0000000000448353

AUTHOR

Pilar Ribera

showing 5 related works from this author

MUC1 deficiency mediates corticosteroid resistance in chronic obstructive pulmonary disease.

2018

Background Lung inflammation in COPD is poorly controlled by inhaled corticosteroids (ICS). Strategies to improve ICS efficacy or the search of biomarkers who may select those patients candidates to receive ICS in COPD are needed. Recent data indicate that MUC1 cytoplasmic tail (CT) membrane mucin can mediate corticosteroid efficacy in chronic rhinosinusitis. The objective of this work was to analyze the previously unexplored role of MUC1 on corticosteroid efficacy in COPD in vitro and in vivo models. Methods MUC1-CT expression was measured by real time PCR, western blot, immunohistochemistry and immunofluorescence. The inflammatory mediators IL-8, MMP9, GM-CSF and MIP3α were measured by EL…

0301 basic medicineMalemedicine.drug_classDrug ResistanceInflammationMUC1Corticosteroid resistancedigestive system03 medical and health sciencesMicePulmonary Disease Chronic Obstructive0302 clinical medicineGlucocorticoid receptorIn vivoAdrenal Cortex HormonesmedicineAnimalsHumansGene Silencingskin and connective tissue diseasesneoplasmsDexamethasoneMUC1Agedlcsh:RC705-779Mice KnockoutCOPDLungbusiness.industryResearchChronic obstructive pulmonary diseaseMucin-1Sputumlcsh:Diseases of the respiratory systemMiddle Agedmedicine.diseasedigestive system diseasesrespiratory tract diseasesMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030228 respiratory systemImmunologyCorticosteroidFemalemedicine.symptombusinessBiomarkersmedicine.drugRespiratory research
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Activation of nuclear factor erythroid 2-related (Nrf2) system as a novel therapeutic approach in COPD

2019

Background: Chronic Obstructive Pulmonary Disease (COPD) is an inflammatory lung disease caused by chronic exposure to cigarette smoke. Oxidative stress is one of the most important mechanisms involved in the physiopathology of COPD. Nuclear Factor Erythroid 2-related (Nrf2) is critical in protection against oxidative stress by inducing expression of antioxidant genes and a decrease in its expression has been observed in COPD patients. Objective: The aim of this study was to characterise the effects of Bardoxolone, Omavexolone and Obacunone as antioxidant drugs in COPD. Methods: Peripheral blood neutrophils from COPD and healthy volunteers and Primary Human Bronchial Epithelial cells were i…

COPDAntioxidantbusiness.industrymedicine.medical_treatmentGlutathionePharmacologymedicine.disease_causemedicine.diseaseProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCytokine030228 respiratory systemchemistryApoptosismedicine030212 general & internal medicineBardoxolonebusinessOxidative stressAirway pharmacology and treatment
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Roflumilast N- oxide combined with sildenafil reverses cellular remodeling on IPF models

2017

Background: Idiopathic pulmonary fibrosis (IPF) is characterized by a rapid progressive lung decline and premature death after its diagnosis. Roflumilast displayed anti-fibrotic effects in animal and cellular models. Recent studies indicate that the combination of PDE4 and PDE5 inhibitors (sildenafil) potentiates anti-fibrotic properties of each drug, suggesting potential beneficts of this combination. Objectives: To study the effects from adding sildenafil to roflumilast N-oxide (RNO) inhibiting TGFβ1-induced human alveolar type II (AECII) epithelial-to-mesenchymal transition (EMT) and human fibrocyte to myofibroblast transition in vitro. Methods: AECII and fibrocytes were isolated from he…

biologybusiness.industrySildenafilMesenchymal stem cellVimentinrespiratory tract diseaseschemistry.chemical_compoundchemistryAnnexinFibrocyteCancer researchbiology.proteinMedicineViability assaybusinessMyofibroblastRoflumilastmedicine.drugAirway Pharmacology and Treatment
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IL-11 promotes pulmonary vascular remodeling and lung fibrosis through the activation of endothelial to mesenchymal transition

2020

Background: Pulmonary hypertension (PH) in idiopathic pulmonary fibrosis (IPF) portends a poor prognosis and currently there is no approved therapy for hypoxemic PH. IL-11 is a novel lung fibrosis mediator but its role on vascular function is unknown. Objective: To analyze the role of IL-11 on pulmonary artery remodeling and lung fibrosis in vitro and in vivo. Methods: IL-11 expression was evaluated in pulmonary arteries and lung sections of control subjects and patients with IPF, IPF+PH and idiopathic PH (PAH). Human pulmonary artery endothelial cells and smooth muscle cells were stimulated with IL-11. Endothelial to mesenchymal transition was evaluated measuring the increase of mesenchyma…

Pathologymedicine.medical_specialtyLungbusiness.industryMesenchymal stem cellrespiratory systemmedicine.diseasePulmonary hypertensionrespiratory tract diseasesIdiopathic pulmonary fibrosismedicine.anatomical_structureFibrosismedicine.arteryPulmonary fibrosisParenchymaPulmonary arteryMedicinebusinessIdiopathic interstitial pneumonias
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Additional file 1: of MUC1 deficiency mediates corticosteroid resistance in chronic obstructive pulmonary disease

2018

Figure S1. Acute cigarette smoke/ lipopolysaccharide lung inflammatory animal model showed resistance to dexamethasone improving lung resistance and bronchoalveolar inflammatory cell extravasation in Muc1 KO animals. Figure S2. IL-8 and IL-13 bronchoalveolar fluid content in Muc1 KO mice exposed to acute cigarette smoke/ lipopolysaccharide is resistant to dexamethasone. Figure S3. Inflammatory lung cell infiltration secondary to acute lipopolysaccharide/ cigarette smoke exposure is resistant to dexamethasone in MUC1 KO mice. (DOCX 1611 kb)

respiratory systemrespiratory tract diseases
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