18 results on '"Ilina O"'
Search Results
2. The Sorption of Radionuclides on Clay Minerals—the Components of Engineering Safety Barriers
- Author
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Semenkova, A. S., Ilina, O. A., Krupskaya, V. V., Zakusin, S. V., Dorzhieva, O. V., Pokidko, B. V., Romanchuk, A. Yu., and Kalmykov, S. N.
- Published
- 2021
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3. New national and regional bryophyte records, 45.
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Ellis, L. T., Ah-Peng, C., Aranda, S. C., Bednarek-Ochyra, H., Borovichev, E. A., Cykowska-Marzencka, B., Duarte, M. C., Enroth, J., Erzberger, P., Fedosov, V., Fojcik, B., Gabriel, R., Coelho, M. C. M., Henriques, D. S. G., Ilina, O. V., Gil-Novoa, J. E., Morales-Puentes, M. E., Gradstein, S. R., Gupta, R., and Nath, V.
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BRYOPHYTES ,ANASTROPHYLLUM ,BRACHYTHECIUM ,BRYUM ,BRACHYTHECIACEAE - Abstract
The article presents new national and regional bryophytes. Some of them are Anastrophyllum michauxii, Antitrichia curtipendula, Anthoceros lamellatus, Brachythecium austrosalebrosum, Bruchia flexuosa, Brachythecium extremorientale, Bryum pseudotriquetrum, Bryum barnesii, Bucklandiella lamprocarpa, Campylium decipiens and Dicranella heteromalla.
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- 2015
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4. Electronic system with series organization for connection the distributed generators of renewable energy to low voltage industrial network.
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Sokol, E. I., Goncharov, Y. P., Eresko, A. V., Zamaruiev, V. V., Krivosheev, S. Y., Ivakhno, V. V., Ilina, O. V., Malyarenko, E. A., Styslo, B. A., and Upyrenko, K. G.
- Published
- 2013
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5. Higher Pedagogical Education for Sustainable Development in Russia and in France: A New Master’s Degree Programs
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Ilina Olga and Brazhnik Evgeniia
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Environmental sciences ,GE1-350 - Abstract
Higher pedagogical education in Russia and France is currently undergoing modernization. In connection with the new challenges of time, global changes in the world community there is a growing public interest in the problems of sustainable development as the only possible way of civilization movement. Under these conditions, there is a need to improve teacher training, the inclusion of new training modules in the educational process, and the creation of new master’s degree programs. This study aims to analyze the situation by introducing the idea of “education for sustainable development (ESD)” into the organization of higher teacher education, which is constantly reforming in the context of the Bologna process, on the example of two countries - Russia and France. The study identifies the main tendencies of pedagogical education modernization, examines the teacher training system in terms of ESD ideas, considers Master’s programs in universities of Russia and France.
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- 2021
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6. pH and ROS Responsiveness of Polymersome Nanovaccines for Antigen and Adjuvant Codelivery: An In Vitro and In Vivo Comparison.
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Jäger E, Ilina O, Dölen Y, Valente M, van Dinther EAW, Jäger A, Figdor CG, and Verdoes M
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- Animals, Mice, Reactive Oxygen Species, CD8-Positive T-Lymphocytes, Dendritic Cells, Antigens chemistry, Adjuvants, Immunologic pharmacology, Ovalbumin, Hydrogen-Ion Concentration, Mice, Inbred C57BL, Nanovaccines, Vaccines chemistry
- Abstract
The antitumor immunity can be enhanced through the synchronized codelivery of antigens and immunostimulatory adjuvants to antigen-presenting cells, particularly dendritic cells (DCs), using nanovaccines (NVs). To study the influence of intracellular vaccine cargo release kinetics on the T cell activating capacities of DCs, we compared stimuli-responsive to nonresponsive polymersome NVs. To do so, we employed "AND gate" multiresponsive (MR) amphiphilic block copolymers that decompose only in response to the combination of chemical cues present in the environment of the intracellular compartments in antigen cross-presenting DCs: low pH and high reactive oxygen species (ROS) levels. After being unmasked by ROS, pH-responsive side chains are exposed and can undergo a charge shift within a relevant pH window of the intracellular compartments in antigen cross-presenting DCs. NVs containing the model antigen Ovalbumin (OVA) and the iNKT cell activating adjuvant α-Galactosylceramide (α-Galcer) were fabricated using microfluidics self-assembly. The MR NVs outperformed the nonresponsive NV in vitro, inducing enhanced classical- and cross-presentation of the OVA by DCs, effectively activating CD8+, CD4+ T cells, and iNKT cells. Interestingly, in vivo, the nonresponsive NVs outperformed the responsive vaccines. These differences in polymersome vaccine performance are likely linked to the kinetics of cargo release, highlighting the crucial chemical requirements for successful cancer nanovaccines.
