Search results for "Protein"

showing 10 items of 21431 documents

Osteoprotegerin: multiple partners for multiple functions.

2013

Osteoprotegerin (OPG) is an essential secreted protein in bone turnover due to its role as a decoy receptor for the Receptor Activator of Nuclear Factor-kB ligand (RANKL) in the osteoclasts, thus inhibiting their differentiation. However, there are additional ligands of OPG that confer various biological functions. OPG can promote cell survival, cell proliferation and facilitates migration by binding TNF-related apoptosis inducing ligand (TRAIL), glycosaminoglycans or proteoglycans. A large number of in vitro, pre-clinical and clinical studies provide evidences of OPG involvement in vascular, bone, immune and tumor biology. This review describes an overview of the different OPG ligands regu…

musculoskeletal diseasesCell SurvivalEndocrinology Diabetes and MetabolismImmunologyOsteoclastsGeneral Biochemistry Genetics and Molecular BiologyTNF-Related Apoptosis-Inducing LigandOsteoprotegerinImmunology and AllergyAnimalsHumansCell adhesionReceptorCell ProliferationbiologyActivator (genetics)Cell growthChemistryRANK LigandOsteoprotegerinCell DifferentiationIn vitroCell biologyBiochemistryRANKLbiology.proteinDecoyCytokinegrowth factor reviews
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Osteogenic differentiation of periodontal fibroblasts is dependent on the strength of mechanical strain

2012

Abstract Objective During orthodontic therapy the correct strength of mechanical strain plays a key role for bone remodelling during tooth movement. Aim of this study was to investigate the osteogenic differentiation of human periodontal ligament fibroblasts (HPdLF) depending on the applied strength of mechanical strain compared to osteoblasts (HOB). Design HPdLF and HOB were loaded with different strengths (1%, 5% and 10%) of static mechanical strain (SMS) for 12 h in vitro. Viability was verified by MTT and apoptosis by TUNEL assay. Gene expression of cyclin D1, collagen type-1 (COL-I), alkaline phosphatase (ALP), osteocalcin, osteoprotegerin (OPG) and receptor activator of the NF-κB liga…

musculoskeletal diseasesCell SurvivalPeriodontal LigamentGene ExpressionDentistryApoptosisEnzyme-Linked Immunosorbent AssayReal-Time Polymerase Chain ReactionCollagen Type IBone remodelingAndrologyCyclin D1OsteoprotegerinOsteogenesisIn Situ Nick-End LabelingHumansPeriodontal fiberCyclin D1RNA MessengerGeneral DentistryCells CulturedAnalysis of VarianceOsteoblastsTUNEL assaybiologybusiness.industryChemistryRANK LigandOsteoprotegerinCell DifferentiationCell BiologyGeneral MedicineFibroblastsAlkaline PhosphataseOtorhinolaryngologyRANKLOsteocalcinbiology.proteinAlkaline phosphataseStress MechanicalbusinessArchives of Oral Biology
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Gastric emptying, small intestinal transit and fecal output in dystrophic (mdx) mice.

2009

Duchenne muscular dystrophy (DMD), which results from deficiency in dystrophin, a sarcolemma protein of skeletal, cardiac and smooth muscle, is characterized by progressive striated muscle degeneration, but various gastrointestinal clinical manifestations have been observed. The aim was to evaluate the possible impact of the dystrophin loss on the gastrointestinal propulsion in mdx mice (animal model for DMD). The gastric emptying of a carboxymethyl cellulose/phenol red dye non-nutrient meal was not significantly different at 20 min from gavaging between wild-type and mdx mice. The intestinal transit and the fecal output were significantly decreased in mdx versus normal animals, although th…

musculoskeletal diseasesCell physiologyDuchenne muscular dystrophyMalecongenital hereditary and neonatal diseases and abnormalitiesmdx mousemedicine.medical_specialtyPhysiologyDuchenne muscular dystrophySettore BIO/09 - FisiologiaMiceIn vivoInternal medicineIntestine SmallMedicineAnimalsmdx mouseMuscular dystrophyDefecationSarcolemmabiologyGastric emptyingbusiness.industryMuscular Dystrophy Animalmusculoskeletal systemmedicine.diseaseMice Inbred C57BLDisease Models AnimalEndocrinologyGastric Emptyingbiology.proteinFecal outputMice Inbred mdxIntestinal transitbusinessDystrophinGastrointestinal MotilityThe journal of physiological sciences : JPS
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Dystroglycan regulates structure, proliferation and differentiation of neuroepithelial cells in the developing vertebrate CNS.

