المؤلفون: Bernabei, I., Hansen, U., Ehirchiou, D., Brinckmann, J., Chobaz, V., Busso, N., Nasi, S.

المصدر: International journal of molecular sciences, vol. 24, no. 11, pp. 9776

مصطلحات موضوعية: Animals, Mice, Apoptosis, Calcinosis/pathology, Cartilage, Articular/metabolism, Chondrocytes/metabolism, Extracellular Matrix/pathology, Integrins/metabolism, Protein-Lysine 6-Oxidase/metabolism, CD11b Antigen/genetics, CD11b, calcium-containing crystals, cartilage calcification, chondrocyte mineralization, integrin, lysyl oxidase, transmission electron microscopy

الوصف: Pathological cartilage calcification is a hallmark feature of osteoarthritis, a common degenerative joint disease, characterized by cartilage damage, progressively causing pain and loss of movement. The integrin subunit CD11b was shown to play a protective role against cartilage calcification in a mouse model of surgery-induced OA. Here, we investigated the possible mechanism by which CD11b deficiency could favor cartilage calcification by using naïve mice. First, we found by transmission electron microscopy (TEM) that CD11b KO cartilage from young mice presented early calcification spots compared with WT. CD11b KO cartilage from old mice showed progression of calcification areas. Mechanistically, we found more calcification-competent matrix vesicles and more apoptosis in both cartilage and chondrocytes isolated from CD11b-deficient mice. Additionally, the extracellular matrix from cartilage lacking the integrin was dysregulated with increased collagen fibrils with smaller diameters. Moreover, we revealed by TEM that CD11b KO cartilage had increased expression of lysyl oxidase (LOX), the enzyme that catalyzes matrix crosslinks. We confirmed this in murine primary CD11b KO chondrocytes, where Lox gene expression and crosslinking activity were increased. Overall, our results suggest that CD11b integrin regulates cartilage calcification through reduced MV release, apoptosis, LOX activity, and matrix crosslinking. As such, CD11b activation might be a key pathway for maintaining cartilage integrity.

العلاقة: info:eu-repo/semantics/altIdentifier/pmid/37298730; info:eu-repo/semantics/altIdentifier/eissn/1422-0067; https://serval.unil.ch/notice/serval:BIB_6F52E416CBF8Test; urn:issn:1422-0067

الإتاحة: https://doi.org/10.3390/ijms24119776Test
https://serval.unil.ch/notice/serval:BIB_6F52E416CBF8Test

المؤلفون: Kusano, T., Ehirchiou, D., Matsumura, T., Chobaz, V., Nasi, S., Castelblanco, M., So, A., Lavanchy, C., Acha-Orbea, H., Nishino, T., Okamoto, K., Busso, N.

المصدر: Nature communications, vol. 10, no. 1, pp. 4904

مصطلحات موضوعية: Animals, Cell Proliferation, Female, Gene Knock-In Techniques, Humans, Macrophages/enzymology, Macrophages/metabolism, Male, Mice, Inbred C57BL, Neoplasms/enzymology, Neoplasms/genetics, Neoplasms/metabolism, Neoplasms/physiopathology, Reactive Oxygen Species/metabolism, Xanthine Dehydrogenase/genetics, Xanthine Dehydrogenase/metabolism, Xanthine Oxidase/genetics, Xanthine Oxidase/metabolism

الوصف: Xanthine oxidoreductase has been implicated in cancer. Nonetheless, the role played by its two convertible forms, xanthine dehydrogenase (XDH) and oxidase (XO) during tumorigenesis is not understood. Here we produce XDH-stable and XO-locked knock-in (ki) mice to address this question. After tumor transfer, XO ki mice show strongly increased tumor growth compared to wild type (WT) and XDH ki mice. Hematopoietic XO expression is responsible for this effect. After macrophage depletion, tumor growth is reduced. Adoptive transfer of XO-ki macrophages in WT mice increases tumor growth. In vitro, XO ki macrophages produce higher levels of reactive oxygen species (ROS) responsible for the increased Tregs observed in the tumors. Blocking ROS in vivo slows down tumor growth. Collectively, these results indicate that the balance of XO/XDH plays an important role in immune surveillance of tumor development. Strategies that inhibit the XO form specifically may be valuable in controlling cancer growth.

