Relevant bibliographies by topics / CXCR2 receptor

Academic literature on the topic 'CXCR2 receptor'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "CXCR2 receptor"

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Zhang, Jing, Shouguo Huang, Lini Quan, Qiu Meng, Haiyan Wang, Jie Wang, and Jin Chen. "Determination of Potential Therapeutic Targets and Prognostic Markers of Ovarian Cancer by Bioinformatics Analysis." BioMed Research International 2021 (March 19, 2021): 1–13. http://dx.doi.org/10.1155/2021/8883800.

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This study is to study the expression of CXCRs in ovarian cancer tissues and their value in prognosis. The expressions of CXCR1-CXCR7 mRNA between ovarian tumor tissues and normal tissues and in different pathological types of ovarian tumor tissues were compared by ONCOMINE online tool. The relationship between the expression of CXCRs and clinical pathological staging was studied by GEPIA. Kaplan-Meier plotter online tool was used to analyze prognosis. Finally, GO and KEGG analyses and protein interaction network analysis were performed for CXCRs by the DAVID software to predict their function, and cBioPortal was used to identify the key functional genes. The expression of CXCR3/4/7 mRNA in ovarian cancer tissues was higher than that in normal ovarian tissues, and the expression of CXCR4 was the highest ( fold change = 306.413 , P < 0.05 ). The expression of CXCR1/2/3/4/7 mRNA in different pathological types of ovarian tumors was significantly different ( P < 0.05 ). Only CXCR5 expression level was associated with tumor staging. Survival analysis showed that high CXCR7 mRNA expression and low CXCR5/6 expression were associated with the shortening of overall survival. High CXCR4/7 expression and low CXCR5/6 expression were associated with the shortening of progression-free survival. High CXCR2/4 expression and low CXCR5/6 expression were closely related to the shortening of postprogressing survival. Protein interaction network analysis showed that GNB1, PTK2, MAPK1, PIK3CA, GNB4, GNA11, KNG1, and ARNT proteins were closely related to the CXC receptor family. CXCR3/4/7 are potential therapeutic targets, and CXCR2/4/5/6/7 are new markers for the prognosis of ovarian cancer.
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Korbecki, Jan, Klaudyna Kojder, Patrycja Kapczuk, Patrycja Kupnicka, Barbara Gawrońska-Szklarz, Izabela Gutowska, Dariusz Chlubek, and Irena Baranowska-Bosiacka. "The Effect of Hypoxia on the Expression of CXC Chemokines and CXC Chemokine Receptors—A Review of Literature." International Journal of Molecular Sciences 22, no. 2 (January 15, 2021): 843. http://dx.doi.org/10.3390/ijms22020843.

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Hypoxia is an integral component of the tumor microenvironment. Either as chronic or cycling hypoxia, it exerts a similar effect on cancer processes by activating hypoxia-inducible factor-1 (HIF-1) and nuclear factor (NF-κB), with cycling hypoxia showing a stronger proinflammatory influence. One of the systems affected by hypoxia is the CXC chemokine system. This paper reviews all available information on hypoxia-induced changes in the expression of all CXC chemokines (CXCL1, CXCL2, CXCL3, CXCL4, CXCL5, CXCL6, CXCL7, CXCL8 (IL-8), CXCL9, CXCL10, CXCL11, CXCL12 (SDF-1), CXCL13, CXCL14, CXCL15, CXCL16, CXCL17) as well as CXC chemokine receptors—CXCR1, CXCR2, CXCR3, CXCR4, CXCR5, CXCR6, CXCR7 and CXCR8. First, we present basic information on the effect of these chemoattractant cytokines on cancer processes. We then discuss the effect of hypoxia-induced changes on CXC chemokine expression on the angiogenesis, lymphangiogenesis and recruitment of various cells to the tumor niche, including myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), regulatory T cells (Tregs) and tumor-infiltrating lymphocytes (TILs). Finally, the review summarizes data on the use of drugs targeting the CXC chemokine system in cancer therapies.
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Konrad, F. M., and J. Reutershan. "CXCR2 in Acute Lung Injury." Mediators of Inflammation 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/740987.

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In pulmonary inflammation, recruitment of circulating polymorphonuclear leukocytes is essential for host defense and initiates the following specific immune response. One pathological hallmark of acute lung injury and acute respiratory distress syndrome is the uncontrolled transmigration of neutrophils into the lung interstitium and alveolar space. Thereby, the extravasation of leukocytes from the vascular system into the tissue is induced by chemokines that are released from the site of inflammation. The most relevant chemokine receptors of neutrophils are CXC chemokine receptor (CXCR) 1 and CXCR2. CXCR2 is of particular interest since several studies implicate a pivotal role of this receptor in development and promotion of numerous inflammatory disorders. CXCR2 gets activated by ELR+chemokines, including MIP-2, KC (rodents) and IL-8 (human). Since multiple ELR+CXC chemokines act on both receptors—CXCR1 and CXCR2—a pharmacologic agent blocking both receptors seems to be advantageous. So far, several CXCR1/2 antagonists have been developed and have been tested successfully in experimental studies. A newly designed CXCR1 and CXCR2 antagonist can be orally administered and was for the first time found efficient in humans. This review highlights the role of CXCR2 in acute lung injury and discusses its potential as a therapeutic target.
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Daniele, Simona, Simona Saporiti, Stefano Capaldi, Deborah Pietrobono, Lara Russo, Uliano Guerrini, Tommaso Laurenzi, et al. "Functional Heterodimerization between the G Protein-Coupled Receptor GPR17 and the Chemokine Receptors 2 and 4: New Evidence." International Journal of Molecular Sciences 24, no. 1 (December 23, 2022): 261. http://dx.doi.org/10.3390/ijms24010261.

