15 results on '"Patoli D"'
Search Results
2. Human Apolipoprotein C1 Transgenesis To Inhibit Cetp And To Attenuate Atherosclerosis In Hypercholesterolemic Rabbits
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Gautier, T., primary, Deckert, V., additional, Aires, V., additional, Le Guern, N., additional, Patoli, D., additional, Lemaire, S., additional, Maquart, G., additional, Bataille, A., additional, Xolin, M., additional, Magnani, C., additional, Masson, D., additional, Harscoët, E., additional, Da Silva, B., additional, Houdebine, L.M., additional, Jolivet, G., additional, and Lagrost, L., additional
- Published
- 2019
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3. Perioperative Albumin Among Adults Undergoing Thoracic Surgery in the United States: Utilization, Associations With Clinical Outcomes, and Contribution to Hospital Costs.
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Al-Qudsi O, Ellis AR, Krishnamoorthy V, Ohnuma T, Patoli D, Taicher B, Mamoun N, Pant P, Wongsripuemtet P, Cobert J, and Raghunathan K
- Abstract
Objectives: To estimate the use of albumin among adults undergoing thoracic surgery in the United States, compare baseline characteristics, clinical and cost outcomes of recipients versus nonrecipients, and determine albumin's contribution to total hospital costs., Design: Retrospective cohort study., Setting: Nationwide sample of US hospitals., Participants: Adults undergoing open and minimally invasive thoracic surgery between 2011 and 2017., Interventions: Albumin on the day of surgery (identified using itemized hospital billing logs)., Measurements and Main Results: Albumin was used in 170 of 342 US hospitals, among 13% and 7% of 14,672 and 22,532 patients who, respectively, underwent open and minimally invasive thoracic surgery (median volume 500 mL). Baseline comorbidities and organ-supportive treatments were several-fold more prevalent among recipients (particularly vasopressors, mechanical ventilation, and red cell transfusions). In standardized mortality ratio propensity score weighted analysis, albumin use was not associated with in-hospital mortality (adjusted relative risk 1.17 [0.72, 1.92] and 1.51 [0.97, 2.34], with open and minimally invasive procedures), but was associated with morbidity and higher costs, more so with minimally invasive procedures than with open surgery. Total costs among recipients were higher by $4,744 ($3,591, $5,897) and $5,088 ($4,075, $6,100) for open and minimally invasive procedures, respectively. Albumin accounted for 2.6% of this difference (median $124 [$83-$189] per patient)., Conclusions: Albumin use varies widely across hospitals, and 9% of patients receive it (median 500 mL). Use was not associated with in-hospital mortality and was associated with more morbidity and cost. The cost of albumin accounted for a trivial portion of hospital costs. Clinical trials must examine the effects of albumin on complications and costs after thoracic surgery., Competing Interests: Declaration of competing interest K.R. is a consultant for Grifols North America, a major supplier of Human-Derived Albumin. This study was conducted via a Cooperative Research and Development Agreement between Grifols and the nonprofit corporation affiliated with the Durham VA Medical Center (the Institute for Medical Research, Durham, NC). All other authors have no relevant disclosures to report., (Copyright © 2024 Elsevier Inc. All rights reserved.)
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- 2024
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4. Functional diversity of NLRP3 gain-of-function mutants associated with CAPS autoinflammation.