وصف الملف: application/pdf

العلاقة: info:eu-repo/semantics/altIdentifier/pmid/31659168; info:eu-repo/semantics/altIdentifier/eissn/2041-1723; info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_AB744ACBDD116; https://serval.unil.ch/notice/serval:BIB_AB744ACBDD11Test; urn:issn:2041-1723; https://serval.unil.ch/resource/serval:BIB_AB744ACBDD11.P001/REF.pdfTest; http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_AB744ACBDD116Test

الإتاحة: https://doi.org/10.1038/s41467-019-12565-zTest
https://serval.unil.ch/notice/serval:BIB_AB744ACBDD11Test
https://serval.unil.ch/resource/serval:BIB_AB744ACBDD11.P001/REF.pdfTest
http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_AB744ACBDD116Test

المؤلفون: Nasi Liu, Guiping Wang, Youming Wu, Tongtong Xue, Gaoxiang Li, Qian Li, Yuzhu Chen, Yanyong Liu, Dexin Kong, Wei Huang, Nan Yang, Mingyue Cao

المصدر: International Journal of Cancer. 149:460-472

مصطلحات موضوعية: Male, MAPK/ERK pathway, Chemokine CXCL5, Cancer Research, Chemokine, Carcinoma, Hepatocellular, MAP Kinase Signaling System, Adrenergic beta-Antagonists, Receptors, Interleukin-8B, Mice, 03 medical and health sciences, Chemokine receptor, 0302 clinical medicine, Cell Line, Tumor, Animals, CXC chemokine receptors, biology, Chemistry, Myeloid-Derived Suppressor Cells, Liver Neoplasms, Propranolol, Gene Expression Regulation, Neoplastic, Oncology, Tumor progression, CXCL5, 030220 oncology & carcinogenesis, Cancer research, biology.protein, Myeloid-derived Suppressor Cell, Signal transduction, Neoplasm Transplantation, Spleen, Stress, Psychological

الوصف: Myeloid-derived suppressor cells (MDSCs) play an important role in tumor immune escape. Recent studies have shown that MDSCs contribute to tumor progression under psychological stress, but the underlying mechanism of MDSCs mobilization and recruitment remains largely unknown. In the present study, a chronic restraint stress paradigm was applied to the H22 hepatocellular carcinoma (HCC) bearing mice to mimic the psychological stress. We observed that chronic restraint stress significantly promoted HCC growth, as well as the mobilization of MDSCs to spleen and tumor sites from bone marrow. Meanwhile, chronic restraint stress enhanced the expression of C-X-C motif chemokine receptor 2 (CXCR2) and pErk1/2 in bone marrow MDSCs, together with elevated chemokine (C-X-C motif) ligand 5 (CXCL5) expression in tumor tissues. In vitro, the treatments of MDSCs with epinephrine (EPI) and norepinephrine (NE) but not corticosterone (CORT)-treated H22 conditioned medium obviously inhibited T-cell proliferation, as well as enhanced CXCR2 expression and extracellular signal-regulated kinase (Erk) phosphorylation. In vivo, β-adrenergic blockade with propranolol almost completely reversed the accelerated tumor growth induced by chronic restraint stress and inactivated CXCL5-CXCR2-Erk signaling pathway. Our findings support the crucial role of β-adrenergic signaling cascade in the mobilization and recruitment of MDSCs under chronic restraint stress.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::996e9fab4ec82ec912e47c13e0326ef2Test
https://doi.org/10.1002/ijc.33552Test

