Search results for "Thyrotropin"

showing 10 items of 93 documents

Serum Thyroid-Stimulating Hormone Levels and Frailty in the Elderly: The Progetto Veneto Anziani Study

2016

High or low thyroid-stimulating hormone (TSH) levels seem to be associated with several negative outcomes in the elderly, but the literature about TSH and frailty is still limited. In this article, we investigated whether TSH is associated with prevalent and incident frailty in a cohort of older community-dwelling subjects. Among 3099 initially screened in the Progetto Veneto Anziani Study, 2571 men and women aged ≥65 years (for cross-sectional analyses) and 1732 (longitudinal, mean follow-up period of 4.4 years) were divided into sex-specific quintiles according to baseline serum TSH concentrations within normal range (0.3 and 4.2 mUI/L). Frailty was defined as the presence of three among …

0301 basic medicineGerontologyMaleAgingmedicine.medical_specialtyFrail ElderlyThyrotropin030209 endocrinology & metabolismfrailtyelderlythyroid03 medical and health sciences0302 clinical medicineThyroid-stimulating hormoneInternal medicinemedicinePrevalencecommunity-dwelling adults.HumansNormal rangeAgedbusiness.industryIncidenceConfoundingThyroidOdds ratioConfidence interval030104 developmental biologymedicine.anatomical_structureCross-Sectional StudiesCohortFemaleGeriatrics and GerontologybusinessHormoneFollow-Up Studies
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Arrestin-β-1 Physically Scaffolds TSH and IGF1 Receptors to Enable Crosstalk

2019

Endogenously expressed TSH receptors (TSHRs) on orbital fibroblasts of patients with Graves ophthalmopathy (GO) use crosstalk with IGF1 receptors (IGF1R) to synergistically stimulate secretion of hyaluronan (HA), a major component of GO pathology. We previously showed crosstalk occurred upstream of mitogen-activated protein kinase (ERK) phosphorylation. Because other G protein-coupled receptors engage arrestin-β-1 (ARRB1) and ERK, we tested whether ARRB1 was a necessary component of TSHR/IGF1R crosstalk. HA secretion was stimulated by the TSHR-stimulating monoclonal antibodies M22 and KSAb1, or immunoglobulins from patients with GO (GO-Igs). Treatment with M22, as previously shown, resulted…

0301 basic medicineMAPK/ERK pathwaymedicine.medical_specialty030209 endocrinology & metabolismStimulationReceptor tyrosine kinaseCell LineReceptor IGF Type 103 medical and health sciencesMice0302 clinical medicineEndocrinologyInternal medicinemedicineArrestinAnimalsHumansPhosphorylationProtein kinase AReceptorResearch ArticlesbiologyChemistryReceptors Thyrotropinbody regionsGraves OphthalmopathyCrosstalk (biology)030104 developmental biologyEndocrinologybeta-Arrestin 1Thyroid Epithelial CellsGene Knockdown Techniquesbiology.proteinPhosphorylationSignal Transduction
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Familial Central Hypothyroidism Caused by a Novel IGSF1 Gene Mutation.

2016

Congenital hypothyroidism of central origin (CH-C) is a rare disease in which thyroid hormone deficiency is caused by insufficient thyrotropin stimulation of a normal thyroid gland. A recently described syndrome of isolated CH-C and macroorchidism was attributed to loss-of-function mutations of the immunoglobulin superfamily, member 1 gene (IGSF1).CH-C was diagnosed in three siblings. The TRH, TRHR, and TSHB genes were sequenced followed by whole-exome sequencing in the proband. A mutation identified in IGSF1 was analyzed by direct PCR sequencing in family members. The effects of the mutation were assessed by in vitro studies in HEK293 cells.The index case was negative for mutations in TRH,…

0301 basic medicineProbandMaleendocrine systemEndocrinology Diabetes and MetabolismDNA Mutational AnalysisImmunoglobulinsThyrotropin030209 endocrinology & metabolismBiology03 medical and health sciences0302 clinical medicineEndocrinologyHypothyroidismmedicineCentral hypothyroidismCongenital HypothyroidismHumansInsertionThyrotropin-Releasing HormoneGeneticsMacroorchidismReceptors Thyrotropin-Releasing HormoneSiblingsThyroidInfant NewbornInfantMembrane Proteinsmedicine.diseaseMolecular biologyCongenital hypothyroidismIGSF1030104 developmental biologymedicine.anatomical_structureHEK293 CellsChild PreschoolMutation (genetic algorithm)MutationThyroid : official journal of the American Thyroid Association
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Evidence That Graves' Ophthalmopathy Immunoglobulins Do Not Directly Activate IGF-1 Receptors