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Cosson C, Riou R, Patoli D, Niu T, Rey A, Groslambert M, De Rosny C, Chatre E, Allatif O, Henry T, Venet F, Milhavet F, Boursier G, Belot A, Jamilloux Y, Merlin E, Duquesne A, Grateau G, Savey L, Jacques Maria AT, Pagnier A, Poutrel S, Lambotte O, Mallebranche C, Ardois S, Richer O, Lemelle I, Rieux-Laucat F, Bader-Meunier B, Amoura Z, Melki I, Cuisset L, Touitou I, Geyer M, Georgin-Lavialle S, and Py BF
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- Humans, Inflammasomes genetics, Drug Development, Syndrome, NLR Family, Pyrin Domain-Containing 3 Protein genetics, Gain of Function Mutation genetics
- Abstract
NLRP3-associated autoinflammatory disease is a heterogenous group of monogenic conditions caused by NLRP3 gain-of-function mutations. The poor functional characterization of most NLRP3 variants hinders diagnosis despite efficient anti-IL-1 treatments. Additionally, while NLRP3 is controlled by priming and activation signals, gain-of-functions have only been investigated in response to priming. Here, we characterize 34 NLRP3 variants in vitro, evaluating their activity upon induction, priming, and/or activation signals, and their sensitivity to four inhibitors. We highlight the functional diversity of the gain-of-function mutants and describe four groups based on the signals governing their activation, correlating partly with the symptom severity. We identify a new group of NLRP3 mutants responding to the activation signal without priming, associated with frequent misdiagnoses. Our results identify key NLRP3 residues controlling inflammasome activity and sensitivity to inhibitors, and antagonistic mechanisms with broader efficacy for therapeutic strategies. They provide new insights into NLRP3 activation, an explanatory mechanism for NLRP3-AID heterogeneity, and original tools for NLRP3-AID diagnosis and drug development., (© 2024 Cosson et al.)
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- 2024
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5. Successful Left Phrenic Nerve Block for Intractable Hiccups in a Patient With LVAD-Induced Diaphragmatic Irritation.
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Patoli D, Chan RC, Tung A, and Rana M
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- Diaphragm diagnostic imaging, Humans, Phrenic Nerve, Anesthesia, Conduction, Hiccup etiology, Hiccup therapy, Nerve Block adverse effects
- Abstract
Competing Interests: Conflict of Interest None.
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- 2022
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6. GPR75: An exciting new target in metabolic syndrome and related disorders.
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Murtaza B, Asghar F, and Patoli D
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- Humans, Obesity, Receptors, G-Protein-Coupled metabolism, Signal Transduction, Cardiovascular Diseases, Dyslipidemias, Metabolic Syndrome drug therapy
- Abstract
The metabolic syndrome is a plethora of related disorders that are frequently associated with morbidity and mortality in addition to economic burden. While various treatment options are available, the need to understand the pathology and find new targets still remains. Recent data have suggested GPR75 as one such exciting target that has shown to a highly druggable potential. In this review, we have discussed the recent findings on GPR75 in terms of its expression and signaling and the way it could be a novel target in diseases associated with metabolic syndrome including obesity, dyslipidemia, diabetes, cardiovascular disease, and cerebrovascular disease. In addition, the opportunities and challenges related with the druggable potential of GPR75 have also been highlighted in this review., Competing Interests: Declaration of competing interest The authors have declared no conflict of interest whatsoever. All authors have read and approved the final article., (Copyright © 2022 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.)
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- 2022
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7. NLRP3 phosphorylation in its LRR domain critically regulates inflammasome assembly.
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Niu T, De Rosny C, Chautard S, Rey A, Patoli D, Groslambert M, Cosson C, Lagrange B, Zhang Z, Visvikis O, Hacot S, Hologne M, Walker O, Wong J, Wang P, Ricci R, Henry T, Boyer L, Petrilli V, and Py BF
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- Animals, Casein Kinase II, Casein Kinase Ialpha, Caspase 1 metabolism, Cytokines metabolism, Deubiquitinating Enzymes, HEK293 Cells, Humans, Macrophages metabolism, Mice, Mice, Knockout, NIMA-Related Kinases metabolism, Phosphorylation, Pyroptosis, Ubiquitination, Inflammasomes metabolism, NLR Family, Pyrin Domain-Containing 3 Protein chemistry, NLR Family, Pyrin Domain-Containing 3 Protein genetics, NLR Family, Pyrin Domain-Containing 3 Protein metabolism
- Abstract
NLRP3 controls the secretion of inflammatory cytokines IL-1β/18 and pyroptosis by assembling the inflammasome. Upon coordinated priming and activation stimuli, NLRP3 recruits NEK7 within hetero-oligomers that nucleate ASC and caspase-1 filaments, but the apical molecular mechanisms underlying inflammasome assembly remain elusive. Here we show that NEK7 recruitment to NLRP3 is controlled by the phosphorylation status of NLRP3 S803 located within the interaction surface, in which NLRP3 S803 is phosphorylated upon priming and later dephosphorylated upon activation. Phosphomimetic substitutions of S803 abolish NEK7 recruitment and inflammasome activity in macrophages in vitro and in vivo. In addition, NLRP3-NEK7 binding is also essential for NLRP3 deubiquitination by BRCC3 and subsequently inflammasome assembly, with NLRP3 phosphomimetic mutants showing enhanced ubiquitination and degradation than wildtype NLRP3. Finally, we identify CSNK1A1 as the kinase targeting NLRP3 S803. Our findings thus reveal NLRP3 S803 phosphorylation status as a druggable apical molecular mechanism controlling inflammasome assembly., (© 2021. The Author(s).)