المؤلفون: Cossarizza, Andrea, Chang, Hyun-Dong, Radbruch, Andreas, Akdis, Mübeccel, Andrä, Immanuel, Annunziato, Francesco, Bacher, Petra, Barnaba, Vincenzo, Battistini, Luca, Bauer, Wolfgang M, Baumgart, Sabine, Becher, Burkhard, Beisker, Wolfgang, Berek, Claudia, Blanco, Alfonso, Borsellino, Giovanna, Boulais, Philip E, Brinkman, Ryan R, Büscher, Martin, Busch, Dirk H., Bushnell, Timothy P, Cao, Xuetao, Cavani, Andrea, Chattopadhyay, Pratip K, Cheng, Qingyu, Chow, Sue, Clerici, Mario, Cooke, Anne, Cosma, Antonio, Cosmi, Lorenzo, Cumano, Ana, Dang, Van Duc, Davies, Derek, De Biasi, Sara, Del Zotto, Genny, Della Bella, Silvia, Dellabona, Paolo, Deniz, Günnur, Dessing, Mark, Diefenbach, Andreas, Santo, James P.Di, Dieli, Francesco, Dolf, Andreas, Donnenberg, Vera S, Dörner, Thomas, Ehrhardt, Götz R A, Endl, Elmar, Engel, Pablo, Engelhardt, Britta, Esser, Charlotte, Everts, Bart, Dreher, Anita, Falk, Christine S, Fehniger, Todd A, Filby, Andrew, Fillatreau, Simon, Follo, Marie, Förster, Irmgard, Foster, John, Foulds, Gemma A, Frenette, Paul S, Galbraith, David, Garbi, Natalio, García-Godoy, Maria Dolores, Geginat, Jens, Ghoreschi, Kamran, Gibellini, Lara, Goettlinger, Christoph, Goodyear, Carl S, Gori, Andrea, Grogan, Jane, Gross, Mor, Grützkau, Andreas, Grummitt, Daryl, Hahn, Jonas, Hammer, Quirin, Hauser, Anja E, Haviland, David L, Hedley, David, Herrera, Guadalupe, Herrmann, Martin, Hiepe, Falk, Holland, Tristan, Hombrink, Pleun, Houston, Jessica P, Hoyer, Bimba F, Huang, Bo, Hunter, Christopher A, Iannone, Anna G., Jäck, Hans-Martin, Jávega, Beatriz, Jonjic, Stipan, Juelke, Kerstin, Jung, Steffen, Kaiser, Toralf, Kalina, Tomas, Keller, Baerbel, Khan, Srijit, Kienhöfer, Deborah, Kroneis, Thomas, Kunkel, Désirée, Kurts, Christian, Kvistborg, Pia, Lannigan, Joanne, Lantz, Olivier, Larbi, Anis, LeibundGut-Landmann, Salome, Leipold, Michael D, Levings, Megan K, Litwin, Virginia, Liu, Yanling, Lohoff, Michael, Lombardi, Giovanna, Lopez, Lilly, Lovett-Racke, Amy, Lubberts, Erik, Ludewig, Burkhard, Lugli, Enrico, Maecker, Holden T, Martrus, Glòria, Matarese, Giuseppe, Maueröder, Christian, McGrath, Mairi, McInnes, Iain B., Mei, Henrik E, Melchers, Fritz, Melzer, Susanne, Mielenz, Dirk, Mills, Kingston, Mirrer, David, Mjösberg, Jenny, Moore, Jonni, Moran, Barry, Moretta, Alessandro, Moretta, Lorenzo, Mosmann, Tim R, Müller, Susann, Müller, Werner, Münz, Christian, Multhoff, Gabriele, Munoz, Luis Enrique, Murphy, Kenneth M, Nakayama, Toshinori, Nasi, Milena, Neudörfl, Christine, Nolan, John J., Nourshargh, Sussan, O'Connor, José-Enrique, Ouyang, Wenjun, Oxenius, Annette, Palankar, Raghav, Panse, Isabel, Peterson, Pärt, Peth, Christian, Petriz, Jordi, Philips, Daisy, Pickl, Winfried, Piconese, Silvia, Pinti, Marcello, Pockley, A Graham, Podolska, Malgorzata Justyna, Pucillo, Carlo, Quataert, Sally A, Radstake, Timothy R D J, Rajwa, Bartek, Rebhahn, Jonathan A, Recktenwald, Diether, Remmerswaal, Ester B M, Rezvani, Katy, Rico, Laura G, Robinson, J Paul, Romagnani, Chiara, Rubartelli, Anna, Ruckert, Beate, Ruland, Jürgen, Sakaguchi, Shimon, Sala-de-Oyanguren, Francisco, Samstag, Yvonne, Sanderson, Sharon, Sawitzki, Birgit, Scheffold, Alexander, Schiemann, Matthias, Schildberg, Frank, Schimisky, Esther, Schmid, Stephan A, Schmitt, Steffen, Schober, Kilian, Schüler, Thomas, Schulz, Axel Ronald, Schumacher, Ton N., Scotta, Cristiano, Shankey, T Vincent, Shemer, Anat, Simon, Anna-Katharina, Spidlen, Josef, Stall, Alan M, Stark, Regina, Stehle, Christina, Stein, Merle, Steinmetz, Tobit, Stockinger, Hannes, Takahama, Yousuke, Tarnok, Attila, Tian, ZhiGang, Toldi, Gergely, Tornack, Julia, Traggiai, Elisabetta, Trotter, Joe, Ulrich, Henning, van der Braber, Marlous, van Lier, René A W, Veldhoen, Marc, Vento-Asturias, Salvador, Vieira, Paulo, Voehringer, David, Volk, Hans-Dieter, von Volkmann, Konrad, Waisman, Ari, Walker, Rachael, Ward, Michael D, Warnatz, Klaus, Warth, Sarah, Watson, James V, Watzl, Carsten, Wegener, Leonie, Wiedemann, Annika, Wienands, Jürgen, Willimsky, Gerald, Wing, James, Wurst, Peter, Yu, Liping, Yue, Alice, Zhang, Qianjun, Zhao, Yi, Ziegler, Susanne, Zimmermann, Jakob