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GPR17, a G protein-coupled receptor, is a pivotal regulator of myelination. Its endogenous ligands trigger receptor desensitization and downregulation allowing oligodendrocyte terminal maturation. In addition to its endogenous agonists, GPR17 could be promiscuously activated by pro-inflammatory oxysterols and chemokines released at demyelinating lesions. Herein, the chemokine receptors CXCR2 and CXCR4 were selected to perform both in silico modelling and in vitro experiments to establish their structural and functional interactions with GPR17. The relative propensity of GPR17 and CXCR2 or CXCR4 to form homo- and hetero-dimers was assessed by homology modelling and molecular dynamics (MD) simulations, and co-immunoprecipitation and immunoenzymatic assay. The interaction between chemokine receptors and GPR17 was investigated by determining receptor-mediated modulation of intracellular cyclic adenosine monophosphate (cAMP). Our data show the GPR17 association with CXCR2 or CXCR4 and the negative regulation of these interactions by CXCR agonists or antagonists. Moreover, GPR17 and CXCR2 heterodimers can functionally influence each other. In contrast, CXCR4 can influence GPR17 functionality, but not vice versa. According to MD simulations, all the dimers reached conformational stability and negative formation energy, confirming the experimental observations. The cross-talk between these receptors could play a role in the development of the neuroinflammatory milieu associated with demyelinating events.
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Uhl, Barbara, Katharina T. Prochazka, Katrin Pansy, Kerstin Wenzl, Johanna Strobl, Claudia Baumgartner, Marta M. Szmyra, et al. "Distinct Chemokine Receptor Expression Profiles in De Novo DLBCL, Transformed Follicular Lymphoma, Richter’s Trans-Formed DLBCL and Germinal Center B-Cells." International Journal of Molecular Sciences 23, no. 14 (July 17, 2022): 7874. http://dx.doi.org/10.3390/ijms23147874.

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Chemokine receptors and their ligands have been identified as playing an important role in the development of diffuse large B-cell lymphoma (DLBCL), follicular lymphoma, and Richter syndrome (RS). Our aim was to investigate the different expression profiles in de novo DLBCL, transformed follicular lymphoma (tFL), and RS. Here, we profiled the mRNA expression levels of 18 chemokine receptors (CCR1–CCR9, CXCR1–CXCR7, CX3CR1 and XCR1) using RQ-PCR, as well as immunohistochemistry of seven chemokine receptors (CCR1, CCR4–CCR8 and CXCR2) in RS, de novo DLBCL, and tFL biopsy-derived tissues. Tonsil-derived germinal center B-cells (GC-B) served as non-neoplastic controls. The chemokine receptor expression profiles of de novo DLBCL and tFL substantially differed from those of GC-B, with at least 5-fold higher expression of 15 out of the 18 investigated chemokine receptors (CCR1–CCR9, CXCR1, CXCR2, CXCR6, CXCR7, CX3CR1 and XCR1) in these lymphoma subtypes. Interestingly, the de novo DLBCL and tFL exhibited at least 22-fold higher expression of CCR1, CCR5, CCR8, and CXCR6 compared with RS, whereas no significant difference in chemokine receptor expression profile was detected when comparing de novo DLBCL with tFL. Furthermore, in de novo DLBCL and tFLs, a high expression of CCR7 was associated with a poor overall survival in our study cohort, as well as in an independent patient cohort. Our data indicate that the chemokine receptor expression profile of RS differs substantially from that of de novo DLBCL and tFL. Thus, these multiple dysregulated chemokine receptors could represent novel clinical markers as diagnostic and prognostic tools. Moreover, this study highlights the relevance of chemokine signaling crosstalk in the tumor microenvironment of aggressive lymphomas.
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Coperchini, Francesca, Laura Croce, Michele Marinò, Luca Chiovato, and Mario Rotondi. "Role of chemokine receptors in thyroid cancer and immunotherapy." Endocrine-Related Cancer 26, no. 8 (August 2019): R465—R478. http://dx.doi.org/10.1530/erc-19-0163.

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Inflammation is currently regarded as an essential component of malignancies. It is now known that the tumor microenvironment may profoundly influence the biological behavior of cancer cells and ultimately the patient’s outcome. Chemokine and their receptor play a major role in determining the immune phenotype of the cells infiltrating the thyroid tumor microenvironment. Experimental evidence shows that both normal and cancer thyroid cells express specific chemokine receptors. The expression of at least some of these receptors exerts several biological effects, which influence the course of the disease. The present review article will take into account the role of the most studied chemokine receptors (CXCR1, CXCR2, CXCR3, CXCR4, CXCR7, DARC, CCR3, CCR6 and CCR7) in the context of thyroid cancer. This review will focus on current knowledge provided by in vitro and in vivo studies specifically performed on thyroid cancer including (i) expression of chemokine receptors in normal and cancer thyroid cells; (ii) role of chemokine receptors in affecting the biological behavior of thyroid tumors including the metastatic process; (iii) current knowledge about immunotherapies through targeting of chemokine receptors in thyroid cancer.
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Richardson, Micheler, Timothy Adekoya, Nikia Smith, and Parag Kothari. "Opposite effects of CXCR1 and CXCR2 overexpression in prostate tumorigenesis." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 178.12. http://dx.doi.org/10.4049/jimmunol.208.supp.178.12.