2007

AbstractIn the developing CNS α- and β-dystroglycan are highly concentrated in the endfeet of radial neuroepithelial cells at the contact site to the basal lamina. We show that injection of anti-dystroglycan Fab fragments, knockdown of dystroglycan using RNAi, and overexpression of a dominant-negative dystroglycan protein by microelectroporation in neuroepithelial cells of the chick retina and optic tectum in vivo leads to the loss of their radial morphology, to hyperproliferation, to an increased number of postmitotic neurons, and to an altered distribution of several basally concentrated proteins. Moreover, these treatments also altered the oriented growth of axons from retinal ganglion c…

musculoskeletal diseasesCentral Nervous Systemcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtySuperior Colliculianimal structuresCellular differentiationNeuroepithelial CellsStem cellsDevelopmentDystrophin-associated protein complexRetinal ganglionAxonal growthMuscular DystrophiesRetina03 medical and health sciences0302 clinical medicineInternal medicineDystroglycanmedicineAnimalsDystroglycansMolecular BiologyCell Shape030304 developmental biologyCell Proliferation0303 health sciencesRetinabiologyfungiCell DifferentiationCell BiologyMuscular dystrophymusculoskeletal systemCell biologyNeuroepithelial cellmedicine.anatomical_structureEndocrinologyRNAiVertebratesbiology.proteinBasal laminaPikachurinStem cellChickens030217 neurology & neurosurgeryDevelopmental BiologyDevelopmental biology
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Bacteria-specific cytotoxic CD8+ T cells: a missing link in the pathogenesis of the HLA-B27-associated spondylarthropathies.

1994

The term seronegative spondylarthropathies is used for an entity of rheumatic syndromes of peripheral joints and the spine (ankylosing spondylitis, reactive arthritis, Reiter's syndrome, arthritis in psoriasis and in inflammatory bowel disease) which are strongly associated with the MHC class I molecule HLA-B27. However, the mechanisms whereby HLA-B27 confers disease susceptibility have so far remained unknown. There is strong evidence that gut inflammation and infection with gram-negative bacteria play a role in the induction of B27-associated disease. HLA-B27, like other MHC class I molecules, physiologically binds antigenic peptides in its binding groove and presents them to CD8+ T lymph…

musculoskeletal diseasesCytotoxicity ImmunologicAnkylosisEpitopeEpitopesAntigenEnterobacteriaceaeMHC class IMedicineCytotoxic T cellAnimalsHumansSpondylarthropathiesHLA-B27 AntigenHLA-B27Antigens Bacterialbiologybusiness.industryArthritisSynovial MembraneGeneral MedicineDisease Models AnimalImmunologybiology.proteinBacterial antigenbusinessCD8Protein BindingT-Lymphocytes CytotoxicAnnals of medicine
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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Targeting of the transcription factor STAT4 by antisense phosphorothioate oligonucleotides suppresses collagen-induced arthritis

2007

Abstract The transcription factor STAT4 mediates signals of various proinflammatory cytokines, such as IL-12, IL-15, and IL-23, that initiate and stabilize Th1 cytokine production. Although Th1 cytokine production has been suggested to play a major pathogenic role in rheumatoid arthritis, the role of STAT4 in this disease is poorly understood. In this study, we demonstrate a key functional role of STAT4 in murine collagen-induced arthritis (CIA). In initial studies we found that STAT4 expression is strongly induced in CD4+ T cells and to a lesser extent in CD11b+ APCs during CIA. To analyze the role of STAT4 for arthritis manifestation, we next investigated the outcome of interfering with S…

musculoskeletal diseasesImmunologyAntigen-Presenting CellsCodon InitiatorArthritisBiologyProinflammatory cytokineArthritis RheumatoidPathogenesisMiceimmune system diseasesmedicineAnimalsImmunology and Allergyskin and connective tissue diseasesSTAT4Cells CulturedMice KnockoutMice Inbred BALB CCD11b Antigenhemic and immune systemsOligonucleotides AntisenseSTAT4 Transcription FactorTh1 CellsThionucleotidesmedicine.diseaseArthritis ExperimentalIntegrin alpha MRheumatoid arthritisImmunologybiology.proteinExperimental pathologyTumor necrosis factor alpha
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H2-M polymorphism in mice susceptible to collagen-induced arthritis involves the peptide binding groove.