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- 2021
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8. Electrocautery-Induced Complete Heart Block.
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Alghanem H, Patoli D, Greenberg SB, Szokol JW, and Silk VL
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- Electrocardiography, Electrocoagulation adverse effects, Humans, Atrioventricular Block
- Published
- 2021
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9. Human apolipoprotein C1 transgenesis reduces atherogenesis in hypercholesterolemic rabbits.
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Gautier T, Deckert V, Aires V, Le Guern N, Proukhnitzky L, Patoli D, Lemaire S, Maquart G, Bataille A, Xolin M, Magnani C, Masson D, Harscoët E, Da Silva B, Houdebine LM, Jolivet G, and Lagrost L
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- Animals, Cholesterol Ester Transfer Proteins genetics, Cholesterol, HDL metabolism, Gene Transfer Techniques, Humans, Mice, Rabbits, Apolipoprotein C-I genetics, Atherosclerosis genetics, Atherosclerosis prevention & control
- Abstract
Background and Aims: Apolipoprotein (apo) C1 is a 6.6 kDa protein associated with HDL and VLDL. ApoC1 alters triglyceride clearance, and it also favors cholesterol accumulation in HDL, especially by inhibiting CETP in human plasma. Apart from studies in mice, which lack CETP, the impact of apoC1 on atherosclerosis in animal models expressing CETP, like in humans, is not known. This study aimed at determining the net effect of human apoC1 on atherosclerosis in rabbits, a species with naturally high CETP activity but with endogenous apoC1 without CETP inhibitory potential., Methods: Rabbits expressing a human apoC1 transgene (HuApoC1Tg) were generated and displayed significant amounts of human apoC1 in plasma., Results: After cholesterol feeding, atherosclerosis lesions were significantly less extensive (-22%, p < 0.05) and HDL displayed a reduced ability to serve as CETP substrates (-25%, p < 0.05) in HuApoC1Tg rabbits than in WT littermates. It was associated with rises in plasma HDL cholesterol level and PON-1 activity, and a decrease in the plasma level of the lipid oxidation markers 12(S)-HODE and 8(S)HETE. In chow-fed animals, the level of HDL-cholesterol was also significantly higher in HuApoC1Tg than in WT animals (0.83 ± 0.11 versus 0.73 ± 0.11 mmol/L, respectively, p < 0.05), and it was associated with significantly lower CETP activity (cholesteryl ester transfer rate, -10%, p < 0.05; specific CETP activity, -14%, p < 0.05)., Conclusions: Constitutive expression of fully functional human apoC1 in transgenic rabbit attenuates atherosclerosis. It was found to relate, at least in part, to the inhibition of plasma CETP activity and to alterations in plasma HDL., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)
- Published
- 2021
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10. Inhibition of mitophagy drives macrophage activation and antibacterial defense during sepsis.