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Abstract Chemokines and their receptors play important role in tumor progression and metastasis. In prostate cancer (PCa), some members of the CXC chemokine receptor have been shown to enhance angiogenesis, proliferation and metastasis. In this study we assess the roles of the interleukin-8 (IL-8/CXCL8) receptors CXCR1 and CXCR2 in prostate tumorigenesis, using MDA PCa 2b and LNCaP cell lines. Our results show that overexpression of CXCR2 enhanced in-vitro cell proliferation, soft agar growth and in-vivo tumor xenograft in nude mice, whereas overexpression of CXCR1 inhibited cell proliferation and tumor growth, relative to control cells. CXCR1 cells showed decrease prostate specific antigen (PSA) expression whereas CXCR2 exhibited decrease androgen receptor (AR) expression. Interestingly, tumor lysates from CXCR1 cells displayed significant increase in ERK and AKT activation as well as chemokines production relative to control and CXCR2 tumors. CXCR1 tumors also exhibited a more mesenchymal phenotype, characterized by reduced E-Cadherin but increased N-Cadherin and Vimentin expression relative to CXCR2 or control tumors. Altogether, these results indicate that CXCR1 and CXCR2 may couple to distinct pathways to modulate prostate tumorigenesis. Supported by CA156735, MD012392
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Yildirim, Sedat, Frank Bautz, Andreas M. Boehmler, Lothar Kanz, and Robert Möhle. "Regulation of CXCR1, CXCR2 and CXCR4 in Human Neutrophils: Potential Role in the Release from the Bone Marrow, Clearance of Senescent Cells, and Cell Function at Sites of Inflammation." Blood 106, no. 11 (November 16, 2005): 3068. http://dx.doi.org/10.1182/blood.v106.11.3068.3068.

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Abstract In the mouse model, it has been shown that the interleukin-8 (IL-8) receptor CXCR2 is involved in the release of mature neutrophils from the bone marrow into the circulation. When neutrophils age, upregulation of CXCR4 and downmodulation of CXCR2 result in homing and subsequent sequestration of senescent cells in the bone marrow. In our study, we observed a similar time-dependent (starting at 3 hrs., maximum at 12–18 hrs.) downregulation of CXCR2 in human neutrophils during aging in ex vivo culture, while expression of the second IL-8 receptor CXCR1, which is mainly responsible for the IL-8-induced chemotaxis, was unchanged. Furthermore, strong upregulation of CXCR4 was noted on the cell surface which could not solely be attributed to re-expression of internalized, intracellular receptors, as an increased amount of CXCR4 mRNA was detected by Northern blot analysis in these cells. The increase in CXCR4 expression was not influenced by inflammatory cytokines such as TNF and IL-1, as well as by IL-8 or G-CSF. Accordingly, SDF-1-induced transendothelial migration of aged neutrophils was 6-fold increased and even exceeded migration in response to IL-8. We conclude that also in human neutrophils, loss of CXCR2 and gain of CXCR4 expression on the cell surface may favor homing and sequestration of senescent cells in the bone marrow. At sites of inflammation however, retained expression of CXCR1 and increased expression of CXCR4 still allow a response of aged, pre-apoptotic neutrophils to the chemotactic mediators IL-8 and SDF-1, as the latter is not only released in the bone marrow, but also at sites of tissue damage and necrosis.
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Schmausser, Bernd, Christine Josenhans, Simon Endrich, Sebastian Suerbaum, Cassian Sitaru, Mindaugas Andrulis, Stephanie Brändlein, Peter Rieckmann, Hans Konrad Müller-Hermelink, and Matthias Eck. "Downregulation of CXCR1 and CXCR2 Expression on Human Neutrophils by Helicobacter pylori: a New Pathomechanism in H. pylori Infection?" Infection and Immunity 72, no. 12 (December 2004): 6773–79. http://dx.doi.org/10.1128/iai.72.12.6773-6779.2004.

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ABSTRACT In Helicobacter pylori gastritis, neutrophil activation and migration, which play central roles in the pathogenesis of the disease, are regulated by the neutrophil attractant chemokines interleukin 8 (IL-8) and Groα, whose secretion is induced by H. pylori. However, the modulation of the corresponding chemokine receptors CXCR1 and CXCR2 on human neutrophils under the influence of H. pylori has not been investigated. Incubation of neutrophils with cag + and cag deletion H. pylori strains resulted in a complete downregulation of the CXCR1 and the CXCR2 receptors after 0.5 h, as tested by fluorescence-activated cell sorter analysis, independent of the cag status. Downregulation of CXCR1 and CXCR2 seems to occur via receptor internalization and rapid degradation, as shown by confocal microscopy and immunoblotting. Neither the proinflammatory cytokines IL-8 and tumor necrosis factor alpha produced by the neutrophils themselves nor H. pylori lipopolysaccharide, which are the known regulators of these two chemokine receptors, was responsible for the downregulation. Reverse transcription-PCR analysis showed that CXCR1 and CXCR2 mRNAs of neutrophils were reduced at a later time than the CXCR1 and CXCR2 proteins. Moreover, cag + H. pylori strains induced significantly stronger downregulation of CXCR1 and CXCR2 mRNAs than the cag deletion mutant. Therefore, receptor protein and mRNA downregulation seem to be mediated by two independent mechanisms. Data obtained by immunohistochemistry suggested that downmodulation of CXCR1 and CXCR2 on neutrophils may also occur in vivo in the human stomach during H. pylori infection. Downregulation of CXCR1 and CXCR2 expression on neutrophils in H. pylori infection by H. pylori itself may represent a new mechanism of modulating neutrophil migration and activation in the gastric mucosa.
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Khandaker, Masud H., Gordon Mitchell, Luoling Xu, Joseph D. Andrews, Rajkumari Singh, Harry Leung, Joaquı́n Madrenas, Stephen S. G. Ferguson, Ross D. Feldman, and David J. Kelvin. "Metalloproteinases Are Involved in Lipopolysaccharide– and Tumor Necrosis Factor-–Mediated Regulation of CXCR1 and CXCR2 Chemokine Receptor Expression." Blood 93, no. 7 (April 1, 1999): 2173–85. http://dx.doi.org/10.1182/blood.v93.7.2173.