المساهمون: Translationele immunologie, Infection & Immunity

مصطلحات موضوعية: Animals, Cell Proliferation, Cell Separation, DNA, False Positive Reactions, Flow Cytometry, Guidelines as Topic, Humans, Immunologic Techniques, Immunophenotyping, Journal Article, Quality Control, RNA, Research Design, Research Support, N.I.H., Extramural, Non-U.S. Gov't, Software, T-Lymphocytes

وصف الملف: image/pdf

العلاقة: https://dspace.library.uu.nl/handle/1874/360250Test

الإتاحة: https://dspace.library.uu.nl/handle/1874/360250Test

المؤلفون: Erik N. Taylor, Nasi Huang, Sunni Lin, Farzad Mortazavi, Van J. Wedeen, Jamila H. Siamwala, Richard J. Gilbert, James A. Hamilton

المصدر: Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance. 24(1)

مصطلحات موضوعية: Magnetic Resonance Spectroscopy, Radiological and Ultrasound Technology, Predictive Value of Tests, Animals, Humans, Radiology, Nuclear Medicine and imaging, Thrombosis, Muscle, Smooth, Rabbits, Cardiology and Cardiovascular Medicine, Atherosclerosis, Lipids, Plaque, Atherosclerotic

الوصف: Background Atherosclerosis is an arterial vessel wall disease characterized by slow, progressive lipid accumulation, smooth muscle disorganization, and inflammatory infiltration. Atherosclerosis often remains subclinical until extensive inflammatory injury promotes vulnerability of the atherosclerotic plaque to rupture with luminal thrombosis, which can cause the acute event of myocardial infarction or stroke. Current bioimaging techniques are unable to capture the pathognomonic distribution of cellular elements of the plaque and thus cannot accurately define its structural disorganization. Methods We applied cardiovascular magnetic resonance spectroscopy (CMRS) and diffusion weighted CMR (DWI) with generalized Q-space imaging (GQI) analysis to architecturally define features of atheroma and correlated these to the microscopic distribution of vascular smooth muscle cells (SMC), immune cells, extracellular matrix (ECM) fibers, thrombus, and cholesteryl esters (CE). We compared rabbits with normal chow diet and cholesterol-fed rabbits with endothelial balloon injury, which accelerates atherosclerosis and produces advanced rupture-prone plaques, in a well-validated rabbit model of human atherosclerosis. Results Our methods revealed new structural properties of advanced atherosclerosis incorporating SMC and lipid distributions. GQI with tractography portrayed the locations of these components across the atherosclerotic vessel wall and differentiated multi-level organization of normal, pro-inflammatory cellular phenotypes, or thrombus. Moreover, the locations of CE were differentiated from cellular constituents by their higher restrictive diffusion properties, which permitted chemical confirmation of CE by high field voxel-guided CMRS. Conclusions GQI with tractography is a new method for atherosclerosis imaging that defines a pathological architectural signature for the atheromatous plaque composed of distributed SMC, ECM, inflammatory cells, and thrombus and lipid. This provides a detailed transmural map of normal and inflamed vessel walls in the setting of atherosclerosis that has not been previously achieved using traditional CMR techniques. Although this is an ex-vivo study, detection of micro and mesoscale level vascular destabilization as enabled by GQI with tractography could increase the accuracy of diagnosis and assessment of treatment outcomes in individuals with atherosclerosis.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ab2cb809d8d4e581671b3150d721b3b3Test
https://pubmed.ncbi.nlm.nih.gov/36544161Test

