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  1. Article ; Online: Ablation of Aquaporin-9 Ameliorates the Systemic Inflammatory Response of LPS-Induced Endotoxic Shock in Mouse.

    Tesse, Angela / Gena, Patrizia / Rützler, Michael / Calamita, Giuseppe

    Cells

    2021  Volume 10, Issue 2

    Abstract: Septic shock is the most severe complication of sepsis, being characterized by a systemic inflammatory response following bacterial infection, leading to multiple organ failure and dramatically high mortality. Aquaporin-9 (AQP9), a membrane channel ... ...

    Abstract Septic shock is the most severe complication of sepsis, being characterized by a systemic inflammatory response following bacterial infection, leading to multiple organ failure and dramatically high mortality. Aquaporin-9 (AQP9), a membrane channel protein mainly expressed in hepatocytes and leukocytes, has been recently associated with inflammatory and infectious responses, thus triggering strong interest as a potential target for reducing septic shock-dependent mortality. Here, we evaluated whether AQP9 contributes to murine systemic inflammation during endotoxic shock. Wild type (
    MeSH term(s) Animals ; Aquaporins/deficiency ; Aquaporins/genetics ; Aquaporins/immunology ; Disease Models, Animal ; Endotoxemia/genetics ; Endotoxemia/immunology ; Endotoxemia/pathology ; Inflammation/genetics ; Inflammation/immunology ; Lipopolysaccharides/pharmacology ; Male ; Mice ; Mice, Knockout ; Shock, Septic/genetics ; Shock, Septic/immunology
    Chemical Substances Aqp9 protein, mouse ; Aquaporins ; Lipopolysaccharides
    Language English
    Publishing date 2021-02-18
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10020435
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Aluminum particles generated during millisecond electric pulse application enhance adenovirus-mediated gene transfer in L929 cells.

    Tesse, Angela / André, Franck M / Ragot, Thierry

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 17725

    Abstract: Gene electrotransfer is an attractive method of non-viral gene delivery. However, the mechanism of DNA penetration across the plasma membrane is widely discussed. To explore this process for even larger structures, like viruses, we applied various ... ...

    Abstract Gene electrotransfer is an attractive method of non-viral gene delivery. However, the mechanism of DNA penetration across the plasma membrane is widely discussed. To explore this process for even larger structures, like viruses, we applied various combinations of short/long and high/low-amplitude electric pulses to L929 cells, mixed with a human adenovirus vector expressing GFP. We observed a transgene expression increase, both in the number of GFP-converted cells and GFP levels, when we added a low-voltage/millisecond-pulse treatment to the adenovirus/cell mixture. This increase, reflecting enhanced virus penetration, was proportional to the applied electric field amplitude and pulse number, but was not associated with membrane permeabilization, nor to direct cell modifications. We demonstrated that this effect is mainly due to adenovirus particle interactions with aggregated aluminum particles released from energized electrodes. Indeed, after centrifugation of the pulsed viral suspension and later on addition to cells, the activity was found mainly associated with the aluminum aggregates concentrated in the lower fraction and was proportional to generated quantities. Overall, this work focused on the use of electrotransfer to facilitate the adenovirus entry into cell, demonstrating that modifications of the penetrating agent can be more important than modifications of the target cell for transfer efficacy.
    MeSH term(s) Adenoviridae ; Aluminum ; Animals ; Cell Line ; Electric Stimulation ; Electroporation/methods ; Fibroblasts ; Gene Transfer Techniques ; Mice
    Chemical Substances Aluminum (CPD4NFA903)
    Language English
    Publishing date 2021-09-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-96781-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: SIRT1 Signaling Is Involved in the Vascular Improvement Induced by Moringa Oleifera Seeds during Aging.

    Conti, Valeria / Randriamboavonjy, Joseph Iharinjaka / Rafatro, Herintsoa / Manzo, Valentina / Dal Col, Jessica / Filippelli, Amelia / Corbi, Graziamaria / Tesse, Angela

    Pharmaceuticals (Basel, Switzerland)

    2023  Volume 16, Issue 5

    Abstract: Vascular aging is linked to reduce NO bioavailability, endothelial dysfunction, oxidative stress, and inflammation. We previously showed that a 4-week treatment of middle-aged Wistar rats (MAWRs, 46 weeks old) ... ...

    Abstract Vascular aging is linked to reduce NO bioavailability, endothelial dysfunction, oxidative stress, and inflammation. We previously showed that a 4-week treatment of middle-aged Wistar rats (MAWRs, 46 weeks old) with
    Language English
    Publishing date 2023-05-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph16050761
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Aluminum particles generated during millisecond electric pulse application enhance adenovirus-mediated gene transfer in L929 cells

    Angela Tesse / Franck M. André / Thierry Ragot

    Scientific Reports, Vol 11, Iss 1, Pp 1-

    2021  Volume 15

    Abstract: Abstract Gene electrotransfer is an attractive method of non-viral gene delivery. However, the mechanism of DNA penetration across the plasma membrane is widely discussed. To explore this process for even larger structures, like viruses, we applied ... ...