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Patoli D, Mignotte F, Deckert V, Dusuel A, Dumont A, Rieu A, Jalil A, Van Dongen K, Bourgeois T, Gautier T, Magnani C, Le Guern N, Mandard S, Bastin J, Djouadi F, Schaeffer C, Guillaumot N, Narce M, Nguyen M, Guy J, Dargent A, Quenot JP, Rialland M, Masson D, Auwerx J, Lagrost L, and Thomas C
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- Animals, Female, Humans, Interferon-gamma immunology, Lipopolysaccharides immunology, Macrophages, Peritoneal microbiology, Macrophages, Peritoneal pathology, Male, Mice, Protein Kinases immunology, RAW 264.7 Cells, Sepsis microbiology, Sepsis pathology, Bacteria immunology, Macrophage Activation, Macrophages, Peritoneal immunology, Mitophagy immunology, Sepsis immunology
- Abstract
Mitochondria have emerged as key actors of innate and adaptive immunity. Mitophagy has a pivotal role in cell homeostasis, but its contribution to macrophage functions and host defense remains to be delineated. Here, we showed that lipopolysaccharide (LPS) in combination with IFN-γ inhibited PINK1-dependent mitophagy in macrophages through a STAT1-dependent activation of the inflammatory caspases 1 and 11. In addition, we demonstrated that the inhibition of mitophagy triggered classical macrophage activation in a mitochondrial ROS-dependent manner. In a murine model of polymicrobial infection (cecal ligature and puncture), adoptive transfer of Pink1-deficient bone marrow or pharmacological inhibition of mitophagy promoted macrophage activation, which favored bactericidal clearance and led to a better survival rate. Reciprocally, mitochondrial uncouplers that promote mitophagy reversed LPS/IFN-γ-mediated activation of macrophages and led to immunoparalysis with impaired bacterial clearance and lowered survival. In critically ill patients, we showed that mitophagy was inhibited in blood monocytes of patients with sepsis as compared with nonseptic patients. Overall, this work demonstrates that the inhibition of mitophagy is a physiological mechanism that contributes to the activation of myeloid cells and improves the outcome of sepsis.
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- 2020
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11. A Rare Cause of a Left Atrial Mass.
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Patoli D, Alghanem H, and Tung A
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- Aged, Echocardiography, Echocardiography, Transesophageal, Hematoma, Humans, Male, Myocardial Infarction, Percutaneous Coronary Intervention
- Abstract
Intramyocardial hematomas are a rare complication of myocardial infarctions. Normally restricted to the left ventricle, in certain scenarios, such as after a percutaneous coronary intervention, intramyocardial hematomas also can occur in the left atrium. Herein, the case of a 74-year-old man who presented to the authors' institution with a large inferior wall myocardial infarction refractory to multiple pressor therapy and thus necessitated venoarterial extracorporeal membrane oxygenation support is described. Through the course of his hospital stay, the patient developed a large left atrial intramyocardial hematoma obstructing mitral inflow as seen on intraoperative transesophageal echocardiography. Ultimately, because of the patient's complex comorbid status, his case was managed conservatively. In this E-challenge, the reason for the conservative approach and the alternative approach of surgically draining the intramyocardial hematoma are discussed., Competing Interests: Declaration of Competing Interest None., (Copyright © 2020 Elsevier Inc. All rights reserved.)
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- 2020
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12. Polysaccharide Chain Length of Lipopolysaccharides From Salmonella Minnesota Is a Determinant of Aggregate Stability, Plasma Residence Time and Proinflammatory Propensity in vivo .