2018

Background: Graves' ophthalmopathy (GO) pathogenesis involves thyrotropin (TSH) receptor (TSHR)-stimulating autoantibodies. Whether there are autoantibodies that directly stimulate insulin-like growth factor 1 receptors (IGF-1Rs), stimulating insulin-like growth factor receptor antibodies (IGFRAbs), remains controversial. This study attempted to determine whether there are stimulating IGFRAbs in patients with GO. Methods: Immunoglobulins (Igs) were purified from normal volunteers (NV-Igs) and patients with GO (GO-Igs). The effects of TSH, IGF-1, NV-Igs, and GO-Igs on pAKT and pERK1/2, members of pathways used by IGF-1R and TSHR, were compared in orbital fibroblasts from GO patients (GOFs) a…

0301 basic medicineendocrine systemendocrine system diseasesEndocrinology Diabetes and MetabolismImmunoglobulins030209 endocrinology & metabolismCell LineReceptor IGF Type 1PathogenesisGraves' ophthalmopathy03 medical and health sciences0302 clinical medicineEndocrinologymedicineHumansImmunology Autoimmunity and Graves' OphthalmopathyPhosphorylationReceptorbiologybusiness.industryAutoantibodyReceptors Thyrotropinmedicine.diseaseeye diseasesGraves Ophthalmopathy030104 developmental biologyImmunologybiology.proteinlipids (amino acids peptides and proteins)AntibodybusinessProto-Oncogene Proteins c-akthormones hormone substitutes and hormone antagonists
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A cyclic peptide significantly improves thyroid function, thyrotropin-receptor antibodies and orbital mucine /collagen content in a long-term Graves’…

2021

BALB/c mice which received long-term immunizations of adenovirus (Ad) expressing thyrotropin receptor A-subunits (TSHR) developed stable Graves' disease (GD). TSHR-derived cyclic peptide 19 (P19) was identified as effective therapy in this model.In Ad-TSHR mice, we investigated shorter disease intervals up to 4 months for histological alterations of the orbits, fine tuning of anti-TSHR antibodies (Ab) and free thyroxine (fT4) hormone levels by using novel detection methods in an independent laboratory. Therapy (0.3 mg/kg P19 or vehicle) was given intravenously after the fourth Ad-TSHR immunization (week 11) and continued until week 19.Thyrotropin binding inhibitory immunoglobulins (TBII, br…

0301 basic medicineendocrine systemmedicine.medical_specialtyendocrine system diseasesGraves' diseaseImmunologyCellThyroid GlandPeptides CyclicThyrotropin receptorMice03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalsHumansImmunology and AllergyBioassay030203 arthritis & rheumatologybiologymedicine.diagnostic_testbusiness.industryMucinsReceptors Thyrotropinmedicine.diseaseGraves Diseaseeye diseasesGraves OphthalmopathyDisease Models Animal030104 developmental biologymedicine.anatomical_structureEndocrinologyImmunoassaybiology.proteinFemaleCollagenAntibodyThyroid functionbusinessOrbithormones hormone substitutes and hormone antagonistsImmunoglobulins Thyroid-StimulatingHormoneJournal of Autoimmunity
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TSH/IGF-1 Receptor Cross-Talk Rapidly Activates Extracellular Signal-Regulated Kinases in Multiple Cell Types

2017

We previously showed that thyrotropin (TSH)/insulinlike growth factor (IGF)-1 receptor cross-talk appears to be involved in Graves’ orbitopathy (GO) pathogenesis and upregulation of thyroid-specific genes in human thyrocytes. In orbital fibroblasts from GO patients, coadministration of TSH and IGF-1 induces synergistic increases in hyaluronan secretion. In human thyrocytes, TSH plus IGF-1 synergistically increased expression of the sodium-iodide symporter that appeared to involve ERK1/2 activation. However, the details of ERK1/2 activation were not known, nor was whether ERK1/2 was involved in this synergism in other cell types. Using primary cultures of GO fibroblasts (GOFs) and human thyr…

0301 basic medicinemedicine.medical_specialtyCell typeendocrine systemendocrine system diseasesMAP Kinase Signaling SystemThyrotropinPertussis toxinReceptor IGF Type 103 medical and health sciencesEndocrinologyDownregulation and upregulationInternal medicinemedicineHumansSecretionHyaluronic AcidInsulin-Like Growth Factor IPhosphorylationReceptorResearch ArticlesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3SymportersChemistryHEK 293 cellsReceptors ThyrotropinReceptor Cross-TalkFibroblastsSignalingGraves Ophthalmopathy030104 developmental biologyEndocrinologyHEK293 CellsThyroid Epithelial CellsSymporterPhosphorylationhormones hormone substitutes and hormone antagonistsEndocrinology
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TSH/IGF-1 Receptor Cross Talk in Graves' Ophthalmopathy Pathogenesis.