    Abstract Abstract Gene electrotransfer is an attractive method of non-viral gene delivery. However, the mechanism of DNA penetration across the plasma membrane is widely discussed. To explore this process for even larger structures, like viruses, we applied various combinations of short/long and high/low-amplitude electric pulses to L929 cells, mixed with a human adenovirus vector expressing GFP. We observed a transgene expression increase, both in the number of GFP-converted cells and GFP levels, when we added a low-voltage/millisecond-pulse treatment to the adenovirus/cell mixture. This increase, reflecting enhanced virus penetration, was proportional to the applied electric field amplitude and pulse number, but was not associated with membrane permeabilization, nor to direct cell modifications. We demonstrated that this effect is mainly due to adenovirus particle interactions with aggregated aluminum particles released from energized electrodes. Indeed, after centrifugation of the pulsed viral suspension and later on addition to cells, the activity was found mainly associated with the aluminum aggregates concentrated in the lower fraction and was proportional to generated quantities. Overall, this work focused on the use of electrotransfer to facilitate the adenovirus entry into cell, demonstrating that modifications of the penetrating agent can be more important than modifications of the target cell for transfer efficacy.
    Keywords Medicine ; R ; Science ; Q
    Subject code 500
    Language English
    Publishing date 2021-09-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Smooth muscle Rac1 contributes to pulmonary hypertension.

    Dilasser, Florian / Rio, Marc / Rose, Lindsay / Tesse, Angela / Guignabert, Christophe / Loirand, Gervaise / Sauzeau, Vincent

    British journal of pharmacology

    2022  Volume 179, Issue 13, Page(s) 3418–3429

    Abstract: Background and purpose: Pulmonary hypertension (PH) is a multifactorial chronic disease characterized by an increase in pulmonary artery (PA) resistance leading to right ventricle (RV) failure. Endothelial dysfunction and alteration of NO/cGMP ... ...

    Abstract Background and purpose: Pulmonary hypertension (PH) is a multifactorial chronic disease characterized by an increase in pulmonary artery (PA) resistance leading to right ventricle (RV) failure. Endothelial dysfunction and alteration of NO/cGMP signalling in PA plays a major role in PH. We recently described the involvement of the Rho protein Rac1 in the control of systemic blood pressure through its involvement in NO-mediated relaxation of arterial smooth muscle cell (SMC). The aim of this study was to analyse the role of SMC Rac1 in PH.
    Experimental approach: PH is induced by exposure of control and SMC Rac1-deficient (SM-Rac1-KO) mice to chronic hypoxia (10% O
    Key results: Rac1 activation in PA of hypoxic mice and patients with idiopathic PH. Hypoxia-induced rise in RV systolic pressure, RV hypertrophy and loss of endothelium-dependent relaxation were significantly decreased in SM-Rac1-KO mice compared to control mice. SMC Rac1 deletion also limited hypoxia-induced PA remodelling and ROS production in pulmonary artery smooth muscle cells (PASMCs).
    Conclusion and implications: Our results provide evidence for a protective effect of SM Rac1 deletion against hypoxic PH. Rac1 activity in PASMCs plays a causal role in PH by favouring ROS-dependent PA remodelling and endothelial dysfunction induced by chronic hypoxia.
    MeSH term(s) Animals ; Cell Proliferation ; Humans ; Hypertension, Pulmonary ; Hypertrophy, Right Ventricular ; Hypoxia/metabolism ; Mice ; Mice, Knockout ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Pulmonary Artery ; Reactive Oxygen Species/metabolism ; Vascular Remodeling ; rac1 GTP-Binding Protein/metabolism
    Chemical Substances RAC1 protein, human ; Reactive Oxygen Species ; rac1 GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2022-02-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.15805
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Ablation of Aquaporin-9 Ameliorates the Systemic Inflammatory Response of LPS-Induced Endotoxic Shock in Mouse

    Angela Tesse / Patrizia Gena / Michael Rützler / Giuseppe Calamita

    Cells, Vol 10, Iss 435, p

    2021  Volume 435

    Abstract: Septic shock is the most severe complication of sepsis, being characterized by a systemic inflammatory response following bacterial infection, leading to multiple organ failure and dramatically high mortality. Aquaporin-9 (AQP9), a membrane channel ... ...

