Adenovirus vector-mediated YKL-40 shRNA attenuates eosinophil airway inflammation in a murine asthmatic model
暂无分享,去创建一个
Suqin Ben | Ying Zheng | A. Bao | Aying Ma | Ling Wang | Yi Wu | Huanxia Shang | Danruo Fang
[1] M. Sugaya,et al. YKL-40 Promotes Proliferation of Cutaneous T-Cell Lymphoma Tumor Cells through Extracellular Signal e Regulated Kinase Pathways , 2020 .
[2] H. Kandikattu,et al. Synergy of Interleukin (IL)-5 and IL-18 in eosinophil mediated pathogenesis of allergic diseases. , 2019, Cytokine & growth factor reviews.
[3] Y. Liu,et al. Chitinase-like protein YKL-40 correlates with inflammatory phenotypes, anti-asthma responsiveness and future exacerbations , 2019, Respiratory Research.
[4] Yan Zhao,et al. YKL-40 promotes the progress of atherosclerosis independent of lipid metabolism in apolipoprotein E−/− mice fed a high-fat diet , 2019, Heart and Vessels.
[5] Y. Prakash,et al. Secretory Inositol Polyphosphate 4‐Phosphatase Protects against Airway Inflammation and Remodeling , 2019, American journal of respiratory cell and molecular biology.
[6] S. Nobs,et al. GM‐CSF intrinsically controls eosinophil accumulation in the setting of allergic airway inflammation , 2019, The Journal of allergy and clinical immunology.
[7] A. Baldi,et al. Helper-dependent adenovirus-mediated gene transfer of a secreted LDL receptor/transferrin chimeric protein reduces aortic atherosclerosis in LDL receptor-deficient mice , 2019, Gene Therapy.
[8] Huabin Li,et al. Fas Signaling in Dendritic Cells Mediates Th2 Polarization in HDM-Induced Allergic Pulmonary Inflammation , 2018, Front. Immunol..
[9] Ying-ying Zhang,et al. Effects of ozone repeated short exposures on the airway/lung inflammation, airway hyperresponsiveness and mucus production in a mouse model of ovalbumin-induced asthma. , 2018, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.
[10] E. Bleecker,et al. Characterisation of asthma subgroups associated with circulating YKL-40 levels , 2017, European Respiratory Journal.
[11] R. Sehmi,et al. Hematopoietic Processes in Eosinophilic Asthma , 2017, Chest.
[12] Rakesh K. Kumar,et al. Modeling TH2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma , 2017, Immunological reviews.
[13] Ying-ying Zhang,et al. Inhalation of progesterone inhibits chronic airway inflammation of mice exposed to ozone , 2017, Molecular immunology.
[14] Shan-Chi Liu,et al. YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells , 2017, International journal of molecular sciences.
[15] Feng-Lai Yuan,et al. Association of interleukin-18 and asthma , 2017, Inflammation.
[16] P. Dzięgiel,et al. The role of YKL-40 in a cancerous process. , 2016, Postepy higieny i medycyny doswiadczalnej.
[17] Anton P. Bussink,et al. New Insights Into the Relationship Between Chitinase-3-Like-1 and Asthma , 2016, Current Allergy and Asthma Reports.
[18] M. Röösli,et al. CHI3L1 polymorphisms, cord blood YKL-40 levels and later asthma development , 2016, BMC Pulmonary Medicine.
[19] J. Elias,et al. Role of Chitinase 3-Like-1 in Interleukin-18-Induced Pulmonary Type 1, Type 2, and Type 17 Inflammation; Alveolar Destruction; and Airway Fibrosis in the Murine Lung. , 2015, American journal of respiratory cell and molecular biology.
[20] Z. Deng,et al. YKL-40 is correlated with FEV1 and the asthma control test (ACT) in asthmatic patients: influence of treatment , 2015, BMC Pulmonary Medicine.
[21] C. Porsbjerg,et al. YKL-40 and genetic status of CHI3L1 in a large group of asthmatics , 2015, European clinical respiratory journal.
[22] Paige Lacy,et al. Eosinophil Cytokines, Chemokines, and Growth Factors: Emerging Roles in Immunity , 2014, Front. Immunol..
[23] Yi Wu,et al. Ovalbumin enhances YKL-40, IL-5, GM-CSF, and eotaxin expression simultaneously in primarily cultured mouse tracheal epithelial cells , 2014, In Vitro Cellular & Developmental Biology - Animal.
[24] S. Kato,et al. IL-18 Induces Airway Hyperresponsiveness and Pulmonary Inflammation via CD4+ T Cell and IL-13 , 2013, PloS one.
[25] H. Ortega,et al. Association of CHI3L1 in African-Americans with Prior History of Asthma Exacerbations and Stress , 2013, The Journal of asthma : official journal of the Association for the Care of Asthma.
[26] Hao Tang,et al. YKL-40 Induces IL-8 Expression from Bronchial Epithelium via MAPK (JNK and ERK) and NF-κB Pathways, Causing Bronchial Smooth Muscle Proliferation and Migration , 2012, The Journal of Immunology.
[27] T. Deneva,et al. Relationship between sonographic parameters and YKL-40 levels in rheumatoid arthritis , 2013, Rheumatology International.
[28] Hao Tang,et al. YKL-40-mediated interleukin 8 production may be closely associated with remodeling of bronchial smooth muscle cells. , 2012, American journal of respiratory and critical care medicine.
[29] C. D. Dela Cruz,et al. YKL-40, a chitinase-like protein at the intersection of inflammation and remodeling. , 2012, American journal of respiratory and critical care medicine.
