Search results for "CCL1"

showing 6 items of 36 documents

Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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CXCR2 blockade impairs angiotensin II-induced CC chemokine synthesis and mononuclear leukocyte infiltration.

2007

Objective—Angiotensin II (Ang-II) and mononuclear leukocytes are involved in atherosclerosis. This study reports the inhibition of Ang-II–induced mononuclear cell recruitment by CXCR2 antagonism and the mechanisms involved.Methods and Results—Ang-II (1 nmol/L, i.p. in rats) induced CXC and CC chemokines, followed by neutrophil and mononuclear cell recruitment. Administration of the CXCR2 antagonist, SB-517785-M, inhibited the infiltration of both neutrophils (98%) and mononuclear cells (60%). SB-517785-M had no effect on the increase in CXC chemokine levels but reduced MCP-1, RANTES, and MIP-1α release by 66%, 63%, and 80%, respectively. Intravital microscopy showed that pretreatment with S…

Malemedicine.medical_specialtyChemokineCXCR3Peripheral blood mononuclear cellLosartanReceptors Interleukin-8BRats Sprague-DawleyChemokine receptorInternal medicinemedicineCell AdhesionCCL17AnimalsHumansCXC chemokine receptorsSplanchnic CirculationChemokine CCL7Chemokine CCL4Chemokine CCL5Cells CulturedChemokine CCL2Chemokine CCL3InflammationbiologyAngiotensin IIMicrocirculationEndothelial CellsMacrophage Inflammatory ProteinsAtherosclerosisAngiotensin IIMonocyte Chemoattractant ProteinsRatsMononuclear cell infiltrationChemotaxis LeukocyteEndocrinologyNeutrophil Infiltrationbiology.proteinLeukocytes MononuclearCardiology and Cardiovascular MedicineAngiotensin II Type 1 Receptor BlockersArteriosclerosis, thrombosis, and vascular biology
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Macrophage inflammatory protein-1.

2003

Macrophage inflammatory protein (MIP)-1alpha was identified 15 years ago as the first of now four members of the MIP-1 CC chemokine subfamily. These proteins termed CCL3 (MIP-1alpha), CCL4 (MIP-1beta), CCL9/10 (MIP-1delta), and CCL15 (MIP-1gamma) according to the revised nomenclature for chemokines are produced by many cells, particularly macrophages, dendritic cells, and lymphocytes. MIP-1 proteins, which act via G-protein-coupled cell surface receptors (CCR1, 3, 5), e.g. expressed by lymphocytes and monocytes/macrophages (MPhi), are best known for their chemotactic and proinflammatory effects but can also promote homoeostasis. The encouraging results of preclinical studies in murine model…

Molecular Sequence DataCCL18Cell BiologyBiologyMacrophage Inflammatory ProteinsCCL7BiochemistryCCL20CXCL2ImmunologyAnimalsHumansDiseaseCCL15Amino Acid SequenceCCL13CC chemokine receptorsChemokine CCL4Macrophage inflammatory proteinChemokine CCL3The international journal of biochemistrycell biology
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2015

Background Acute exacerbation (AE) of idiopathic pulmonary fibrosis (IPF) is a common cause of disease acceleration in IPF and has a major impact on mortality. The role of macrophage activation in AE of IPF has never been addressed before. Methods We evaluated BAL cell cytokine profiles and BAL differential cell counts in 71 IPF patients w/wo AE and in 20 healthy volunteers. Twelve patients suffered from AE at initial diagnosis while sixteen patients developed AE in the 24 months of follow-up. The levels of IL-1ra, CCL2, CCL17, CCL18, CCL22, TNF-α, IL-1β, CXCL1 and IL-8 spontaneously produced by BAL-cells were analysed by ELISA. Results In patients with AE, the percentage of BAL neutrophils…

Pathologymedicine.medical_specialtyMultidisciplinaryExacerbationbusiness.industrymedicine.medical_treatmentCCL18respiratory systemmedicine.diseaseM2 Macrophagerespiratory tract diseasesCXCL1Idiopathic pulmonary fibrosisCytokinePulmonary fibrosisImmunologymedicineTumor necrosis factor alphabusinessPLOS ONE
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Influencia de la situación postprandial sobre el eje CCL11/CCR3 en sujetos con hipercolesterolemia

2020

Introducción: La enfermedad cardiovascular es la principal causa de morbilidad y mortalidad a nivel mundial y su base patogénica es la arteriosclerosis (AE). La hipercolesterolemia primaria es uno de los factores de riesgo más importantes para la AE y este proceso está asociado a cierto grado de inflamación sistémica, habiéndose descrito en la actualidad varias citoquinas quimiotácticas involucradas en el proceso arteriosclerótico. Se ha detectado la influencia de la eotaxina-1 (CCL11) y de su receptor, CCR3, en la aparición y desarrollo de la arteriosclerosis, así como la influencia de la lipemia postprandial (LPP) como factor de riesgo independiente de enfermedad cardiovascular, aunque no…

inflamaciónUNESCO::CIENCIAS MÉDICASeotaxinapostprandialhipercolesterolemiaCCR3:CIENCIAS MÉDICAS [UNESCO]CCL11
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Growth and differentiation factor 11 (GDF11): Functions in the regulation of erythropoiesis and cardiac regeneration

2015

International audience; Members of the TGF-β superfamily transduce their signals through type I and II receptor serine/threonine kinases. The binding of activins to activin type IIA (ActRIIA) or type IIB (ActRIIB) receptors induces the recruitment and phosphorylation of an activin type I receptor (ALK4 and/or ALK7), which then phosphorylates the Smad2 and Smad3 intracellular signaling proteins. The regulation of members of the TGF-β family is known to be complex, because many proteins able to bind the ligands and inhibit their activities have been identified. Growth and differentiation factor 11 (Gdf11) belongs to the TGF-β family. GDF11, like other members of the TGF-β superfamily, is prod…

medicine.medical_specialtySmad2 ProteinProtein Serine-Threonine Kinases030204 cardiovascular system & hematologyBiology03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicineTGF beta signaling pathway[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumansRegeneration[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPharmacology (medical)PhosphorylationCCL11Activin type 2 receptors030304 developmental biologyPharmacology0303 health sciencesR-SMADcardiac regenerationGrowth differentiation factorHeartActivins[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemCell biologyBMPR2Growth Differentiation FactorsEndocrinologyBone Morphogenetic ProteinsGDF11Smad2 ProteinSignal transductionActivin Receptors Type IerythropoiesisACVR2BSignal TransductionPharmacology & Therapeutics
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