    Abstract Septic shock is the most severe complication of sepsis, being characterized by a systemic inflammatory response following bacterial infection, leading to multiple organ failure and dramatically high mortality. Aquaporin-9 (AQP9), a membrane channel protein mainly expressed in hepatocytes and leukocytes, has been recently associated with inflammatory and infectious responses, thus triggering strong interest as a potential target for reducing septic shock-dependent mortality. Here, we evaluated whether AQP9 contributes to murine systemic inflammation during endotoxic shock. Wild type ( Aqp9 +/+

    WT) and Aqp9 gene knockout ( Aqp9 −/−

    KO) male mice were submitted to endotoxic shock by i.p. injection of lipopolysaccharide (LPS; 40 mg/kg) and the related survival times were followed during 72 h. The electronic paramagnetic resonance and confocal microscopy were employed to analyze the nitric oxide (NO) and superoxide anion (O 2 − ) production, and the expression of inducible NO-synthase (iNOS) and cyclooxigenase-2 (COX-2), respectively, in the liver, kidney, aorta, heart and lung of the mouse specimens. LPS-treated KO mice survived significantly longer than corresponding WT mice, and 25% of the KO mice fully recovered from the endotoxin treatment. The LPS-injected KO mice showed lower inflammatory NO and O 2 − productions and reduced iNOS and COX-2 levels through impaired NF-κB p65 activation in the liver, kidney, aorta, and heart as compared to the LPS-treated WT mice. Consistent with these results, the treatment of FaO cells, a rodent hepatoma cell line, with the AQP9 blocker HTS13268 prevented the LPS-induced increase of inflammatory NO and O 2 − . A role for AQP9 is suggested in the early acute phase of LPS-induced endotoxic shock involving NF-κB signaling. The modulation of AQP9 expression/function may reveal to be useful in developing novel endotoxemia therapeutics.
    Keywords membrane transport ; hydrogen peroxide ; peroxiporins ; aquaglyceroporins ; LPS ; sepsis ; Biology (General) ; QH301-705.5
    Subject code 630
    Language English
    Publishing date 2021-02-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: NO-ferroheme is a signaling entity in the vasculature.

    Kleschyov, Andrei L / Zhuge, Zhengbing / Schiffer, Tomas A / Guimarães, Drielle D / Zhang, Gensheng / Montenegro, Marcelo F / Tesse, Angela / Weitzberg, Eddie / Carlström, Mattias / Lundberg, Jon O

    Nature chemical biology

    2023  Volume 19, Issue 10, Page(s) 1267–1275

    Abstract: Despite wide appreciation of the biological role of nitric oxide (NO) synthase (NOS) signaling, questions remain about the chemical nature of NOS-derived bioactivity. Here we show that NO-like bioactivity can be efficiently transduced by mobile NO- ... ...

    Abstract Despite wide appreciation of the biological role of nitric oxide (NO) synthase (NOS) signaling, questions remain about the chemical nature of NOS-derived bioactivity. Here we show that NO-like bioactivity can be efficiently transduced by mobile NO-ferroheme species, which can transfer between proteins, partition into a hydrophobic phase and directly activate the sGC-cGMP-PKG pathway without intermediacy of free NO. The NO-ferroheme species (with or without a protein carrier) efficiently relax isolated blood vessels and induce hypotension in rodents, which is greatly potentiated after the blockade of NOS activity. While free NO-induced relaxations are abolished by an NO scavenger and in the presence of red blood cells or blood plasma, a model compound, NO-ferroheme-myoglobin preserves its vasoactivity suggesting the physiological relevance of NO-ferroheme species. We conclude that NO-ferroheme behaves as a signaling entity in the vasculature.
    MeSH term(s) Nitric Oxide ; Erythrocytes ; Heme ; Signal Transduction
    Chemical Substances Nitric Oxide (31C4KY9ESH) ; Heme (42VZT0U6YR)
    Language English
    Publishing date 2023-09-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2202962-X
    ISSN 1552-4469 ; 1552-4450
    ISSN (online) 1552-4469
    ISSN 1552-4450
    DOI 10.1038/s41589-023-01411-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Vasorelaxant Effect of Moroccan

    Mahou, Youssef / Chda, Alae / Es-Safi, Nour Eddine / Tesse, Angela / Fettoukh, Nezha / El Bouri, Aziz / Stambouli, Hamid / El Abida, Kaouakib / Bencheikh, Rachid

    Evidence-based complementary and alternative medicine : eCAM

    2023  Volume 2023, Page(s) 1265103

    Abstract: Introduction: Ethanolic fraction of Moroccan : Methods: Free radical scavenging capacity of EFCS was assessed using DPPH method. The EFCS vasodilation activities in phenylephrine-precontracted isolated rat mesenteric arterial beds were investigated ... ...