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Sali W, Patoli D, Pais de Barros JP, Labbé J, Deckert V, Duhéron V, Le Guern N, Blache D, Chaumont D, Lesniewska E, Gasquet B, Paul C, Moreau M, Denat F, Masson D, Lagrost L, and Gautier T
- Abstract
Lipopolysaccharides (LPS) originate from the outer membrane of Gram-negative bacteria and trigger an inflammatory response via the innate immune system. LPS consist of a lipid A moiety directly responsible for the stimulation of the proinflammatory cascade and a polysaccharide chain of variable length. LPS form aggregates of variable size and structure in aqueous media, and the aggregation/disaggregation propensity of LPS is known as a key determinant of their biological activity. The aim of the present study was to determine to which extent the length of the polysaccharide chain can affect the nature of LPS structures, their pharmacokinetics, and eventually their proinflammatory properties in vivo . LPS variants of Salmonella Minnesota with identical lipid A but with different polysaccharide moieties were used. The physical properties of LPS aggregates were analyzed by zetametry, dynamic light scattering, and microscopy. The stability of LPS aggregates was tested in the presence of plasma, whole blood, and cultured cell lines. LPS pharmacokinetics was performed in wild-type mice. The accumulation in plasma of rough LPS (R-LPS) with a short polysaccharidic chain was lower, and its hepatic uptake was faster as compared to smooth LPS (S-LPS) with a long polysaccharidic chain. The inflammatory response was weaker with R-LPS than with S-LPS. As compared to S-LPS, R-LPS formed larger aggregates, with a higher hydrophobicity index, a more negative zeta potential, and a higher critical aggregation concentration. The lower stability of R-LPS aggregates could be illustrated in vitro by a higher extent of association of LPS to plasma lipoproteins, faster binding to blood cells, and increased uptake by macrophages and hepatocytes, compared to S-LPS. Our data indicate that a long polysaccharide chain is associated with the formation of more stable aggregates with extended residence time in plasma and higher inflammatory potential. These results show that polysaccharide chain length, and overall aggregability of LPS might be helpful to predict the proinflammatory effect that can be expected in experimental settings using LPS preparations. In addition, better knowledge and control of LPS aggregation and disaggregation might lead to new strategies to enhance LPS detoxification in septic patients.
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- 2019
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13. LPCAT3 deficiency in hematopoietic cells alters cholesterol and phospholipid homeostasis and promotes atherosclerosis.
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Thomas C, Jalil A, Magnani C, Ishibashi M, Queré R, Bourgeois T, Bergas V, Ménégaut L, Patoli D, Le Guern N, Labbé J, Gautier T, de Barros JPP, Lagrost L, and Masson D
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- 1-Acylglycerophosphocholine O-Acyltransferase genetics, ATP Binding Cassette Transporter 1 genetics, ATP Binding Cassette Transporter 1 metabolism, ATP Binding Cassette Transporter, Subfamily G, Member 1 genetics, ATP Binding Cassette Transporter, Subfamily G, Member 1 metabolism, Animals, Apolipoproteins E genetics, Apolipoproteins E metabolism, Arachidonic Acid metabolism, Atherosclerosis genetics, Atherosclerosis pathology, Cells, Cultured, Disease Models, Animal, Genetic Predisposition to Disease, Hematopoietic Stem Cell Transplantation, Liver X Receptors metabolism, Macrophages transplantation, Mice, Inbred C57BL, Mice, Knockout, Phenotype, Receptors, LDL deficiency, Receptors, LDL genetics, 1-Acylglycerophosphocholine O-Acyltransferase deficiency, Atherosclerosis enzymology, Cholesterol metabolism, Hematopoietic Stem Cells enzymology, Macrophages enzymology, Phospholipids metabolism, Plaque, Atherosclerotic
- Abstract
Background and Aims: LPCAT3 plays a major role in phospholipid metabolism in the liver and intestine. However, the impact of LPCAT3 on hematopoietic cell and macrophage functions has yet to be described. Our aim was to understand the functions of LPCAT3 in macrophages and to investigate whether LPCAT3 deficiency in hematopoietic cells may affect atherosclerosis development., Methods: Mice with constitutive Lpcat3 deficiency (Lpcat3
-/- ) were generated. We used fetal hematopoietic liver cells to generate WT and Lpcat3-/- macrophages in vitro and to perform hematopoietic cell transplantation in recipient Ldlr-/- mice., Results: Lpcat3-deficient macrophages displayed major reductions in the arachidonate content of phosphatidylcholines, phosphatidylethanolamines and, unexpectedly, plasmalogens. These changes were associated with altered cholesterol homeostasis, including an increase in the ratio of free to esterified cholesterol and a reduction in cholesterol efflux in Lpcat3-/- macrophages. This correlated with the inhibition of some LXR-regulated pathways, related to altered cellular availability of the arachidonic acid. Indeed, LPCAT3 deficiency was associated with decreased Abca1, Abcg1 and ApoE mRNA levels in fetal liver cells derived macrophages. In vivo, these changes translated into a significant increase in atherosclerotic lesions in Ldlr-/- mice with hematopoietic LPCAT3 deficiency., Conclusions: This study identifies LPCAT3 as a key factor in the control of phospholipid homeostasis and arachidonate availability in myeloid cells and underlines a new role for LPCAT3 in plasmalogen metabolism. Moreover, our work strengthens the link between phospholipid and sterol metabolism in hematopoietic cells, with significant consequences on nuclear receptor-regulated pathways and atherosclerosis development., (Copyright © 2018 Elsevier B.V. All rights reserved.)- Published
- 2018
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14. Correction: Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon cancer cells via the mitochondrial apoptotic pathway.