المؤلفون: Milena Nasi, Anna De Gaetano, Gianluca Carnevale, Laura Bertoni, Valentina Selleri, Giada Zanini, Alessandra Pisciotta, Stefania Caramaschi, Luca Reggiani Bonetti, Alberto Farinetti, Andrea Cossarizza, Marcello Pinti, Antonio Manenti, Anna Vittoria Mattioli

المصدر: Nutrients; Volume 14; Issue 9; Pages: 1928

مصطلحات موضوعية: Nutrition and Dietetics, energy drinks, fibrosis, Coffee, Rats, Gastrointestinal Tract, Rats, Sprague-Dawley, Gastrointestinal tract, Caffeine, Animals, Energy Drinks, caffeine, eosinophils, Food Science

الوصف: Energy drinks (EDs) are non-alcoholic beverages containing high amounts of caffeine and other psychoactive substances. EDs also contain herbal extract whose concentration is usually unknown. EDs can have several adverse effects on different organs and systems, but their effects on the gastrointestinal (GI) tract have been poorly investigated. To determine the acute effects of EDs on the GI tract, we administered EDs, coffee, soda cola, or water to Sprague–Dawley rats (n = 7 per group, randomly assigned) for up to five days, and analyzed the histopathological changes in the GI tract. Data were compared among groups by Kruskal–Wallis or Mann–Whitney tests. We found that, while EDs did not cause any evident acute lesion to the GI tract, they triggered eosinophilic infiltration in the intestinal mucosa; treatment with caffeine alone at the same doses found in EDs leads to the same effects, suggesting that it is caffeine and not other substances present in the EDs that causes this infiltration. The interruption of caffeine administration leads to the complete resolution of eosinophilic infiltration. As no systemic changes in pro-inflammatory or immunomodulating molecules were observed, our data suggest that caffeine present in ED can cause a local, transient inflammatory status that recruits eosinophils.

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::63f161785bb8af90f019ad2b198bd7ceTest
https://hdl.handle.net/11380/1275199Test

المؤلفون: Nasi, S., Ea, H.K., Lioté, F., So, A., Busso, N.

المصدر: PloS one, vol. 11, no. 7, pp. e0158196

مصطلحات موضوعية: Animals, Bone Marrow Cells/cytology, Calcium/chemistry, Calcium Phosphates/chemistry, Cartilage/pathology, Cartilage, Articular/pathology, Chemokine CCL2/metabolism, Chondrocytes/cytology, Crystallization, Female, Gene Expression Regulation, Humans, Interleukin-6/metabolism, Macrophages/cytology, Mice, Inbred C57BL, Osteoarthritis/therapy, Reactive Oxygen Species/metabolism, Thiosulfates/pharmacology, X-Ray Microtomography