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- 2024
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7. Correction to: Multiscale imaging of therapeutic anti-PD-L1 antibody localization using molecularly defined imaging agents Iris.
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Hagemans IM, Wierstra PJ, Steuten K, Molkenboer-Kuenen JDM, van Dalen D, Ter Beest M, van der Schoot JMS, Ilina O, Gotthardt M, Figdor CG, Scheeren FA, Heskamp S, and Verdoes M
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- 2022
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8. Multiscale imaging of therapeutic anti-PD-L1 antibody localization using molecularly defined imaging agents.
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Hagemans IM, Wierstra PJ, Steuten K, Molkenboer-Kuenen JDM, van Dalen D, Ter Beest M, van der Schoot JMS, Ilina O, Gotthardt M, Figdor CG, Scheeren FA, Heskamp S, and Verdoes M
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- Animals, B7-H1 Antigen metabolism, Cell Line, Tumor, Humans, Immunohistochemistry, Mice, Tissue Distribution, Immunoconjugates metabolism, Neoplasms diagnostic imaging
- Abstract
Background: While immune checkpoint inhibitors such as anti-PD-L1 antibodies have revolutionized cancer treatment, only subgroups of patients show durable responses. Insight in the relation between clinical response, PD-L1 expression and intratumoral localization of PD-L1 therapeutics could improve patient stratification. Therefore, we present the modular synthesis of multimodal antibody-based imaging tools for multiscale imaging of PD-L1 to study intratumoral distribution of PD-L1 therapeutics., Results: To introduce imaging modalities, a peptide containing a near-infrared dye (sulfo-Cy5), a chelator (DTPA), an azide, and a sortase-recognition motif was synthesized. This peptide and a non-fluorescent intermediate were used for site-specific functionalization of c-terminally sortaggable mouse IgG1 (mIgG1) and Fab anti-PD-L1. To increase the half-life of the Fab fragment, a 20 kDa PEG chain was attached via strain-promoted azide-alkyne cycloaddition (SPAAC). Biodistribution and imaging studies were performed with
111 In-labeled constructs in 4T1 tumor-bearing mice. Comparing our site-specific antibody-conjugates with randomly conjugated antibodies, we found that antibody clone, isotype and method of DTPA conjugation did not change tumor uptake. Furthermore, addition of sulfo-Cy5 did not affect the biodistribution. PEGylated Fab fragment displayed a significantly longer half-life compared to unPEGylated Fab and demonstrated the highest overall tumor uptake of all constructs. PD-L1 in tumors was clearly visualized by SPECT/CT, as well as whole body fluorescence imaging. Immunohistochemistry staining of tumor sections demonstrated that PD-L1 co-localized with the fluorescent and autoradiographic signal. Intratumoral localization of the imaging agent could be determined with cellular resolution using fluorescent microscopy., Conclusions: A set of molecularly defined multimodal antibody-based PD-L1 imaging agents were synthesized and validated for multiscale monitoring of PD-L1 expression and localization. Our modular approach for site-specific functionalization could easily be adapted to other targets., (© 2022. The Author(s).)- Published
- 2022
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9. Collective invasion induced by an autocrine purinergic loop through connexin-43 hemichannels.
