffeine) is required to trigger periodic calcium release through ryanodine receptors in afferent arterioles.
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Dissertations / Theses on the topic "Calcium channel sensitizers"

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Alomari, Abdul-Hakeem Hussein Electrical Engineering &amp Telecommunications Faculty of Engineering UNSW. "Spectral analysis of arterial blood prssure and stroke volume variability: the role of Calcium channel blockers and sensitizers." Publisher:University of New South Wales. Electrical Engineering & Telecommunications, 2008. http://handle.unsw.edu.au/1959.4/43923.

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In this thesis, we included results from two studies. The first one considered the effects of the blood volume changes, during blood donation, on the heart rate variability (HRV) measured, non-invasively, form electrocardiographic (ECG) and photoplethysmographic (PPG) signals. Our results showed that, during blood donation, there were no significant changes in the pulsatile area of PPG signal, while heart rate increased. No significant changes were noticed in HRV extracted from both signals. Error analysis between the HRV extracted from ECG and peak interval variability (PIV) suggested that the error during blood donation was increased which means that the use of PIV extracted from PPG signal, used as a replacement diagnostic tool in clinical applications, needs further investigations and should be carefully studied in non-stationary cardiovascular situations such as blood donation. The imbalance between the two branches of the autonomic nervous system, sympathetic and parasympathetic, vagal, may result in a harmful activation of myocardial tissues which cause arrhythmias and sudden cardiac death. Although the study of the sympathovagal balance have been attracting many researchers, further studies are needed to elucidate the effects of many kinds of drugs on the autonomic modulation of the cardiac muscle, specifically, the cells of sinoatrial (SA) node. The aim of the second part of this thesis was to assess the effects of calcium channel blocker (Verapamil), calcium channel sensitizer (Levosimendan), calcium chloride (CaCl2), the combinations of verapamil/ CaCl2, levosimendan/ CaCl2, and noradrenaline infusion on beat-to-beat cardiovascular variability represented, in this research, by systolic blood pressure variability (SBPV), and stroke volume variability (SVV) signals. We used Fat Fourier Transform (FFT) to evaluate the power spectral density of the fluctuations in both signals to evaluate the effects of short-term treatments with those drugs on the sympathovagal balance in normal rats. Then, we compared the spectra obtained from SBPV and SVV to decide which of these fluctuations along with corresponding spectrum was more able to provide a clear feedback about the autonomic nervous system. Our data suggests that there were a significant correlations between low- (LF), mid- (MF), and high-frequency (HF) spectra obtained from SBPV and SVV except between the HF spectra estimated from after the infusion of levosimendan where a poor correlation (r = 0.530, p = 0.281) was noticed. This that both HF components obtained provide different information regarding the autonomic nervous system modulation of the SA node cells, while the results obtained from the rest of experiments showed that both signals provide same information about the modulation of sympathetic and parasympathetic tone due to all stages of different drugs infusion studied in this thesis. Besides that, we found that both spectra may be used to track the fluctuations in the cardiac output as a result of the drugs infusion.
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Florent, Romane. "Intérêt de la modulation pharmacologique des voies de signalisation calcique pour restaurer le contrôle de l'apoptose dans les cancers ovariens chimiorésistants Inhibition of store-operated channels by carboxyamidotriazole sensitizes ovarian carcinoma cells to anti-BclxL strategies through Mcl-1 down-regulation Drug Repositioning of the α1-Adrenergic Receptor Antagonist Naftopidil: A Potential New Anti-Cancer Drug? Bim, Puma and Noxa upregulation by Naftopidil sensitizes ovarian cancer to the BH3-mimetic ABT-737 and the MEK inhibitor Trametinib." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC413.