الوصف: Calcium-containing crystals participate in the pathogenesis of OA. Sodium thiosulfate (STS) has been shown to be an effective treatment in calcification disorders such as calciphylaxis and vascular calcification. This study investigated the effects and mechanisms of action of STS in a murine model of OA and in chondrocyte calcification. Hydroxyapatite (HA) crystals-stimulated murine chondrocytes and macrophages were treated with STS. Mineralization and cellular production of IL-6, MCP-1 and reactive oxygen species (ROS) were assayed. STS's effects on genes involved in calcification, inflammation and cartilage matrix degradation were studied by RT-PCR. STS was administered in the menisectomy model of murine OA, and the effect on periarticular calcific deposits and cartilage degeneration was investigated by micro-CT-scan and histology. In vitro, STS prevented in a dose-dependent manner calcium crystal deposition in chondrocytes and inhibited Annexin V gene expression. In addition, there was a reduction in crystal-induced IL-6 and MCP-1 production. STS also had an antioxidant effect, diminished HA-induced ROS generation and abrogated HA-induced catabolic responses in chondrocytes. In vivo, administration of STS reduced the histological severity of OA, by limiting the size of new periarticular calcific deposits and reducing the severity of cartilage damage. STS reduces the severity of periarticular calcification and cartilage damage in an animal model of OA via its effects on chondrocyte mineralization and its attenuation of crystal-induced inflammation as well as catabolic enzymes and ROS generation. Our study suggests that STS may be a disease-modifying drug in crystal-associated OA.

وصف الملف: application/pdf

العلاقة: info:eu-repo/semantics/altIdentifier/pmid/27391970; info:eu-repo/semantics/altIdentifier/eissn/1932-6203; info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_7920E7051A8B0; https://serval.unil.ch/notice/serval:BIB_7920E7051A8BTest; urn:issn:1932-6203; https://serval.unil.ch/resource/serval:BIB_7920E7051A8B.P001/REF.pdfTest; http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_7920E7051A8B0Test

الإتاحة: https://doi.org/10.1371/journal.pone.0158196Test
https://serval.unil.ch/notice/serval:BIB_7920E7051A8BTest
https://serval.unil.ch/resource/serval:BIB_7920E7051A8B.P001/REF.pdfTest
http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_7920E7051A8B0Test

المؤلفون: Nasi Huang, Yandan Wang, Erik N. Taylor, James A. Hamilton, Kathleen G. Morgan, Jonathan J. Wisco

المصدر: Journal of Translational Medicine, Vol 18, Iss 1, Pp 1-11 (2020)
Journal of Translational Medicine

مصطلحات موضوعية: 0301 basic medicine, Pathology, medicine.medical_specialty, Aging, Thalamus, lcsh:Medicine, Brain imaging, General Biochemistry, Genetics and Molecular Biology, White matter, Mice, 03 medical and health sciences, 0302 clinical medicine, Neuroimaging, Fractional anisotropy, Vascular contributions to cognitive impairment and dementia (VCID), medicine, Animals, Dementia, Gray Matter, Vascular dementia, Cerebral Hemorrhage, business.industry, Gradient-recalled echo MRI, diffusion tensor imaging, Research, lcsh:R, Brain, General Medicine, medicine.disease, Magnetic Resonance Imaging, Diffusion Magnetic Resonance Imaging, 030104 developmental biology, medicine.anatomical_structure, Cerebral microbleeds (CMBs), business, 030217 neurology & neurosurgery, Ex vivo, Tractography

الوصف: Background Brain aging is a major risk factor in the progression of cognitive diseases including Alzheimer’s disease (AD) and vascular dementia. We investigated a mouse model of brain aging up to 24 months old (mo). Methods A high field (11.7T) MRI protocol was developed to characterize specific features of brain aging including the presence of cerebral microbleeds (CMBs), morphology of grey and white matter, and tissue diffusion properties. Mice were selected from age categories of either young (3 mo), middle-aged (18 mo), or old (24 mo) and fed normal chow over the duration of the study. Mice were imaged in vivo with multimodal MRI, including conventional T2-weighted (T2W) and T2*-weighted (T2*W) imaging, followed by ex vivo diffusion-weighted imaging (DWI) and T2*W MR-microscopy to enhance the detection of microstructural features. Results Structural changes observed in the mouse brain with aging included reduced cortical grey matter volume and enlargement of the brain ventricles. A remarkable age-related change in the brains was the development of CMBs found starting at 18 mo and increasing in total volume at 24 mo, primarily in the thalamus. CMBs presence was confirmed with high resolution ex vivo MRI and histology. DWI detected further brain tissue changes in the aged mice including reduced fractional anisotropy, increased radial diffusion, increased mean diffusion, and changes in the white matter fibers visualized by color-coded tractography, including around a large cortical CMB. Conclusions The mouse is a valuable model of age-related vascular contributions to cognitive impairment and dementia (VCID). In composite, these methods and results reveal brain aging in older mice as a multifactorial process including CMBs and tissue diffusion alterations that can be well characterized by high field MRI.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2ce4ee216589677c3fd620ccaad86749Test
http://link.springer.com/article/10.1186/s12967-020-02441-6Test