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Khalil AA, Ilina O, Vasaturo A, Venhuizen JH, Vullings M, Venhuizen V, Bilos A, Figdor CG, Span PN, and Friedl P
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- Adenosine Triphosphate genetics, Breast Neoplasms pathology, Cell Communication genetics, Cell Line, Tumor, Epithelial Cells metabolism, Epithelial Cells pathology, Female, Gap Junctions genetics, Gene Expression Regulation, Neoplastic genetics, Humans, Intercellular Junctions genetics, Neoplasm Invasiveness pathology, Proto-Oncogene Proteins c-akt genetics, Signal Transduction genetics, Breast Neoplasms genetics, Connexin 43 genetics, Neoplasm Invasiveness genetics, Receptors, Purinergic P1 genetics
- Abstract
Progression of epithelial cancers predominantly proceeds by collective invasion of cell groups with coordinated cell-cell junctions and multicellular cytoskeletal activity. Collectively invading breast cancer cells express the gap junction protein connexin-43 (Cx43), yet whether Cx43 regulates collective invasion remains unclear. We here show that Cx43 mediates gap-junctional coupling between collectively invading breast cancer cells and, via hemichannels, adenosine nucleotide/nucleoside release into the extracellular space. Using molecular interference and rescue strategies, we identify that Cx43 hemichannel function, but not intercellular communication, induces leader cell activity and collective migration through the engagement of the adenosine receptor 1 (ADORA1) and AKT signaling. Accordingly, pharmacological inhibition of ADORA1 or AKT signaling caused leader cell collapse and halted collective invasion. ADORA1 inhibition further reduced local invasion of orthotopic mammary tumors in vivo, and joint up-regulation of Cx43 and ADORA1 in breast cancer patients correlated with decreased relapse-free survival. This identifies autocrine purinergic signaling, through Cx43 hemichannels, as a critical pathway in leader cell function and collective invasion., (© 2020 Khalil et al.)
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- 2020
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10. Cell-cell adhesion and 3D matrix confinement determine jamming transitions in breast cancer invasion.
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Ilina O, Gritsenko PG, Syga S, Lippoldt J, La Porta CAM, Chepizhko O, Grosser S, Vullings M, Bakker GJ, Starruß J, Bult P, Zapperi S, Käs JA, Deutsch A, and Friedl P
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- Adherens Junctions pathology, Animals, Cell Line, Cell Line, Tumor, Down-Regulation physiology, Female, Gene Expression Regulation, Neoplastic physiology, HEK293 Cells, Humans, Intercellular Junctions pathology, MCF-7 Cells, Mice, Inbred BALB C, Breast Neoplasms pathology, Cell Adhesion physiology, Neoplasm Invasiveness pathology
- Abstract
Plasticity of cancer invasion and metastasis depends on the ability of cancer cells to switch between collective and single-cell dissemination, controlled by cadherin-mediated cell-cell junctions. In clinical samples, E-cadherin-expressing and -deficient tumours both invade collectively and metastasize equally, implicating additional mechanisms controlling cell-cell cooperation and individualization. Here, using spatially defined organotypic culture, intravital microscopy of mammary tumours in mice and in silico modelling, we identify cell density regulation by three-dimensional tissue boundaries to physically control collective movement irrespective of the composition and stability of cell-cell junctions. Deregulation of adherens junctions by downregulation of E-cadherin and p120-catenin resulted in a transition from coordinated to uncoordinated collective movement along extracellular boundaries, whereas single-cell escape depended on locally free tissue space. These results indicate that cadherins and extracellular matrix confinement cooperate to determine unjamming transitions and stepwise epithelial fluidization towards, ultimately, cell individualization.
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- 2020
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11. Molecular Repolarisation of Tumour-Associated Macrophages.
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van Dalen FJ, van Stevendaal MHME, Fennemann FL, Verdoes M, and Ilina O
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- Animals, Humans, Immunotherapy methods, Macrophages metabolism, Neoplasms immunology, Neoplasms therapy, Tumor Microenvironment immunology
- Abstract
The tumour microenvironment (TME) is composed of extracellular matrix and non-mutated cells supporting tumour growth and development. Tumour-associated macrophages (TAMs) are among the most abundant immune cells in the TME and are responsible for the onset of a smouldering inflammation. TAMs play a pivotal role in oncogenic processes as tumour proliferation, angiogenesis and metastasis, and they provide a barrier against the cytotoxic effector function of T lymphocytes and natural killer (NK) cells. However, TAMs are highly plastic cells that can adopt either pro- or anti-inflammatory roles in response to environmental cues. Consequently, TAMs represent an attractive target to recalibrate immune responses in the TME. Initial TAM-targeted strategies, such as macrophage depletion or disruption of TAM recruitment, have shown beneficial effects in preclinical models and clinical trials. Alternatively, reprogramming TAMs towards a proinflammatory and tumouricidal phenotype has become an attractive strategy in immunotherapy. This work summarises the molecular wheelwork of macrophage biology and presents an overview of molecular strategies to repolarise TAMs in immunotherapy.