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Abstract The neutrophil-specific G-protein–coupled chemokine receptors, CXCR1 and CXCR2, bind with high affinity to the potent chemoattractant interleukin-8 (IL-8). The mechanisms of IL-8 receptor regulation are not well defined, although previous studies have suggested a process of ligand-promoted internalization as a putative regulatory pathway. Herein, we provide evidence for two distinct processes of CXCR1 and CXCR2 regulation. Confocal microscopy data showed a redistribution of CXCR1 expression from the cell surface of neutrophils to internal compartments after stimulation with IL-8, whereas stimulation with bacterial lipopolysaccharide (LPS) or tumor necrosis factor- (TNF-) did not induce CXCR1 internalization but instead mediated a significant loss of membrane-proximal CXCR1 staining intensity. To investigate whether proteolytic cleavage was the mechanism responsible for LPS- and TNF-–induced downmodulation of IL-8 receptors, we tested a panel of proteinase inhibitors. The downmodulation of CXCR1 and CXCR2 by LPS and TNF- was most dramatically inhibited by metalloproteinase inhibitors; 1,10-phenanthroline and EDTA significantly attenuated LPS- and TNF-–induced loss of CXCR1 and CXCR2 cell surface expression. Metalloproteinase inhibitors also blocked the release of CXCR1 cleavage fragments into the cell supernatants of LPS- and TNF-–stimulated neutrophils. In addition, while treatment of neutrophils with LPS and TNF- inhibited IL-8 receptor–mediated calcium mobilization and IL-8–directed neutrophil chemotaxis, both 1,10-phenanthroline and EDTA blocked these inhibitory processes. In contrast, metalloproteinase inhibitors did not affect IL-8–mediated downmodulation of CXCR1 and CXCR2 cell surface expression or receptor signaling. Thus, these findings may provide further insight into the mechanisms of leukocyte regulation during immunologic and inflammatory responses.
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Dissertations / Theses on the topic "CXCR2 receptor"

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Williams, Mark Anthony. "DISPARATE REGULATION OF NEUTROPHIL PRO-INFLAMMATORY FUNCTIONING BY CXCR2-SELECTIVE CHEMOKINES." University of Cincinnati / OhioLINK, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=ucin971879221.

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RACCOSTA, LAURA. "Tumour-released Liver X Receptor ligands attract tumour promoting neutrophils in a CXCR2 dependent manner." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/28479.

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Tumour formation is the result of molecular alterations involving cellular regulators as well as the ability of tumor cells to affect the tumor microenvironment through smoldering inflammation, or even taking advantage of inflammation to grow and metastasize. Tumour microenvironment is composed of various cell types, among them neutrophils are recognized as playing an important pro-tumorigenic role, by promoting neoangiogenesis and/or by suppressing antitumor immune responses. We have recently shown that ligands of liver X receptors (LXRs), which are involved in cholesterol homeostasis and in modulating immune responses, are released by cancer cells and suppress antitumor immune responses by dampening dendritic cell migration to draining lymph nodes. Here, we report that natural and tumour-derived LXR ligands attract a subpopulation of bone marrow (BM)- derived cells in a LXR independent, CXCR2 dependent manner. These cells have phenotypic (CD11bhighGr1highLy6G+) and morphological features of neutrophils and favour initial tumour angiogenesis. Moreover, the in vivo inactivation of LXR ligands, the depletion of neutrophils, as well as the pharmacologic and genetic inactivation of CXCR2 inhibit neutrophil recruitment to the tumour and delay tumour growth. Our data reveal an unanticipated chemoattractant role for tumour-derived LXR ligands in promoting tumour growth that relies on the CXCR2-mediated recruitment of neutrophils, thus identifying a new therapeutic target for cancer patients.
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Padovani-Claudio, Dolly Ann. "Functional analysis of the chemokine receptor Cxcr2 in the normal and demyelinated adult central nervous system." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1152193193.

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Padovani-Claudio, Dolly Ann. "FUNCTIONAL ANALYSES OF THE CHEMOKINE RECEPTOR CXCR2 IN THE NORMAL AND DEMYELINATED ADULT CENTRAL NERVOUS SYSTEM." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1152193193.

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Russo, Remo de Castro. "Efeito da administração do antagonista de receptor CXCR2 no modelo de fibrose pulmonar induzida por bleomicina." Universidade Federal de Minas Gerais, 2005. http://hdl.handle.net/1843/UCSD-8FTN2Z.

