Search results for "FIBROBLASTS"

showing 10 items of 445 documents

Influence of nifedipine on the metabolism of gingival fibroblasts.

1994

Calcium antagonists are the gold standard in the therapy of coronary heart disease and hypertension. The prototype of these drugs is nifedipine which, as well as its therapeutic effects on the cells of the cardiovascular system, also has unpleasant side effects on other organ systems. One side effect can be a missive hyperplasia of the gingiva, the reason for which are unclear. In vitro experiments were designed to elucidate the influence of nifedipine on the growth of human gingival fibroblasts in short and long term (72 hours, 6 weeks) cell culture. The following cellular parameters were determined quantitatively: cell proliferation (cell count, [3H]thymidine incorporation), protein synth…

AdultSide effectNifedipineCell SurvivalCellGingivaPharmacologyBiochemistrychemistry.chemical_compoundNifedipineCyclosporin aLactate dehydrogenasemedicineHumansCells CulturedDose-Response Relationship DrugChemistryCell growthDNAHyperplasiaFibroblastsmedicine.diseaseChromatography Ion Exchangemedicine.anatomical_structureCell cultureProtein BiosynthesisProteoglycansCell Divisionmedicine.drugBiological chemistry Hoppe-Seyler
researchProduct

Myofibroblasts Are Evidence of Chronic Tissue Microtrauma at the Endometrial-Myometrial Junctional Zone in Uteri With Adenomyosis.

2017

Background Adenomyosis (AM) uteri exhibit hyperperistalsis. The latter causes a chronic tissue trauma at the endometrial-myometrial junctional zone (EMJZ). Upon tissue trauma, microdehiscences in the myometrium facilitate the translocation of basal endometrial fragments into the myometrium. There, a metaplasia (mediated by transforming growth factor β1 [TGFβ1] and connective tissue growth factor [CTGF]) occurs and AM lesions develop. The abundance of myofibroblasts in a tissue hallmarks metaplasia and points to a tissue microtrauma. Materials and methods To study if myofibroblasts-as an evidence of tissue microtrauma-are more abundant at EMJZ in AM-uteri, a case-control experimental study w…

Adultadenomyosis pathogenesiPathologymedicine.medical_specialtyUterusConnective tissueEndometriummicrotraumaDesmin03 medical and health sciencesEndometrium0302 clinical medicineendometrial–myometrial junctional zoneMetaplasiaMedicineHumansAdenomyosisMyofibroblastscollagen I030219 obstetrics & reproductive medicineurogenital systembusiness.industryMyometriumConnective Tissue Growth FactorObstetrics and Gynecologymedicine.diseaseActinsCTGFmedicine.anatomical_structure030220 oncology & carcinogenesisCase-Control StudiesMyometriumDesminFemalemedicine.symptombusinessReceptors Transforming Growth Factor betaAdenomyosisBiomarkersReproductive sciences (Thousand Oaks, Calif.)
researchProduct

In vitro synthesis of glycosaminoglycans in endocrine ophthalmopathy

1992

The effects of humoral and cell-mediated immunity on the glycosaminoglycan synthesis of retrobulbar fibroblasts was evaluated in patients with endocrine ophthalmopathy. After incubation with IgG and sera, secreted glycosaminoglycans, radiolabeled with D-6-3H-glucosamine and 35sulfate, were precipitated with cetylpyridinium chloride and ethanol. Hyaluronic acid synthesis of human retrobulbar fibroblasts after incubation with sera and IgG and after co-culture with lymphocytes was assessed by means of a radiometric test. Patients' IgG, compared to controls', accounted for a higher secretory stimulation of porcine retrobulbar fibroblasts (as measured by cetylpyridinium chloride precipitation) a…

Adultmedicine.medical_specialtyEye Diseasesgenetic structuresSwineEndocrinology Diabetes and MetabolismStimulationEndocrine System DiseasesCetylpyridinium chlorideIncubation periodGlycosaminoglycanchemistry.chemical_compoundEndocrinologyInternal medicineHyaluronic acidAnimalsHumansMedicineLymphocytesHyaluronic AcidFibroblastIncubationAgedGlycosaminoglycansbusiness.industryOsmolar ConcentrationGeneral MedicineFibroblastsMiddle Agedeye diseasesIn vitroEndocrinologymedicine.anatomical_structurechemistryImmunoglobulin Gsense organsbusinessOrbit
researchProduct

CARDIAC PUNCTURE OF FETUS WITH HURLER'S DISEASE AVOIDING ABORTION OF UNAFFECTED CO-TWIN

1978

Adultmedicine.medical_specialtyFetal ResorptionMucopolysaccharidosis IFetal heartPuncturesDiseaseAbortionIduronidaseFetal HeartPregnancyPrenatal DiagnosisDiseases in TwinsHumansMedicineFetal DeathGlucuronidaseGlycosaminoglycansFetusPregnancyFetal deathbusiness.industryObstetricsInfant NewbornFollow up studiesInfantFetal ResorptionGeneral MedicineFibroblastsAmniotic Fluidbeta-Galactosidasemedicine.diseaseAnesthesiaFemalebusinessFollow-Up StudiesThe Lancet
researchProduct

Progerin expression induces a significant downregulation of transcription from human repetitive sequences in iPSC-derived dopaminergic neurons.