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- 2018
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12. Intravital microscopy of collective invasion plasticity in breast cancer.
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Ilina O, Campanello L, Gritsenko PG, Vullings M, Wang C, Bult P, Losert W, and Friedl P
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- Actins metabolism, Animals, Cell Line, Tumor, Cell Proliferation, Female, HEK293 Cells, Humans, Imaging, Three-Dimensional, Mammary Neoplasms, Animal blood supply, Mice, Inbred BALB C, Neoplasm Invasiveness, Neoplasm Metastasis, Neovascularization, Pathologic pathology, Stromal Cells pathology, Cell Plasticity, Intravital Microscopy, Mammary Neoplasms, Animal diagnostic imaging, Mammary Neoplasms, Animal pathology
- Abstract
Cancer invasion programs are adaptive by switching between metastatic collective and single-cell dissemination; however, current intravital microscopy models for epithelial cancer in mice fail to reliably recreate such invasion plasticity. Using microimplantation of breast cancer spheroids into the murine mammary fat pad and live-cell monitoring, we show microenvironmental conditions and cytoskeletal adaptation during collective to single-cell transition in vivo E-cadherin-expressing 4T1 and E-cadherin-negative MMT tumors both initiated collective invasion along stromal structures, reflecting invasion patterns in 3D organotypic culture and human primary ductal and lobular carcinoma. Collectively invading cells developed weakly oscillatory actin dynamics, yet provided zones for single-cell transitions with accentuated, more chaotic actin fluctuations. This identifies collective invasion in vivo as a dynamic niche and efficient source for single-cell release., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2018. Published by The Company of Biologists Ltd.)
- Published
- 2018
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13. Collective invasion in ductal and lobular breast cancer associates with distant metastasis.
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Khalil AA, Ilina O, Gritsenko PG, Bult P, Span PN, and Friedl P
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- Adult, Aged, Breast Neoplasms mortality, Carcinoma, Ductal, Breast mortality, Carcinoma, Lobular mortality, Disease-Free Survival, Female, Humans, Kaplan-Meier Estimate, Middle Aged, Breast Neoplasms pathology, Carcinoma, Ductal, Breast pathology, Carcinoma, Lobular pathology, Neoplasm Invasiveness pathology
- Abstract
Breast cancer undergoes collective tissue invasion and, in experimental models, can collectively metastasize. The prevalence of collective invasion and its contribution to distant metastasis in clinical disease, however, remains poorly defined. We here scored the adipose tissue invasion of primary invasive ductal carcinoma (IDC), expressing E-cadherin, and E-cadherin negative invasive lobular carcinoma (ILC) and identified predominantly collective invasion patterns (86/86 samples) in both carcinoma types. Whereas collective invasion in IDC lesions retained adherens junctions, multicellular clusters and "Indian files" in ILC, despite the absence of adherens junctions (AJ) proteins E-cadherin and β-catenin, retained CD44 at cell-cell contacts. By histomorphological scoring and semi-automated image analysis, we show that the extent of collective invasion into the adipose tissue correlated with decreased distant metastasis-free survival (5-year follow-up; hazard ratio: 2.32 and 2.29, respectively). Thus, collective invasion represents the predominant invasion mode in breast cancer, develops distinct junctional subtypes in IDC and ILC, and associates with distant metastasis, suggesting a critical role in systemic dissemination.
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- 2017
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14. Hypoxia Induces a HIF-1-Dependent Transition from Collective-to-Amoeboid Dissemination in Epithelial Cancer Cells.