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Pulmonary fibrosis is a disease characterized by progressive interstitial collagen deposition, which causes changes in the normal lung architecture and loss of function, which could lead to death. Acute pulmonary inflammatory processes and their chronification are associated with fibrotic phenomena acting as triggering events. The inflammation that precedes the emergence of pulmonary fibrosis is characterized by an increased cell influx, which culminates in the liberation of inflammatory mediators, which perpetuate the initial lesion. Therefore it is likely that the inhibition of the inflammatory response might be able to decrease the interstitial collagen deposition. The bleomycin-induced pulmonary fibrosis model is characterized by intense neutrophil influx concomitant with cytokine production, high levels of chemokines CXCL1-3/KC and CXCL1-2/MIP-2, followed by collagen deposition on the pulmonary parenchyma. In this study, we analyzed the effects of DF2162 administration, which is a CXCR2 chemokine receptor antagonist on bleomycin-induced pulmonary fibrosis model in mice. Our results show that the administration of 6 mg/kg of DF2162 twice a day significantly inhibited the neutrophilic influx peaks caused by intra-tracheal instillation of 0,125 U of bleomycin. However, DF2162 did not promote changes in the levels of modulatory cytokines such as IFN, IL-10 e VEGF, which are important for the inflammatory process. We did not observe changes in the levels of chemokines CXCL1-3/KC, CXCL1-2/MIP-2, CCL2/JE, CCL3/MIP-1 and CXCL10/IP-10 with the exception of CCL5/RANTES, whose production was inhibited and CXCL9/MIG, whose levels incresased during the early phase of DF2162 treatment. Furthermore, we observed pathological changes revealing less severe and reduced interstitial collagen deposition in the lungs of DF2162-treated animals. In spite of the observed improvement in all inflammatory aspects studied, the animals receiving DF2162 had a higher mortality (66.6%) than the animals in the control group, which showed only 25% lethality.These data suggest that the CXCR2 receptor exerts an important role in the regulation of the inflammatory process and pulmonary fibrosis induced by bleomycin. Notwithstanding, the increment in letality in the group of mice that received DF2162 treatment after bleomycin instillation is likely not associated with the fibrotic process itself, but depends on factors which shall be later studied.
A fibrose pulmonar é uma doença caracterizada pela deposição intersticial progressiva de colágeno, que acarreta alterações na arquitetura normal pulmonar e perda da função, podendo levar ao óbito. As inflamações agudas pulmonares e a sua cronificação estão associadas a fenômenos fibróticos, sendo responsáveis por seu desencadeamento. A inflamação que precede a instalação da fibrose pulmonar é caracterizada pelo influxo de células inflamatórias, culminando na liberação de mediadores que perpetuam o dano inicial. Desta forma, é provável que a inibição da resposta inflamatória seja capaz de diminuir a deposição de colágeno intersticial. O modelo de fibrose pulmonar induzido por bleomicina é caracterizado por um intenso influxo de neutrófilos, concomitantemente com uma produção de citocinas, níveis elevados das quimiocinas CXCL1-3/KC e CXCL1-2/MIP-2, e posterior deposição de colágeno no parênquima pulmonar.No presente trabalho, estudamos os efeitos da administração do DF2162, um antagonista de receptores de quimiocinas CXCR2, no modelo experimental de fibrose pulmonar induzida por bleomicina em camundongos. Nossos dados mostram que a administração da dose de 6 mg/kg de DF2162, duas vezes ao dia, inibiu de forma significativa os picos de influxo neutrofílicos após administração de 0,125 U de bleomicina por via intra-traqueal. Entretanto, DF2162 não alterou os níveis das citocinas de caráter modulatório tais como IFN, IL-10 e VEGF, importantes para o processo inflamatório. As quimiocinas CXCL1-3/KC, CXCL1-2/MIP-2, CCL2/JE, CCL3/MIP-1 e CXCL10/IP-10 quantificadas também não apresentaram mudanças no seu perfil de produção, com exceção para CCL5/RANTES, que foi inibida, e CXCL9/MIG, que apresentou níveis elevados numa fase mais inicial, pelo tratamento com este antagonista. Além disso, foram verificadas alterações patológicas que revelaram uma inflamação menos severa e uma menor de deposição de colágeno intersticial no pulmão dos animais tratados com DF2162. Entretanto, apesar de uma melhora em todos os aspectos inflamatórios estudados, os animais que receberam DF2162 apresentaram um índice de letalidade de 66,6%; enquanto que no grupo controle foi observado a morte de apenas 25% dos animais.Estes dados em conjunto sugerem que o receptor CXCR2 exerça papel importante na regulação do processo inflamatório e fibrose pulmonar induzida por bleomicina. Apesar disso, o incremento na taxa de letalidade no grupo de animais que receberam tratamento com DF2162 após instilação de bleomicina provavelmente não está relacionado ao processo fibrótico em si, mas depende de outros fatores que serão investigados em estudos posteriores.
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Wilson, Shirley Risk. "Oligomerisation of chemokine receptors CXCR1 and CXCR2." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418346.

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Trevelin, Silvia Cellone. "Papel do receptor toll-like 9 na falência de migração dos neutrófilos na sepse." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-14082013-055722/.

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O recrutamento de neutrófilos para o sítio da infecção é um evento crucial para o combate aos microrganismos e sobrevivência na sepse. A migração destes polimorfonucleares é dirigida através de um gradiente quimiotático por meio do reconhecimento de quimiocinas por receptores acoplados a proteína G (GPCRs), os quais são regulados por quinases específicas (GRKs). Estudos prévios demonstraram que na sepse ocorre uma falência na migração de neutrófilos para o foco infeccioso em função da dessensibilização de receptores quimiotáticos via GRKs induzida pela ativação de receptores toll-like (TLRs), TLR2 e TLR4. Apesar de a ausência de TLR9 em células dendriticas ter sido relacionada a maior sobrevivência de camundongos sépticos, o papel do TLR9 atuando diretamente em neutrófilos não foi avaliado. Objetivando preencher esta lacuna, propôs-se avaliar o papel direto de TLR9 na falência de migração de neutrófilos na sepse. Os camundongos TLR9-/- apresentaram maior sobrevivência a sepse polimicrobiana avaliada por meio do modelo de ligadura e perfuração do ceco (CLP). A deficiência de TLR9 também acarretou em aumento na migração de neutrófilos para o foco da infecção, menor seqüestro de neutrófilos no pulmão, bem como, menor número de bactérias no lavado peritoneal e sangue. A ativação de TLR9 por oligodeoxinucleotídeo contendo o dinucleotídeo CpG não metilado (ODN CpG) nos neutrófilos reduziu a quimiotaxia destes em direção a quimiocina CXCL2 e expressão do receptor quimiotático CXCR2. Além disso, neutrófilos estimulados com ODN CpG apresentaram aumento na expressão da quinase tipo 2 relacionada a receptores acoplados a proteína G (GRK2). Dessa forma, a ativação de TLR9 em neutrófilos circulantes no sangue é prejudicial na sepse por reduzir a quimiotaxia destes para o foco da infecção ao induzir a dessensibilização de CXCR2 via GRK2.
The recruitment of neutrophils to the site of infection is a crucial event for combating the microorganisms and survival on sepsis. The neutrophil migration is directed by a chemotactic gradient through the recognition of chemokines by G protein-coupled receptors (GPCRs), which are regulated by specific kinases (GRKs). Previous studies have shown a failure of neutrophil migration into infectious focus on sepsis due to chemotactic receptor desensitization via GRKs induced by activation of toll- like receptors (TLRs), TLR2 and TLR4. Despite the absence of activation of TLR9 in dendritic cells have been related to increase survival of septic mice, the role of TLR9 acting directly on neutrophils was not evaluated. We proposed to verify the direct role of TLR9 in the failure of neutrophil migration on sepsis. The TLR9 knockout mice (TLR9-/-) showed high survival to polymicrobial sepsis using cecal ligation and puncture model (CLP). TLR9-/- mice had high neutrophil migration to the focus of infection, low neutrophil sequestration in the lung, as well as, few bacteria in the peritoneal exudates and blood. The activation of TLR9 by oligodeoxinucleotide containing unmethylated dinucleotide CpG (CpG ODN) in neutrophils also reduced chemotaxis toward CXCL2 and the expression of chemokine receptor CXCR2. In addition, neutrophils stimulated with CpG ODN showed increased expression of kinase-related G protein-coupled receptor type 2 (GRK2). Thus, the activation of TLR9 in blood circulating neutrophils is harmful on sepsis by reducing their chemotaxis into the site of the infection by inducing CXCR2 desensitization via GRK2.
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Kiss, Debra Lois. "Regulation of the Chemokine Receptors CXCR4, CXCR7 , and the Androgen Receptor in Prostate Cancer." Thesis, Griffith University, 2013. http://hdl.handle.net/10072/367690.