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Le sombre pronostic du cancer de l’ovaire s’explique notamment par une fréquence importante de résistance à la chimiothérapie conventionnelle présentée par les patientes. La mise en place de stratégies thérapeutiques alternatives à la chimiothérapie, mais aussi la découverte de biomarqueurs prédictifs de la réponse à ce traitement, représentent donc un enjeu majeur pour améliorer la prise en charge de cette pathologie. La chimiorésistance des cellules cancéreuses ovariennes s’explique principalement par leur résistance à l’apoptose, résultant d’un déséquilibre entre les membres pro- et anti-apoptotiques de la famille Bcl-2 qui contrôlent cette mort cellulaire. De ce fait, toutes stratégies capables de moduler le ratio [pro ]/[anti apoptotiques] en faveur des [pro-] restaure efficacement l’apoptose de ces cellules. Or, la signalisation calcique est connue pour réguler l’expression de ces protéines et apparait ainsi comme une cible pertinente pour restaurer l’apoptose des cellules cancéreuses ovariennes chimiorésistantes. Dans ce contexte, nous avons mis en évidence que trois modulateurs du signal calcique sont capables d’induire la mort de ces dernières en association à l’ABT-737, un BH3-mimétique ciblant l’activité de l’anti apoptotique Bcl-xL. Cette sensibilisation à l’ABT-737 est permise par le fait que le carboxyamidotriazole réprime l’expression de l’anti apoptotique Mcl-1 via l’inhibition des courants SOCE, le naftopidil augmente l’expression des protéines pro apoptotiques via l’induction d’un stress du RE ou l’activation de JNK et que la thapsigargine semble préparer à la mort cellulaire grâce à une augmentation de la concentration calcique intracellulaire via STIM1 et, peut-être, via l’induction de l’expression de Noxa. En outre, les acteurs de la signalisation calcique, connus pour subir un remodelage au cours des processus de cancérogenèse pourraient se révéler comme des outils de prédiction de réponse à la chimiothérapie. Dans ce contexte, nous avons mis en évidence que l’expression de la pompe calcique SERCA2 semble jouer le rôle de biomarqueur prédictif de la réponse à la chimiothérapie des patientes atteintes d’un cancer de l’ovaire
The poor prognosis of ovarian cancer is mainly explained by a high rate of resistance to conventional chemotherapy presented by patients. Therefore, discovery of both alternative therapeutic strategies to chemotherapy and predictive biomarkers for response to this treatment represent a major challenge for improving the management of this pathology. Chemoresistance of ovarian cancer cells is mainly due to their resistance to apoptosis, resulting from an imbalance between the pro- and anti-apoptotic members of the Bcl-2 family that control this type of cell death. Thus, all strategies able to modulate the [pro]/[anti-apoptotic] protein ratio in favor of [pro-] effectively restore apoptosis in these cells. However, calcium signaling is known to regulate the expression of these proteins and thus appears to be a relevant target for restoring apoptosis in chemoresistant ovarian cancer cells. In this context, we have shown that three calcium signal modulators are able to induce the death of these cells in association with ABT-737, a BH3-mimetic targeting the activity of the anti-apoptotic Bcl-xL. This sensitization to ABT-737 is enabled by the fact that carboxyamidotriazole represses the expression of the anti apoptotic Mcl-1 via the inhibition of SOCE currents, naftopidil increases pro-apoptotic protein expression via ER stress induction or JNK activation and thapsigargin seems to prepare cell death through increasing intracellular calcium concentration via STIM1 and, maybe, through Noxa expression induction. In addition, players of the calcium signaling toolkit, known to undergo remodeling during carcinogenesis could be proven as tools for predicting response to chemotherapy. In this context, we have shown that the expression of the calcium pump SERCA2 seems to play a role as a predictive biomarker for response to chemotherapy of patients with ovarian cancer
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Conference papers on the topic "Calcium channel sensitizers"

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Oraevsky, Alexander A., Olga A. Cabello, Qin Shan, Frank K. Tittel, and Philip D. Henry. "Detection of calcium activity in human monocytes by the fura-2 fluorescence method: in vitro differentiation sensitizes cells to dihydropyridine calcium channel modulators." In OE/LASE '94, edited by George S. Abela. SPIE, 1994. http://dx.doi.org/10.1117/12.179909.

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Casarez, Eli V., Lloyd Gray, Amir A. Jazaeri, and Jill K. Slack-Davis. "Abstract 945: Inhibition of T-type calcium channels sensitizes ovarian cancer cell growth and metastasis to platinum-based chemotherapy." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-945.

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Dziegielewski, Jaroslaw, Nicholas C. K. Valerie, Barbara Dziegielewska, Amol S. Hosing, Lloyd S. Gray, and James M. Larner. "Abstract LB-262: Targeting T-type calcium channels induces the extrinsic apoptotic pathway and sensitizes glioblastoma cancer cells to radio- and chemotherapy." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-262.

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