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Lehmann S, Te Boekhorst V, Odenthal J, Bianchi R, van Helvert S, Ikenberg K, Ilina O, Stoma S, Xandry J, Jiang L, Grenman R, Rudin M, and Friedl P
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- Breast Neoplasms metabolism, Cell Adhesion, Cell Line, Tumor, Cell Movement, Female, Head and Neck Neoplasms metabolism, Humans, Neoplasm Metastasis, Nuclear Proteins metabolism, Tumor Hypoxia, Twist-Related Protein 1 metabolism, Breast Neoplasms pathology, Epithelial-Mesenchymal Transition, Head and Neck Neoplasms pathology, Hypoxia-Inducible Factor 1 metabolism, Mechanotransduction, Cellular
- Abstract
Cancer metastases arise from a multi-step process that requires metastasizing tumor cells to adapt to signaling input from varying tissue environments [1]. As an early metastatic event, cancer cell dissemination occurs through different migration programs, including multicellular, collective, and single-cell mesenchymal or amoeboid migration [2-4]. Migration modes can interconvert based on changes in cell adhesion, cytoskeletal mechanotransduction [5], and/or proteolysis [6], most likely under the control of transcriptional programs such as the epithelial-to-mesenchymal transition (EMT) [7, 8]. However, how plasticity of tumor cell migration and EMT is spatiotemporally controlled and connected upon challenge by the tumor microenvironment remains unclear. Using 3D cultures of collectively invading breast and head and neck cancer spheroids, here we identify hypoxia, a hallmark of solid tumors [9], as an inducer of the collective-to-amoeboid transition (CAT), promoting the dissemination of amoeboid-moving single cells from collective invasion strands. Hypoxia-induced amoeboid detachment was driven by hypoxia-inducible factor 1 (HIF-1), followed the downregulation of E-cadherin, and produced heterogeneous cell subsets whose phenotype and migration were dependent (∼30%) or independent (∼70%) of Twist-mediated EMT. EMT-like and EMT-independent amoeboid cell subsets showed stable amoeboid movement over hours as well as leukocyte-like traits, including rounded morphology, matrix metalloproteinase (MMP)-independent migration, and nuclear deformation. Cancer cells undergoing pharmacological stabilization of HIFs retained their constitutive ability for early metastatic seeding in an experimental model of lung metastasis, indicating that hypoxia-induced CAT enhances cell release rather than early organ colonization. Induced by metabolic challenge, amoeboid movement may thus constitute a common endpoint of both EMT-dependent and EMT-independent cancer dissemination programs., (Copyright © 2017. Published by Elsevier Ltd.)
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- 2017
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15. Ca(2+)-activated K(+) channel-3.1 blocker TRAM-34 attenuates airway remodeling and eosinophilia in a murine asthma model.
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Girodet PO, Ozier A, Carvalho G, Ilina O, Ousova O, Gadeau AP, Begueret H, Wulff H, Marthan R, Bradding P, and Berger P
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- Animals, Cytokines biosynthesis, Enzyme-Linked Immunosorbent Assay, Female, Flow Cytometry, Immunohistochemistry, Mice, Mice, Inbred BALB C, Airway Remodeling drug effects, Disease Models, Animal, Eosinophilia prevention & control, Potassium Channels, Calcium-Activated antagonists & inhibitors, Pyrazoles pharmacology
- Abstract
Key features of asthma include bronchial hyperresponsiveness (BHR), eosinophilic airway inflammation, and bronchial remodeling, characterized by subepithelial collagen deposition, airway fibrosis, and increased bronchial smooth muscle (BSM) mass. The calcium-activated K(+) channel K(Ca)3.1 is expressed by many cells implicated in the pathogenesis of asthma, and is involved in both inflammatory and remodeling responses in a number of tissues. The specific K(Ca)3.1 blocker 5-[(2-chlorophenyl)(diphenyl)methyl]-1H-pyrazole (TRAM-34) attenuates BSM cell proliferation, and both mast cell and fibrocyte recruitment in vitro. We aimed to examine the effects of K(Ca)3.1 blockade on BSM remodeling, airway inflammation, and BHR in a murine model of chronic asthma. BALB/c mice were sensitized with intraperitoneal ovalbumin (OVA) on Days 0 and 14, and then challenged with intranasal OVA during Days 14-75. OVA-sensitized/challenged mice received TRAM-34 (120 mg/kg/day, subcutaneous) from Days -7 to 75 (combined treatment), Days -7 to 20 (preventive treatment), or Days 21 to 75 (curative treatment). Untreated mice received daily injections of vehicle (n = 8 per group). Bronchial remodeling was assessed by histological and immunohistochemical analyses. Inflammation was evaluated using bronchoalveolar lavage and flow cytometry. We also determined BHR in both conscious and anesthetized mice via plethysmography. We demonstrated that curative treatment with TRAM-34 abolishes BSM remodeling and subbasement collagen deposition, and attenuates airway eosinophilia. Although curative treatment alone did not significantly reduce BHR, the combined treatment attenuated nonspecific BHR to methacholine. This study indicates that K(Ca)3.1 blockade could provide a new therapeutic strategy in asthma.
- Published
- 2013
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16. Interstitial guidance of cancer invasion.