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The chemokine receptor CXCR4 contributes to tumour cell migration and invasion during the progression of prostate cancer. In particular, this pathway is central to the metastasis of prostate cancer to the bone marrow. Limited therapeutic options exist for prostate cancer patients who have progressed to advanced metastatic disease, and pharmacological interference of the chemokine network may serve to control tumour cell dissemination and the establishment of metastasis. A more detailed knowledge of the mechanisms regulating chemokine receptors is required, in order to further characterise and explore the capacity and effectiveness of targeting these pathways for therapeutic intervention in prostate cancer. Here, the regulation of CXCR4 protein expression and function was investigated in relation to androgens and the extracellular matrix. Accumulating evidence of CXCR4 regulation by androgens and the androgen receptor have indicated that androgens not only promote the growth and development of prostate cancer, but may actively contribute to the metastatic progression of prostate through modulation of the chemokine network. In the current study, the endogenous protein expression and functionality of the androgen receptor were firstly characterised in the androgen-insensitive prostate cancer cell lines DU145 and PC3, using the androgen-sensitive LNCaP cells as a basis for comparison. Investigations were performed using two-dimensional culture in conjunction with the more physiologically relevant three-dimensional in vitro culture model.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Eskitis Institute for Cell and Molecular Therapies
Science, Environment, Engineering and Technology
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Bento, Allisson Freire. "Efeito do SB225002, antagonista seletivo do receptor para quimiocinas CXCR2, no modelo de colite induzida pelo ácido 2,4,6-trinitrobenzeno sulfônico (TNBS) em camundongos." reponame:Repositório Institucional da UFSC, 2012. http://repositorio.ufsc.br/xmlui/handle/123456789/92097.

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Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas, Programa de Pos-Graduação em Farmacologia, Florianópolis, 2008.
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Os neutrófilos são células importantes para a eliminação de patógenos, no entanto, o recrutamento excessivo dessas células pode levar a lesão tecidual. Essa migração é mediada pelas quimiocinas CXC, e seus receptores, CXCR1 e CXCR2 presentes nos neutrófilos. Dessa forma, a redução do influxo de células durante o processo inflamatório, através da inibição desses receptores, pode ser uma alternativa terapêutica apropriada para o tratamento de inúmeras doenças inflamatórias, como as doenças inflamatórias intestinais (IBD). O presente estudo buscou avaliar se o tratamento sistêmico curativo com antagonista seletivo para o receptor CXCR2, SB225002, era capaz de reduzir a inflamação intestinal, no modelo de colite induzida pelo TNBS em camundongos. O SB225002 (SB) ou dexametasona (DEX) (controle positivo) foram administrados 24 h após a indução da colite, de 12 em 12 horas por três dias. No terceiro dia após a indução da colite, os animais foram sacrificados e diferentes parâmetros inflamatórios foram avaliados. A administração do TNBS induziu danos macro e microscópicos no cólon dos animais, encurtamento e edema desse tecido, além de aumento do peso do baço, causando, em muitos casos, a morte dos animais. Os tratamentos com SB ou DEX reduziram de forma significativa todos os parâmetros analisados, demonstrando uma melhoria no quadro inflamatório. Alguns dos mecanismos envolvidos nos efeitos do SB também foram analisados. O tratamento sistêmico reduziu o influxo de neutrófilos, a atividade da enzima MPO, os níveis de IL-1ß e KC além da expressão das proteínas VEGF, iNOS e COX-2, no cólon dos animais. Adicionalmente, os níveis das citocinas antiinflamatórias IL-4 e IL-10 estavam aumentados no cólon de animais que receberam SB. Dessa forma, nossos resultados demonstraram que o bloqueio seletivo do receptor CXCR2, através da ação do antagonista SB, se mostrou eficaz em reduzir a inflamação colonica no modelo de colite induzida por TNBS, sugerindo que o SB é um potencial agente terapêutico para o tratamento das doenças inflamatórias intestinais.
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Khurram, Syed Ali. "The chemokine receptors XCR1, CXCR1 and CXCR2 regulate oral epithelial cell behaviour." Thesis, University of Sheffield, 2008. http://etheses.whiterose.ac.uk/10311/.