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Zeriouh W, Nani A, Belarbi M, Dumont A, de Rosny C, Aboura I, Ghanemi FZ, Murtaza B, Patoli D, Thomas C, Apetoh L, Rébé C, Delmas D, Khan NA, Ghiringhelli F, Rialland M, and Hichami A
- Abstract
[This corrects the article DOI: 10.1371/journal.pone.0170823.].
- Published
- 2017
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15. Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon cancer cells via the mitochondrial apoptotic pathway.
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Zeriouh W, Nani A, Belarbi M, Dumont A, de Rosny C, Aboura I, Ghanemi FZ, Murtaza B, Patoli D, Thomas C, Apetoh L, Rébé C, Delmas D, Khan NA, Ghiringhelli F, Rialland M, and Hichami A
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- Animals, Cell Death drug effects, Cell Line, Tumor, Cell Proliferation drug effects, Endoplasmic Reticulum Stress drug effects, Gene Expression Regulation, Neoplastic drug effects, Humans, Membrane Potential, Mitochondrial drug effects, Mice, Mice, Nude, Mitochondria pathology, Phenol chemistry, Reactive Oxygen Species metabolism, Transcription Factor CHOP metabolism, Xenograft Model Antitumor Assays, Apoptosis drug effects, Caspases metabolism, Colonic Neoplasms pathology, Mitochondria drug effects, Olea chemistry, Plant Extracts pharmacology, Plant Leaves chemistry
- Abstract
Dietary polyphenols, derived from natural products, have received a great interest for their chemopreventive properties against cancer. In this study, we investigated the effects of phenolic extract of the oleaster leaves (PEOL) on tumor growth in mouse model and on cell death in colon cancer cell lines. We assessed the effect of oleaster leaf infusion on HCT116 (human colon cancer cell line) xenograft growth in athymic nude mice. We observed that oleaster leaf polyphenol-rich infusion limited HCT116 tumor growth in vivo. Investigations of PEOL on two human CRC cell lines showed that PEOL induced apoptosis in HCT116 and HCT8 cells. We demonstrated an activation of caspase-3, -7 and -9 by PEOL and that pre-treatment with the pan-caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk), prevented PEOL-induced cell death. We observed an involvement of the mitochondrial pathway in PEOL-induced apoptosis evidenced by reactive oxygen species (ROS) production, a decrease of mitochondrial membrane potential, and cytochrome c release. Increase in intracellular Ca2+ concentration induced by PEOL represents the early event involved in mitochondrial dysfunction, ROS-induced endoplasmic reticulum (ER) stress and apoptosis induced by PEOL, as ruthenium red, an inhibitor of mitochondrial calcium uptake inhibited apoptotic effect of PEOL, BAPTA/AM inhibited PEOL-induced ROS generation and finally, N-acetyl-L-cysteine reversed ER stress and apoptotic effect of PEOL. These results demonstrate that polyphenols from oleaster leaves might have a strong potential as chemopreventive agent in colorectal cancer.
- Published
- 2017
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