Search results for "CTGF"

showing 7 items of 17 documents

TGF-β Signaling Pathways in Different Compartments of the Lower Airways of Patients With Stable COPD

2017

Background: The expression and localization of transforming growth factor-β (TGF-β) pathway proteins in different compartments of the lower airways of patients with stable COPD is unclear. We aimed to determine TGF-β pathway protein expression in patients with stable COPD. Methods: The expression and localization of TGF-β pathway components was measured in the bronchial mucosa and peripheral lungs of patients with stable COPD (n = 44), control smokers with normal lung function (n = 24), and control nonsmoking subjects (n = 11) using immunohistochemical analysis. Results: TGF-β1, TGF-β3, and connective tissue growth factor expression were significantly decreased in the bronchiolar epithelium…

MaleCCN2 connective tissue growth factorSmad Proteinsairway inflammationCritical Care and Intensive Care MedicineTRAP-1 transforming growth factor-β receptor-associated binding proteinPulmonary Disease Chronic ObstructiveLAP latency-associated peptideSMAD small mother against decapentaplegicBAMBI CTGF SMAD TGF-B airway inflammation autoimmunityLungTGF transforming growth factorLLC large latent complexBAMBI CTGF SMAD TGF-β Airway Inflammation AutoimmunityautoimmunityMiddle Agedrespiratory systemLTBP latent transforming growth factor-β binding proteinImmunohistochemistryTGIF 5′-TG-3′-interacting factorECM extracellular matrixTGFBI transforming growth factor-β-induced proteinFemaleCardiology and Cardiovascular MedicinePI3K phosphoinositide 3-kinaseSignal TransductionTGF-βPulmonary and Respiratory MedicineTGF-βR TGF-β receptorSocio-culturaleBronchiRespiratory MucosaArticleTGF-BTransforming Growth Factor beta1Transforming Growth Factor beta3Macrophages AlveolarHumansAgedBAMBI; CTGF; SMAD; TGF-β; airway inflammation; autoimmunityBAMBIMembrane ProteinsCTGFBMP bone morphogenetic proteinBAMBI; CTG; SMAD; TGF-β; airway inflammation; autoimmunityCTGBAMBI bone morphogenetic proteins and activin membrane-bound inhibitorrespiratory tract diseasesairway inflammation; autoimmunity; BAMBI; CTGF; SMAD; TGF-β; Pulmonary and Respiratory Medicine; Critical Care and Intensive Care Medicine; Cardiology and Cardiovascular MedicineCase-Control StudiesBiomarkersMAPK mitogen-activated protein kinaseSMAD
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Myocardial hypertrophy is associated with inflammation and activation of endocannabinoid system in patients with aortic valve stenosis.

2013

article i nfo Article history: Received 1 February 2013 Accepted 22 March 2013 Aims: Endocannabinoids and their receptors have been associated with cardiac adaptation to injury, inflam- mation and fibrosis. Experimental studies suggested a role for inflammatory reaction and active remodeling in myocardial hypertrophy, but they have not been shown in human hypertrophy. We investigated the asso- ciation of the endocannabinoid system with myocardial hypertrophy in patients with aortic stenosis. Main methods: Myocardial biopsies were collected from patients with aortic stenosis (AS) and atrial myxoma as controls during surgery. Histological and molecular analysis of endocannabinoids and their r…

Malemedicine.medical_specialtyInflammationCardiomegalyGeneral Biochemistry Genetics and Molecular BiologyMuscle hypertrophyFibrosisInternal medicinemedicineHumansGeneral Pharmacology Toxicology and PharmaceuticsAgedPressure overloadInflammationbiologybusiness.industryTenascin CGeneral MedicineAortic Valve Stenosismedicine.diseaseEndocannabinoid systemCTGFEndocrinologyAortic valve stenosisbiology.proteinlipids (amino acids peptides and proteins)Femalemedicine.symptombusinessEndocannabinoidsLife sciences
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Transcript profiling identifies novel key players mediating the growth inhibitory effect of NS-398 on human pancreatic cancer cells

2010

Pancreatic cancer is one of the most aggressive human malignancies with an increasing incidence worldwide. Despite an increase in the number of systemic treatments available for pancreatic cancer, the impact of therapy on the clinical course of the disease has been modest, underscoring an urgent need for new therapeutic options. Although selective cyclooxygenase-2 inhibitors have been demonstrated to have cancer-preventive effects, the mechanism of their effects is not clearly known. Moreover, there have been no unbiased studies to identify novel molecular targets of NS-398 regarding pancreatic cancer. Here we undertook a gene expression profiling study to identify novel molecular targets m…

Pancreatic diseaseDown-RegulationApoptosisBiologyDownregulation and upregulationCell Line TumorPancreatic cancermedicineHumansNitrobenzenesCell ProliferationOligonucleotide Array Sequence AnalysisPharmacologySulfonamidesCell growthGene Expression ProfilingCancermedicine.diseaseAryl hydrocarbon receptorUp-RegulationPancreatic NeoplasmsCTGFGene expression profilingImmunologyCancer researchbiology.proteinEuropean Journal of Pharmacology
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FGF-9 overexpression prevents pleural fibrosis induced by intra-pleural adenovirus injection in mice