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Chemokines are chemoattractant cytokines which act on specific receptors and play an important role in tumour biology. The aim of this project was to determine whether the chemokine receptors XCRl, CXCRl and CXCR2 and their respective ligands lymphotactin, IL-8 (CXCRl&2) and GRO-a regulate the behaviour of normal and malignant oral epithelial cells. XCRl, CXCRl and CXCR2 mRNA and surface protein expression was detected in normal and oral cancer cell lines. Lymphotactin, IL-8 and GRO-a facilitated intracellular activation of ERK1/2 signaling pathway and stimulated migration, invasion and proliferation of all cells. These effects were mediated through XCRl for lymphotactin, CXCRl and CXCR2 for IL-8 and CXCR2 for GRO-a. The cancer cells showed a greater response than normal cells and a direct relationship between receptor expression and migration, invasion and proliferation was observed. XCRl but not lymphotactin was expressed by epithelial cells in normal oral mucosa in vivo and both were expressed and upregulated in inflammation and cancer. Constitutive expression of both XCRl and lymphotactin was found in regional lymph nodes and on metastatic tumours. Lymphotactin mRNA al}d constitutive intracellular protein was detected in normal and cancerous oral cells. Exposure of normal cells to lymphotactin resulted in increased adhesion to fibronectin but not collagen and stimulated MMP-2 and -9 release whereas exposure of cancer cells resulted in increased adhesion to both collagen and fibronectin and stimulated MMP-2, 9 and MMP-7 release. These findings show for the first time that XCRl and its ligand lymphotactin are expressed by epithelial cells in a range of oral conditions and strongly suggest that they play an important role in regulating the behaviour of normal and malignant epithelial cells. Similarly CXCRl and CXCR2 are upregulated on malignant oral cells in vitro and may be important in the biology of oral cancer.
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Books on the topic "CXCR2 receptor"

1

Fruehauf, Stefan, W. Jens Zeller, and Gary Calandra. Novel Developments in Stem Cell Mobilization: Focus on CXCR4. Springer, 2014.

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Fruehauf, Stefan, W. Jens Zeller, and Gary Calandra. Novel Developments in Stem Cell Mobilization: Focus on CXCR4. Springer, 2012.

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Livingston, Schuyler, Benjamin Young, Martin Markowitz, Poonam Mathur, and Bruce L. Gilliam. HIV Virology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0017.

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HIV is a member of the lentivirus subfamily of retroviruses. Two distinct groups of viruses are pathogenic in humans: HIV-1 and HIV-2. Both are transmitted sexually and known to cause immunodeficiency disease. HIV enters the cell through use of the CD4 receptor and chemokine co-receptors, primarily CCR5 and CXCR4. The viral genome is transcribed from RNA to DNA by reverse transcriptase and integrated into the host genome by integrase. The HIV genome encodes 15 proteins, comprising three categories: structural, regulatory, and accessory. After budding from the host cell, the virus matures into its infectious form through cleavage of viral precursor proteins by protease.
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Noels, Heidi, and Jürgen Bernhagen, eds. The CXCR4 Ligand/Receptor Family and the DPP4 Protease in High-Risk Cardiovascular Patients. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-858-0.

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Novel Developments In Stem Cell Mobilization Focus On Cxcr4. Springer, 2012.

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Book chapters on the topic "CXCR2 receptor"

1

Sarau, Henry M., Katherine L. Widdowson, Michael R. Palovich, John R. White, David C. Underwood/surname, and Don E. Griswold. "Interleukin-8 Receptor (CXCR2) Antagonists." In New Drugs for Asthma, Allergy and COPD, 293–96. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062157.

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Lam, Clarissa, Mahmud Arif Pavel, Parul Kashyap, Zahra Salehi-Najafabadi, Victoria Valentino, and Yong Yu. "Detection of CXCR2 Cytokine Receptor Surface Expression Using Immunofluorescence." In Cytokine Bioassays, 193–200. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0928-5_17.

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Blay, Jonathan. "Chemokine Receptor CXCR4." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1067-3.

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Blay, Jonathan. "Chemokine Receptor CXCR4." In Encyclopedia of Cancer, 932–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_1067.

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Furusato, Bungo, and Johng S. Rhim. "CXCR4 and Cancer." In Chemokine Receptors in Cancer, 31–45. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-267-4_2.

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Li, Yanchun, and Amy M. Fulton. "The CXCR3/CXCL3 Axis in Cancer." In Chemokine Receptors in Cancer, 79–91. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-267-4_5.

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Wijtmans, Maikel, Iwan J. P. de Esch, and Rob Leurs. "Therapeutic Targeting of the CXCR3 Receptor." In Methods and Principles in Medicinal Chemistry, 301–22. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527631995.ch13.

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Woodard, Lauren E., and Sridhar Nimmagadda. "Molecular Imaging of CXCR4 Receptor Expression in Tumors." In Novel Developments in Stem Cell Mobilization, 399–420. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-1960-0_21.

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Calì, Corrado, Julie Marchaland, Osvaldo Mirante, and Paola Bezzi. "Chemokines as Neuromodulators: Regulation of Glutamatergic Transmission by CXCR4-Mediated Glutamate Release From Astrocytes." In Chemokine Receptors and NeuroAIDS, 271–300. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_12.

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Sengupta, Rajarshi, and Olimpia Meucci. "Regulation of Neuronal Chemokine Receptor CXCR4 by μ-Opioid Agonists and Its Involvement in NeuroAIDS." In Chemokine Receptors and NeuroAIDS, 379–97. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_17.

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Conference papers on the topic "CXCR2 receptor"

1

Sharma, Bhawna, Dhananjay M. Nawandar, Michelle L. Varney, and Rakesh K. Singh. "Abstract 693: Evaluating the role of CXCR2 receptor and its ligand in breast cancer therapy resistance." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-693.

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Wade, R. C., D. Xing, V. Lin, Y. Wu, C. Song, X. Xu, N. Harris, J. M. Wells, and G. A. Payne. "Inflammatory Ligands of CXC Chemokine Receptor 2 (CXCR2) Are Associated with Coronary Artery Calcification in COPD." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2401.

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Sharma, Bhawna, Dhananjay Nawandar, Michelle L. Varney, Kalyan C. Nannuru, and Rakesh K. Singh. "Abstract 5462: Enhancing efficacy of drugs by targeting CXCR2 receptor signaling for the treatment of malignant breast cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5462.

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Dong, Yuanlin, Syeda M. Kabir, Eunsook Lee, and Deok-Soo Son. "Abstract 527: Proinflammatory chemokine receptor CXCR2 promotes cellular proliferation through suppression of cell cycle inhibitor p21 protein in ovarian cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-527.