1996

The ability to develop type II collagen (CII)-induced arthritis (CIA) in mice is associated with the major histocompatibilityI-A gene and with as yet poorly defined regulatory molecules of the major histocompatibility complex (MHC) class II antigen processing and presentation pathway. H2-M molecules are thought to be involved in the loading of antigenic peptides into the MHC class II binding cleft. We sequencedH2-Ma, H2-Mb1, andH2-Mb2 genes from CIA-susceptible and-resistant mouse strains and identified four differentMa andMb2 alleles and three differentMb1 alleles defined by polymorphic residues within the predicted peptide binding groove. Most CIA-resistant mouse strains share commonMa, M…

musculoskeletal diseasesImmunologyGenes MHC Class IIMolecular Sequence DataGenes MHC Class IPeptide bindingMice Inbred StrainsMajor histocompatibility complexEpitopeMiceAntigenMHC class IGeneticsAnimalsAmino Acid SequencePhylogenyDNA PrimersMHC class IIPolymorphism GeneticbiologyBase SequenceSequence Homology Amino AcidAntigen processingH-2 AntigensHistocompatibility Antigens Class IIMolecular biologyArthritis ExperimentalHistocompatibilityHaplotypesbiology.proteinCollagenSequence AlignmentImmunogenetics
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Altered (oxidized) C1q induces a rheumatoid arthritis-like destructive and chronic inflammation in joint structures in arthritis-susceptible rats.

1997

Previous studies have identified an altered C1q molecule in synovial fluids from the joints of rheumatoid arthritis patients. We therefore immunized arthritis-susceptible Lewis 1A.AVN rats with either native C1q (C1q nat), altered (oxidized) C1q (C1q ox), or type II collagen (CII, induces arthritis in these animals), in order to induce arthritis. Unlike C1q nat, both CII and C1q ox were able to induce swelling and erythema of joints consistent with an arthritis-like inflammatory reaction. Histopathological evaluation of individual joint sections revealed synovitis, bursitis and tendovaginitis, massive joint destruction, and severe pannus formation. In a time-course study, no differences in …

musculoskeletal diseasesImmunologyType II collagenArthritischemical and pharmacologic phenomenaInflammationPathology and Forensic Medicinefluids and secretionsAntigenimmune system diseasesSynovitismedicineImmunology and AllergyAnimalsskin and connective tissue diseasesAutoimmune diseaseInflammationbiologybusiness.industryArthritisComplement C1qmedicine.diseaseRatsRats Inbred LewRheumatoid arthritisImmunologybiology.proteinFemaleJointsmedicine.symptomAntibodybusinessOxidation-ReductionClinical immunology and immunopathology
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Fertility in McCune Albright syndrome female: A case study focusing on AMH as a marker of ovarian dysfunction and a literature review.

2021

Abstract Background The molecular basis of McCune Albright syndrome (MAS) is a recurrent GNAS Postzygotic gain of function sporadic mutation, resulting in a mosaic disease. Most of girls present precocious puberty, caused by the development of recurrent ovarian cysts with autonomous Hyperestrogenic stimulation. After menarche, the majority of patients with ovarian GNAS mutation have menstrual disturbances and infertility. Objectives We wanted to focus on the fertility of MAS females and propose an appropriate management, by a detailed case report and an exhaustive review of the literature on fertility and pregnancy in MAS females. Results We present the case of a 29-year-old MAS female, who…

musculoskeletal diseasesInfertilityAdultAnti-Mullerian Hormoneendocrine systemmedicine.medical_specialtyendocrine system diseasesGenetic counselingmedicine.medical_treatmentOvariectomyFertilization in VitroFibrous Dysplasia PolyostoticMcCune–Albright syndrome03 medical and health sciences0302 clinical medicineFollicular phasemedicineGNAS complex locusPrecocious pubertyHumansGynecology030219 obstetrics & reproductive medicineIn vitro fertilisationbiologybusiness.industryObstetrics and GynecologyOophorectomymedicine.diseasefemale genital diseases and pregnancy complicationsReproductive Medicine030220 oncology & carcinogenesisbiology.proteinFemalebusinessInfertility Femalehormones hormone substitutes and hormone antagonistsJournal of gynecology obstetrics and human reproduction
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