2015

Introduction: Lung fibrosis is associated with the reactivation of molecular pathways involved in lung development. Mesothelial cells are involved in the fibrotic lung process but their exact role is debated. Fibroblast Growth Factor-9 (FGF-9) is expressed by epithelial cells and visceral pleura during embryonic lung development. Mice homozygous for a targeted disruption of FGF-9 exhibit lung hypoplasia with reduced mesenchyme and early postnatal death. The aim of this study was to evaluate the role of FGF-9 expression by mesothelial cells in the adult lung. We used adenovirus-mediated (FGF-9) gene transfer in mesothelial cells in vivo. Material and Methods: AdFGF9 or a control adenovirus (…

Pathologymedicine.medical_specialtyLungbiologybusiness.industryMesenchymeInflammationrespiratory systemFibroblast growth factorrespiratory tract diseasesCTGFFibronectinmedicine.anatomical_structuremedicinebiology.proteinmedicine.symptombusinessFibroblastMesothelial Cell1.5 Diffuse Parenchymal Lung Disease
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Lovastatin attenuates ionizing radiation-induced normal tissue damage in vivo.

2009

Abstract Background and purpose HMG-CoA-reductase inhibitors (statins) are widely used lipid-lowering drugs. Moreover, they have pleiotropic effects on cellular stress responses, proliferation and apoptosis in vitro . Here, we investigated whether lovastatin attenuates acute and subchronic ionizing radiation-induced normal tissue toxicity in vivo . Materials and methods Four hours to 24h after total body irradiation (6Gy) of Balb/c mice, acute pro-inflammatory and pro-fibrotic responses were analyzed. To comprise subchronic radiation toxicity, mice were irradiated twice with 2.5Gy and analyses were performed 3weeks after the first radiation treatment. Molecular markers of inflammation and f…

Programmed cell deathPathologymedicine.medical_specialtyStatinmedicine.drug_classCell SurvivalPharmacologyRadiation DosageMiceRandom AllocationIn vivoFibrosisReference ValuesRadiation IonizingmedicineAnimalsHumansRadiology Nuclear Medicine and imagingLovastatinRNA MessengerRadiation InjuriesLungProbabilityMice Inbred BALB CChemistryTumor Necrosis Factor-alphaNF-kappa BDose-Response Relationship RadiationHematologymedicine.diseaseCTGFIntestinesDisease Models AnimalRadiation Injuries ExperimentalOncologyLiverApoptosisToxicitylipids (amino acids peptides and proteins)FemaleLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsInflammation Mediatorsmedicine.drugDNA DamageRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
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Progressive pulmonary fibrosis is mediated by TGF-β isoform 1 but not TGF-β3

2007

Tissue repair is a well-orchestrated biological process involving numerous soluble mediators, and an imbalance between these factors may result in impaired repair and fibrosis. Transforming growth factor (TGF)-beta is a key profibrotic element in this process and it is thought that its three isoforms act in a similar way. Here, we report that TGF-beta3 administered to rat lungs using transient overexpression initiates profibrotic effects similar to those elicited by TGF-beta1, but causes less severe and progressive changes. The data suggest that TGF-beta3 does not lead to inhibition of matrix degradation in the same way as TGF-beta1, resulting in non-fibrotic tissue repair. Further, TGF-bet…

medicine.medical_specialtyPulmonary FibrosisSMADBiologyBiochemistryArticleCell LineRats Sprague-DawleyTransforming Growth Factor beta1Extracellular matrixTransforming Growth Factor beta3Downregulation and upregulationFibrosisInternal medicinePulmonary fibrosismedicineAnimalsLungCell Biologymedicine.diseaseRatsCTGFEndocrinologyCancer researchFemaleWound healingReceptors Transforming Growth Factor betaTransforming growth factorThe International Journal of Biochemistry & Cell Biology
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Inhibition of Rac1 signaling by lovastatin protects against anthracycline-induced cardiac toxicity

2011

Normal tissue damage limits the efficacy of anticancer therapy. For anthracyclines, the clinically most relevant adverse effect is cardiotoxicity. The mechanisms involved are poorly understood and putative cardioprotectants are controversially discussed. Here, we show that the lipid-lowering drug lovastatin protects rat H9c2 cardiomyoblasts from doxorubicin in vitro. Protection by lovastatin is related to inhibition of the Ras-homologous GTPase Rac1. It rests on a reduced formation of DNA double-strand breaks, resulting from the inhibition of topoisomerase II by doxorubicin. Doxorubicin transport and reactive oxygen species are not involved. Protection by lovastatin was confirmed in vivo. I…

rac1 GTP-Binding ProteinCancer ResearchAnthracyclineDoxorubicin transportCardiac fibrosismedicine.medical_treatmentImmunologyPharmacologyBiologyDNA damage responsestatinsMiceCellular and Molecular NeuroscienceRho GTPasespolycyclic compoundsmedicineAnimalsDNA Breaks Double-StrandedMyocytes CardiacDoxorubicinLovastatinanthracyclinesCardiotoxicityAntibiotics AntineoplasticTroponin IConnective Tissue Growth FactorCell Biologymedicine.diseaseRatsCTGFDNA Topoisomerases Type IICytokinenormal tissue damageDoxorubicinOriginal Articlelipids (amino acids peptides and proteins)LovastatinAtrial Natriuretic FactorSignal Transductionmedicine.drugCell Death & Disease
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