2019

Repetitive DNA sequences represent about half of the human genome. They have a central role in human biology, especially neurobiology, but are notoriously difficult to study. The purpose of this study was to quantify the transcription from repetitive sequences in a progerin-expressing cellular model of neuronal aging. Progerin is a nuclear protein causative of the Hutchinson–Gilford progeria syndrome that is also incrementally expressed during the normal aging process. A dedicated pipeline of analysis allowed to quantify transcripts containing repetitive sequences from RNAseq datasets oblivious of their genomic localization, tolerating a sufficient degree of mutational noise, all with low c…

AgingRetroelementsTranscription GeneticAluInduced Pluripotent Stem CellsAlu elementDown-RegulationSettore BIO/11 - Biologia MolecolareRetrotransposonComputational biologyBiologySettore BIO/19 - Microbiologia GeneraleProgerinProgeriaSettore BIO/13 - Biologia ApplicataAlu ElementsRepetitive sequencemedicineRetrotransposonHumansDNA transposonRepeated sequenceGeneCellular SenescenceProgeriaintegumentary systemDopaminergic NeuronsFibroblastsmedicine.diseaseProgerinLamin Type ASettore BIO/18 - GeneticaSatelliteHuman genomeOriginal ArticleGeriatrics and GerontologyGeroScience
researchProduct

Primary mouse fibroblasts deficient for c-Fos, p53 or for both proteins are hypersensitive to UV light and alkylating agent-induced chromosomal break…

2000

The important regulatory proteins, c-Fos and p53 are induced by exposure of cells to a variety of DNA damaging agents. To investigate their role in cellular defense against genotoxic compounds, we comparatively analysed chromosomal aberrations and apoptosis induced by ultraviolet (UV-C) light and the potent alkylating agent methyl methanesulfonate (MMS) in primary diploid mouse fibroblasts knockout for either c-Fos or p53, or double knockout for both genes. We show that c-Fos and p53 deficient fibroblasts are more sensitive than the corresponding wild-type cells as to the induction of chromosomal aberrations and apoptosis. Double knockout fibroblasts lacking both c-Fos and p53 are viable an…

Alkylating AgentsUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisDrug ResistanceMutagenesis (molecular biology technique)ApoptosisBiologyRadiation ToleranceCell LineMicechemistry.chemical_compoundGeneticsAnimalsMolecular BiologyGene knockoutChromosome AberrationsMice KnockoutGenes fosFibroblastsCell cycleGenes p53Molecular biologyMethyl methanesulfonatechemistryApoptosisCell cultureTumor Suppressor Protein p53Proto-Oncogene Proteins c-fosDNA DamageMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
researchProduct

Central role of IL-6 and MMP-1 for cross talk between human intestinal mast cells and human intestinal fibroblasts.

2012

Mast cells (MC) are key effector cells in allergic reactions but also involved in host defence, tissue remodeling, angiogenesis, and fibrogenesis. Here, we show that human intestinal fibroblasts (FB) suppress apoptosis in human intestinal MC dependent on IL-6. Intestinal FB produced IL-6 upon direct stimulation by intestinal MC in co-culture or by MC mediators such as TNF-α, IL-1β, tryptase or histamine. MC incubated with IL-6 survived for up to 3 weeks similar to MC co-cultured with FB and MC survival could be blocked by neutralizing anti-IL-6 Abs. Moreover, FB stimulated by MC mediators upregulated their expression of matrix metalloproteinase-1 (MMP-1), a key fibrolytic enzyme. Noteworthy…

AngiogenesisCell SurvivalImmunologyInflammationTryptaseApoptosisCell CommunicationMatrix metalloproteinaseBiologychemistry.chemical_compoundDownregulation and upregulationmedicineImmunology and AllergyHumansMast CellsIntestinal MucosaInterleukin 6Protein Kinase InhibitorsFlavonoidsInterleukin-6HematologyReceptor Cross-TalkFibroblastsMolecular biologyCoculture TechniqueschemistryApoptosisImmunologybiology.proteinmedicine.symptomMatrix Metalloproteinase 1HistamineImmunobiology
researchProduct

Succinobucol’s New Coat — Conjugation with Steroids to Alter Its Drug Effect and Bioavailability