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Ustach, Carolyn V., Aprill Watanabe, Meraj Aziz, Caroline Diep, Galen Hostetter, Demeure Michael, Haiyong Han, and Daniel D. Von Hoff. "Abstract 393: The chemokine receptor, CXCR2/IL8RB, contributes to the survival of pancreatic adenocarcinoma, and may play a role in stroma-tumor communication." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-393.

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Adekoya, Timothy O., Nikia Smith, Parag Kothari, and Ricardo M. Richardson. "Abstract PO-134: Differential effects of CXCR1 and CXCR2 receptors on prostate tumorigenesis." In Abstracts: AACR Virtual Conference: 14th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; October 6-8, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/1538-7755.disp21-po-134.

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Silva, Mariane Ricciardi da, Nádia Calvo Martins Okuyama, and Karen Brajão De Oliveira. "PAPEL DAS VARIANTES GENÉTICAS DE CXCL12 (RS1801157) E DE CXCR4 (RS2228014) NA EXPRESSÃO PROTEICA DO RECEPTOR E EM PARÂMETROS CLINICOPATOLÓGICOS DO CÂNCER DE COLO DE ÚTERO." In II Congresso Brasileiro de Saúde On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1519.

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Introdução: O câncer cervical é o terceiro câncer mais comum em mulheres no mundo e a inflamação é um componente crucial na progressão do tumor, mas outros cofatores devem estar presentes para o desenvolvimento da malignidade, como fatores genéticos individuais. Nesse contexto, os genes CXCL12 e CXCR4 podem ter uma variação de nucleotídeo único (SNV) rs1801157 e rs2228014, respectivamente, que estão envolvidas na sobrevivência, angiogênese e invasão de células malignas. Objetivos: O objetivo do presente estudo foi verificar uma possível associação entre SNVs de CXCL12 e CXCR4 e sua influência na expressão de CXCR4 em tecido tumoral de câncer cervical, analisar associação entre as variantes de nucleotídeo único de CXCL12 e CXCR4 com parâmetros clinicopatológicos (tumor, grau da histologia e estágio) e a expressão de CXCR4 em tecido tumoral. Material e métodos: CXCL12 e CXCR4 foram avaliados por PCR, seguida de digestão enzimática para 90 pacientes, e imuno-histoquímica foi realizada em 35 amostras de tumor cervical fixado em formalina e incluso em parafina. Resultados: Não foi encontrada diferença na distribuição genotípica entre os grupos para cada variável. Nem o efeito principal dos SNVs, nem as interações (GA + AA por CT +TT) foram associadas com as características clinicopatológicas analisadas. Em relação a marcação proteica de CXCR4, não houve relação significativa com os parâmetros clinicopatológicos analisados. A avaliação de rs1801157 de CXCL12 e rs2228014 de CXCR4 e a imunocoloração não demonstraram relação significativa entre os graus de imunocoloração de CXCR4 e cada modelo de SNVs de CXCL12 e CXCR4. Conclusão: Os resultados demonstram que não foi comprovada associação entre os SNVs e os parâmetros analisados. Essa é a primeira vez que os SNVs de CXCL12 e CXCR4 foram analisados com o objetivo de verificar a possibilidade de associação com a imunocoloração de CXCR4 e parâmetros clinicopatológicos.
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Pham, Kien, Che Liu, Defang Luo, Brent A. Reynolds, and Jeffrey K. Harrison. "Abstract 5194: Heterogenous expression of chemokine receptors in primary patient-derived GBM lines; association of CXCR3, CXCR4, and CXCR7 with a slow cycling sub-population." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5194.

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Miekus, Katarzyna, Danuta Jarocha, Elzbieta Trzyna, and Marcin Majka. "Abstract B113: Role of I‐TAC‐binding receptors CXCR3 and CXCR7 in biology of various tumor cell lines." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b113.

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Costa, Leonardo, Jürgen Haas, Henriette Rudolph, Saskia Libicher, Sven Jarius, Tobias Tenenbaum, Horst Schroten, and Brigitte Brigitte Wildemann. "The Choroid Plexus Is Permissive for a Preactivated Antigen-Experienced Memory B Cell Subset in Multiple Sclerosis." In Building Bridges in Medical Science 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.03.001.2.

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Background: The role of B cells in multiple sclerosis (MS) is increasingly recognized. B cells undergo compartmentalized redistribution in blood and cerebrospinal fluid (CSF) during active MS, whereby memory B cells accumulate in the CSF. While B-cell trafficking across the blood– brain barrier has been intensely investigated, cellular diapedesis through the blood–CSF barrier (BCSFB) is incompletely understood. Objectives: To investigate how B cells interact with the choroid plexus to transmigrate into the CSF, we isolated circulating B cells from healthy donors (HC) and MS patients, utilized an inverted cell culture filter system of human choroid plexus papilloma (HIBCPP) cells to determine transmigration rates of B-cell subsets, immunofluorescence, and electron microscopy to analyze migration routes, and qRT-PCR to determine cytokines/chemokines mediating B-cell diapedesis. We also screened the transcriptome of intrathecal B cells from MS patients. Results: We found that spontaneous transmigration of HC- and MS-derived B cells was scant yet increased significantly in response to B-cell specific chemokines CXCL-12/CXCL-13, was further boosted upon pre-activation and occurred via paracellular and transcellular pathways. Migrating cells exhibited upregulation of several genes involved in B-cell activation/migration and enhanced expression of chemokine receptors CXCR4/CXCR5 and were predominantly of isotype class switched memory phenotype. This antigen-experienced migratory subset displayed more pronounced chemotactic activities in MS than in HC and was retrieved in intrathecal B cells from patients with active MS. Trafficking of class-switched memory B cells was downscaled in a small cohort of natalizumab-exposed MS patients and the proportions of these phenotypes were reduced in peripheral blood yet were enriched intrathecally in patients who experienced recurrence of disease activity after withdrawal of natalizumab. Conclusion: Our findings highlight the relevance of the BCSFB as an important gate for the entry of potentially harmful activated B cells into the CSF.
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