[30] Min Zhang,et al. Breast regression protein-39 (BRP-39) promotes dendritic cell maturation in vitro and enhances Th2 inflammation in murine model of asthma , 2012, Acta Pharmacologica Sinica.
[31] W. LaFramboise,et al. Exacerbation of Experimental Autoimmune Encephalomyelitis in the Absence of Breast Regression Protein 39/Chitinase 3-Like 1 , 2012, Journal of neuropathology and experimental neurology.
[32] G. Delespesse,et al. Hematopoietic progenitor cells are innate Th2 cytokine‐producing cells , 2012, Allergy.
[33] B. Ma,et al. Role of chitin and chitinase/chitinase-like proteins in inflammation, tissue remodeling, and injury. , 2011, Annual review of physiology.
[34] H. Hammad,et al. The role of dendritic and epithelial cells as master regulators of allergic airway inflammation , 2010, The Lancet.
[35] H. Vestergaard,et al. Low grade inflammation as measured by levels of YKL-40: association with an increased overall and cardiovascular mortality rate in an elderly population. , 2010, International journal of cardiology.
[36] I. Pavord,et al. Eosinophil protein in airway macrophages: a novel biomarker of eosinophilic inflammation in patients with asthma. , 2010, The Journal of allergy and clinical immunology.
[37] Zheng Liu,et al. Clara cell 10-kD protein suppresses chitinase 3-like 1 expression associated with eosinophilic chronic rhinosinusitis. , 2010, American journal of respiratory and critical care medicine.
[38] J. Elias,et al. Role of breast regression protein-39/YKL-40 in asthma and allergic responses , 2009, Allergy, asthma & immunology research.
[39] R. Flavell,et al. Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis , 2009, The Journal of experimental medicine.
[40] J. Kastrup,et al. High serum YKL-40 concentration is associated with cardiovascular and all-cause mortality in patients with stable coronary artery disease. , 2009, European heart journal.
[41] G. Chupp,et al. Novel biomarkers in asthma: chemokines and chitinase-like proteins , 2009, Current opinion in allergy and clinical immunology.
[42] Dirk E. Smith,et al. CD34+ hemopoietic progenitor cells are potent effectors of allergic inflammation. , 2009, The Journal of allergy and clinical immunology.
[43] L. Tarnow,et al. YKL-40, a Marker of Inflammation and Endothelial Dysfunction, Is Elevated in Patients With Type 1 Diabetes and Increases With Levels of Albuminuria , 2009, Diabetes Care.
[44] H. Shen,et al. Treatment with anti‐CC chemokine receptor 3 monoclonal antibody or dexamethasone inhibits the migration and differentiation of bone marrow CD34+ progenitor cells in an allergic mouse model , 2008, Allergy.
[45] Ying Sun,et al. Effect of variation in CHI3L1 on serum YKL-40 level, risk of asthma, and lung function. , 2008, The New England journal of medicine.
[46] J. Dziura,et al. A chitinase-like protein in the lung and circulation of patients with severe asthma. , 2007, The New England journal of medicine.
[47] Andrew D Rowan,et al. The Mammalian Chitinase-like Lectin, YKL-40, Binds Specifically to Type I Collagen and Modulates the Rate of Type I Collagen Fibril Formation* , 2006, Journal of Biological Chemistry.
[48] K. Akashi,et al. Identification of eosinophil lineage–committed progenitors in the murine bone marrow , 2005, The Journal of experimental medicine.
[49] Sarah J. McMillan,et al. Therapeutic administration of Budesonide ameliorates allergen‐induced airway remodelling , 2005, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.
[50] H. Ling,et al. The chitinase 3-like protein human cartilage glycoprotein 39 (HC-gp39) stimulates proliferation of human connective-tissue cells and activates both extracellular signal-regulated kinase- and protein kinase B-mediated signalling pathways. , 2002, The Biochemical journal.
[51] Rakesh K. Kumar,et al. Eotaxin Expression by Epithelial Cells and Plasma Cells in Chronic Asthma , 2002, Laboratory Investigation.
[52] M. Takigawa,et al. Recognition of YKL-39, a human cartilage related protein, as a target antigen in patients with rheumatoid arthritis , 2001, Annals of the rheumatic diseases.
[53] P. O'Byrne,et al. Systemic aspects of allergic disease: bone marrow responses. , 2000, The Journal of allergy and clinical immunology.
[54] M. Rehli,et al. Molecular characterization of the gene for human cartilage gp-39 (CHI3L1), a member of the chitinase protein family and marker for late stages of macrophage differentiation. , 1997, Genomics.
[55] L. Shackelton,et al. Identification of a 38-kDa Heparin-binding Glycoprotein (gp38k) in Differentiating Vascular Smooth Muscle Cells as a Member of a Group of Proteins Associated with Tissue Remodeling (*) , 1995, The Journal of Biological Chemistry.
[56] J. Roth,et al. Safety evaluation of Ad5CMV-p53 in vitro and in vivo. , 1995, Human gene therapy.
[57] D. Leung. Steroid-resistant asthma. , 1995, The Western journal of medicine.
[58] M. Welsh,et al. Safety and efficacy of repetitive adenovirus–mediated transfer of CFTR cDNA to airway epithelia of primates and cotton rats , 1994, Nature Genetics.
[59] Brian,et al. Human cartilage gp-39, a major secretory product of articular chondrocytes and synovial cells, is a mammalian member of a chitinase protein family. , 1993, The Journal of biological chemistry.
[60] J. Gamble,et al. Recombinant human granulocyte-macrophage colony-stimulating factor stimulates in vitro mature human neutrophil and eosinophil function, surface receptor expression, and survival. , 1986, The Journal of clinical investigation.