2011

Synthesis, detailed structural characterization (X-ray, NMR, MS, IR, elemental analysis), and studies of toxicity, antioxidant activity and bioavailability of unique potent anti-atherosclerotic succinobucol-steroid conjugates are reported. The conjugates consist of, on one side, the therapeutically important drug succinobucol ([4-{2,6-di-tert-butyl-4-[(1-{[3-tert-butyl-4-hydroxy-5-(propan-2-yl)phenyl]sulfanyl}ethyl)sulfanyl]phenoxy}-4-oxo-butanoic acid]) possessing an antioxidant and anti-inflammatory activity, and on the other side, plant stanol/sterols (stigmastanol, β-sitosterol and stigmasterol) possessing an ability to lower the blood cholesterol level. A cholesterol-succinobucol prodr…

AntioxidantFree RadicalsStereochemistrymedicine.medical_treatmentStatic ElectricityAnti-Inflammatory AgentsBiological AvailabilityPharmaceutical ScienceprobucolArticleAntioxidantsAnalytical Chemistrylcsh:QD241-441Micechemistry.chemical_compoundPicrateslcsh:Organic chemistrySulfanylDrug DiscoverymedicineAnimalsHumansPhysical and Theoretical Chemistrysuccinobucol; phytosterol; atherosclerosis; cholesterol; probucolta317phytosterolStigmastanolClinical Trials as TopicMice Inbred BALB CMolecular StructurePhytosterolBiphenyl CompoundsOrganic Chemistrycholesterol3T3 CellsFibroblastsProdrugAscorbic acidBioavailabilityBiphenyl compoundchemistryChemistry (miscellaneous)Molecular MedicineSteroidsatherosclerosissuccinobucolMolecules; Volume 16; Issue 11; Pages: 9404-9420
researchProduct

Sub-lethal Doses of Polybrominated Diphenyl Ethers, in Vitro, Promote Oxidative Stress and Modulate Molecular Markers Related to Cell Cycle, Antioxid…

2019

In the present study, we evaluated the effects of different concentrations of the polybrominated diphenyl ethers (PBDEs) BDE-209, BDE-47 and BDE-99, on the vitality and oxidative stress of a HS-68 human cell culture exposed to the compounds for three days. The results showed that for this exposure time, only the highest concentrations produced a significant vitality reduction and oxidative stress induction (p &lt

AntioxidantPBDEsmedicine.medical_treatmentHealth Toxicology and Mutagenesisproliferationlcsh:Medicine010501 environmental sciencesPharmacologyPBDEmedicine.disease_cause01 natural sciencesAntioxidantsArticleCell Line03 medical and health sciencesPolybrominated diphenyl ethersSettore AGR/20 - ZoocoltureHalogenated Diphenyl EthersmedicineHumansoxidative stressSettore BIO/06 - Anatomia Comparata E Citologia030304 developmental biology0105 earth and related environmental scienceschemistry.chemical_classification0303 health sciencesReactive oxygen speciesoxidative streCell growthCell Cyclelcsh:RPublic Health Environmental and Occupational HealthAMPKbiomarkersMetabolismFibroblastsCell cyclechemistrybiomarkerEnvironmental PollutantsEnergy MetabolismmetabolismOxidative stressInternational Journal of Environmental Research and Public Health
researchProduct

DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK).

2009

Abstract The impact of DNA damage-induced replication blockage for early activation of stress kinases [stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)] is largely unknown. Here, we show that induction of dual phosphorylation of SAPK/JNK by the DNA polymerase inhibitor aphidicolin was not ameliorated by additional exposure to ultraviolet (UV) light, indicating that overlapping mechanisms participate in signaling to SAPK/JNK triggered by both agents. UV-induced DNA replication blockage, cyclobutane pyrimidine dimer formation and DNA strand break induction coincided with SAPK/JNK phosphorylation at early (≤ 30 min) but not late (≥ 2 h) time points after exposure. Genotoxin…

AphidicolinDNA ReplicationDNA damageUltraviolet RaysPoly ADP ribose polymeraseCell Linechemistry.chemical_compoundMiceAphidicolinStructural BiologyCricetinaeAnimalsHumansLymphocytesPhosphorylationProtein kinase AMolecular BiologyNucleic Acid Synthesis InhibitorsBRCA2 ProteinMice KnockoutbiologyKinaseCell CycleDNA replicationJNK Mitogen-Activated Protein KinasesFibroblastsMolecular biologyProliferating cell nuclear antigenDNA-Binding ProteinsEnzyme ActivationchemistryPyrimidine Dimersbiology.proteinPhosphorylationApoptosis Regulatory ProteinsDNA DamageJournal of molecular biology
researchProduct