    Abstract Introduction: Ethanolic fraction of Moroccan
    Methods: Free radical scavenging capacity of EFCS was assessed using DPPH method. The EFCS vasodilation activities in phenylephrine-precontracted isolated rat mesenteric arterial beds were investigated in presence of L-NAME (nitric oxide synthase inhibitor), indomethacin (cyclooxygenase inhibitor), potassium channel blockers (namely tetraetylamonium, barium chloride, and glibenclamide), and atropine. Nitric oxide vascular release was measured by electron paramagnetic resonance (EPR) using a spin trap in rat aortic rings.
    Results: EFCS induced dose-dependent vasorelaxation on mesenteric vascular bed. Incubation of the preparations with L-NAME, ODQ (a soluble guanylyl cyclase inhibitor), or potassium channel blockers reduced the fall of perfusion pressure caused by EFCS. Endothelial denudation or atropine abolished the EFCS's vasorelaxant effect, suggesting involvement of muscarinic receptors and endothelium-relaxing factors. The extract induced nitric oxide release in aortic rings in a similar manner as acetylcholine suggesting an effect of EFCS on the muscarinic receptor and the conductance arteries. Chemical investigation of EFCS identified potential active components namely apigenin and derivatives of luteolin skeleton and also additional components such as neophytadiene, squalene, and
    Language English
    Publishing date 2023-04-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2171158-6
    ISSN 1741-4288 ; 1741-427X
    ISSN (online) 1741-4288
    ISSN 1741-427X
    DOI 10.1155/2023/1265103
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Concomitant Administration of Capecitabine and Folate Supplements: Need to Encourage Medication Reconciliation.

    Stefanelli, Berenice / Sellitto, Carmine / De Bellis, Emanuela / Torsiello, Martina / Bertini, Nicola / Pezzullo, Angelo Maria / Corbi, Graziamaria / Sabbatino, Francesco / Pepe, Stefano / Tesse, Angela / Conti, Valeria / Filippelli, Amelia

    Pharmaceuticals (Basel, Switzerland)

    2022  Volume 15, Issue 11

    Abstract: Hand-Foot syndrome (HFS) and diarrhoea are dose-limiting Adverse Drug Reactions (ADRs) of capecitabine-based chemotherapy. Four polymorphisms in ... ...

    Abstract Hand-Foot syndrome (HFS) and diarrhoea are dose-limiting Adverse Drug Reactions (ADRs) of capecitabine-based chemotherapy. Four polymorphisms in the
    Language English
    Publishing date 2022-11-10
    Publishing country Switzerland
    Document type Case Reports
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph15111388
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Changes in Key Mitochondrial Lipids Accompany Mitochondrial Dysfunction and Oxidative Stress in NAFLD.

    Durand, Manon / Coué, Marine / Croyal, Mikaël / Moyon, Thomas / Tesse, Angela / Atger, Florian / Ouguerram, Khadija / Jacobi, David

    Oxidative medicine and cellular longevity

    2021  Volume 2021, Page(s) 9986299

    Abstract: Nonalcoholic fatty liver disease (NAFLD) is a dysmetabolic hepatic damage of increasing severity: simple fat accumulation (steatosis), nonalcoholic steatohepatitis (NASH), and hepatic fibrosis. Oxidative stress is considered an important factor in ... ...

    Abstract Nonalcoholic fatty liver disease (NAFLD) is a dysmetabolic hepatic damage of increasing severity: simple fat accumulation (steatosis), nonalcoholic steatohepatitis (NASH), and hepatic fibrosis. Oxidative stress is considered an important factor in producing hepatocyte injury associated with NAFLD progression. Studies also suggest a link between the accumulation of specific hepatic lipid species, mitochondrial dysfunction, and the progression of NAFLD. However, it is unclear whether mitochondrial lipid modifications are involved in NAFLD progression. To gain insight into the relationship between mitochondrial lipids and disease progression through different stages of NAFLD, we performed lipidomic analyses on mouse livers at different stages of western diet-induced NAFLD, with or without hepatic fibrosis. After organelle separation, we studied separately the mitochondrial and the "nonmitochondrial" hepatic lipidomes. We identified 719 lipid species from 16 lipid families. Remarkably, the western diet triggered time-dependent changes in the mitochondrial lipidome, whereas the "nonmitochondrial" lipidome showed little difference with levels of hepatic steatosis or the presence of fibrosis. In mitochondria, the changes in the lipidome preceded hepatic fibrosis. In particular, two critical phospholipids, phosphatidic acid (PA) and cardiolipin (CL), displayed opposite responses in mitochondria. Decrease in CL and increase in PA were concurrent with an increase of coenzyme Q. Electron paramagnetic resonance spectroscopy superoxide spin trapping and Cu
    MeSH term(s) Animals ; Humans ; Lipid Metabolism/genetics ; Male ; Mice ; Mitochondria/pathology ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/pathology ; Oxidative Stress/genetics
    Language English
    Publishing date 2021-06-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2021/9986299
    Database MEDical Literature Analysis and Retrieval System OnLINE

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