المؤلفون: VAN VLIET, NATHALIE, MILNER-GULLAND, E. J., BOUSQUET, FRANCOIS, SAQALLI, MEHDI, NASI, ROBERT

المصدر: Conservation Biology, 2010 Oct 01. 24(5), 1327-1337.

الوصول الحر: https://www.jstor.org/stable/40864033Test

المؤلفون: Alexander So, Mariela Castelblanco, Hans Acha-Orbea, Tomohiro Matsumura, Véronique Chobaz, Nathalie Busso, Teruo Kusano, Takeshi Nishino, Driss Ehirchiou, Ken Okamoto, Sonia Nasi, Christine Lavanchy

المصدر: Nature Communications, Vol 10, Iss 1, Pp 1-14 (2019)
Nature communications, vol. 10, no. 1, pp. 4904
Nature Communications

مصطلحات موضوعية: Male, 0301 basic medicine, Xanthine Oxidase, Adoptive cell transfer, Xanthine Dehydrogenase, Science, General Physics and Astronomy, medicine.disease_cause, Article, General Biochemistry, Genetics and Molecular Biology, Mice, 03 medical and health sciences, 0302 clinical medicine, Neoplasms, Gene knockin, medicine, Animals, Humans, Gene Knock-In Techniques, lcsh:Science, Cell Proliferation, Cancer, chemistry.chemical_classification, Oxidase test, Reactive oxygen species, Multidisciplinary, Chemistry, Cell growth, Macrophages, Wild type, General Chemistry, Female, Macrophages/enzymology, Macrophages/metabolism, Mice, Inbred C57BL, Neoplasms/enzymology, Neoplasms/genetics, Neoplasms/metabolism, Neoplasms/physiopathology, Reactive Oxygen Species/metabolism, Xanthine Dehydrogenase/genetics, Xanthine Dehydrogenase/metabolism, Xanthine Oxidase/genetics, Xanthine Oxidase/metabolism, 030104 developmental biology, Xanthine dehydrogenase, 030220 oncology & carcinogenesis, Cancer research, Tumour immunology, lcsh:Q, Reactive Oxygen Species, Carcinogenesis

الوصف: Xanthine oxidoreductase has been implicated in cancer. Nonetheless, the role played by its two convertible forms, xanthine dehydrogenase (XDH) and oxidase (XO) during tumorigenesis is not understood. Here we produce XDH-stable and XO-locked knock-in (ki) mice to address this question. After tumor transfer, XO ki mice show strongly increased tumor growth compared to wild type (WT) and XDH ki mice. Hematopoietic XO expression is responsible for this effect. After macrophage depletion, tumor growth is reduced. Adoptive transfer of XO-ki macrophages in WT mice increases tumor growth. In vitro, XO ki macrophages produce higher levels of reactive oxygen species (ROS) responsible for the increased Tregs observed in the tumors. Blocking ROS in vivo slows down tumor growth. Collectively, these results indicate that the balance of XO/XDH plays an important role in immune surveillance of tumor development. Strategies that inhibit the XO form specifically may be valuable in controlling cancer growth.
The roles of the convertible forms, xanthine dehydrogenase (XDH) and xanthine oxidase (XO) during tumorigenesis is not known. Here, the authors develop XDH-stable and XO-locked knock-in (ki) mice and show increased tumor growth in XO ki mice, via macrophage-mediated immunoregulatory responses.

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::64bc8d18e5e6e17285be9cac5cbdc0f2Test
https://doaj.org/article/a917fab180ef4bcfad65767813174f1dTest