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Gritsenko PG, Ilina O, and Friedl P
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- Adipose Tissue pathology, Blood Vessels pathology, Cadherins physiology, Cell Adhesion Molecules physiology, Cell Movement physiology, Collagen physiology, Dystroglycans physiology, Extracellular Matrix pathology, Female, Humans, Hyaluronan Receptors physiology, Immunoglobulin G physiology, Integrins physiology, Mammary Glands, Human pathology, Neoplasm Invasiveness pathology, Nerve Fibers, Myelinated pathology, Receptors, Cell Surface physiology, Syndecans physiology, Brain Neoplasms pathology, Breast Neoplasms pathology, Carcinoma, Ductal, Breast pathology, Glioma pathology
- Abstract
Cancer cell invasion into healthy tissues develops preferentially along pre-existing tracks of least resistance, followed by secondary tissue remodelling and destruction. The tissue scaffolds supporting or preventing guidance of invasion vary in structure and molecular composition between organs. In the brain, the guidance is provided by myelinated axons, astrocyte processes, and blood vessels which are used as invasion routes by glioma cells. In the human breast, containing interstitial collagen-rich connective tissue, disseminating breast cancer cells preferentially invade along bundled collagen fibrils and the surface of adipocytes. In both invasion types, physical guidance prompted by interfaces and space is complemented by molecular guidance. Generic mechanisms shared by most, if not all, tissues include (i) guidance by integrins towards fibrillar interstitial collagen and/or laminins and type IV collagen in basement membranes decorating vessels and adipocytes, and, likely, CD44 engaging with hyaluronan; (ii) haptotactic guidance by chemokines and growth factors; and likely (iii) physical pushing mechanisms. Tissue-specific, resticted guidance cues include ECM proteins with restricted expression (tenascins, lecticans), cell-cell interfaces, and newly secreted matrix molecules decorating ECM fibres (laminin-332, thrombospondin-1, osteopontin, periostin). We here review physical and molecular guidance mechanisms in interstitial tissue and brain parenchyma and explore shared principles and organ-specific differences, and their implications for experimental model design and therapeutic targeting of tumour cell invasion., (Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.)
- Published
- 2012
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17. Two-photon laser-generated microtracks in 3D collagen lattices: principles of MMP-dependent and -independent collective cancer cell invasion.
- Author
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Ilina O, Bakker GJ, Vasaturo A, Hofmann RM, and Friedl P
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- Animals, Cell Movement, Female, Humans, Lasers, Mammary Neoplasms, Animal metabolism, Mice, Microtechnology, Neoplasms metabolism, Neoplasms pathology, Spheroids, Cellular, Tissue Scaffolds chemistry, Tumor Cells, Cultured, Collagen metabolism, Mammary Neoplasms, Animal pathology, Matrix Metalloproteinases metabolism, Neoplasm Invasiveness pathology
- Abstract
Cancer invasion into an extracellular matrix (ECM) results from a biophysical reciprocal interplay between the expanding cancer lesion and tissue barriers imposed by the adjacent microenvironment. In vivo, connective tissue provides both densely packed ECM barriers adjacent to channel/track-like spaces and loosely organized zones, both of which may impact cancer invasion mode and efficiency; however little is known about how three-dimensional (3D) spaces and aligned tracks present in interstitial tissue guide cell invasion. We here describe a two-photon laser ablation procedure to generate 3D microtracks in dense 3D collagen matrices that support and guide collective cancer cell invasion. Whereas collective invasion of mammary tumor (MMT) breast cancer cells into randomly organized collagen networks required matrix metalloproteinase (MMP) activity for cell-derived collagen breakdown, re-alignment and track generation, preformed tracks supported MMP-independent collective invasion down to a track caliber of 3 µm. Besides contact guidance along the track of least resistance and initial cell deformation (squeezing), MMP-independent collective cell strands led to secondary track expansion by a pushing mechanism. Thus, two-photon laser ablation is useful to generate barrier-free microtracks in a 3D ECM which guide collective invasion independently of pericellular proteolysis.
- Published
- 2011
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18. Mechanisms of collective cell migration at a glance.
- Author
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Ilina O and Friedl P
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- Animals, Cell Adhesion, Cell Polarity, Humans, Morphogenesis, Neoplasms pathology, Wound Healing, Cell Movement
- Published
- 2009
- Full Text
- View/download PDF
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