2016

AbstractContext:The TSH receptor (TSHR) is considered the main target of stimulatory autoantibodies in the pathogenesis of Graves' ophthalmopathy (GO); however, it has been suggested that stimulatory IGF-1 receptor (IGF-1R) autoantibodies also play a role.Objective:We previously demonstrated that a monoclonal stimulatory TSHR antibody, M22, activates TSHR/IGF-1R cross talk in orbital fibroblasts/preadipocytes obtained from patients with GO (GO fibroblasts [GOFs]). We show that cross talk between TSHR and IGF-1R, not direct IGF-1R activation, is involved in the mediation of GO pathogenesis stimulated by Graves' autoantibodies.Design/Setting/Participants:Immunoglobulins were purified from the…

0301 basic medicinemedicine.medical_specialtyLinsitinibEndocrinology Diabetes and MetabolismClinical Biochemistry030209 endocrinology & metabolismContext (language use)BiochemistryThyrotropin receptorReceptor IGF Type 1Graves' ophthalmopathyPathogenesis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyInternal medicineCyclic AMPMedicineHumansHyaluronic AcidReceptorCells Culturedbusiness.industryBiochemistry (medical)AutoantibodyReceptors ThyrotropinReceptor Cross-TalkOriginal Articlesmedicine.diseaseGraves Ophthalmopathy030104 developmental biologyEndocrinologychemistryMonoclonalbusinessOrbitThe Journal of clinical endocrinology and metabolism
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Alterations in circadian rhythm of serum thyrotropin in critically ill patients.

1992

To evaluate the 24-h pattern of serum thyrotropin (TSH) in critically ill patients, we measured serum concentrations of TSH in blood samples collected every 2 h for 24 h from nine patients (six with malignancy, two with liver cirrhosis, one with chronic renal failure), who had subnormal levels of both triiodothyronine (T3) and thyroxine (T4), in the absence of history, symptoms or signs of thyroid disease. Analysis of the data, performed using a second-order inferential statistical methodology for rhythmometry (cosinor method), demonstrated that critically ill patients still had daily oscillations of serum TSH which significantly adapted to the function approximating the circadian rhythms (…

AdultLiver CirrhosisMaleendocrine systemmedicine.medical_specialtyCirrhosisEndocrinology Diabetes and MetabolismCritical IllnessRadioimmunoassayThyrotropinMalignancylaw.inventionEndocrinologyRhythmlawInternal medicineNeoplasmsmedicineHumansCircadian rhythmAgedTriiodothyroninebusiness.industryCritically illThyroid diseaseGeneral MedicineMiddle Agedmedicine.diseaseIntensive care unitCircadian RhythmThyroxineEndocrinologyKidney Failure ChronicTriiodothyronineFemalebusinessActa endocrinologica
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Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness

1994

Custro N, Scafidi V, Gallo S, Notarbartolo A. Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness. Eur J Endocrinol 1994;130:132–6. ISSN 0804–4643. Twenty-four-hour thyrotropin (TSH) profiles in eight severely ill patients were compared with those of six healthy subjects. The profiles were assessed using the cosinor method to evaluate circadian variations and using the Pulsar algorithm to analyze episodic secretion. In the normal subjects, the typical periodicity of TSH secretion showed a mean level in the rhythm (mesor) of 2.03 mU/l, The amplitude (half the extent of rhythmic change in the cycle) was 0.58 mU/l; the acrophase (the delay…

AdultLiver CirrhosisMaleendocrine systemmedicine.medical_specialtyTriiodothyronine Reverseendocrine system diseasesEndocrinology Diabetes and MetabolismPulsatile flowThyrotropinBiologyThyroxine-Binding ProteinsEndocrinologyRhythmHypothyroidismThyrotropic cellNeoplasmsInternal medicinemedicineHumansCircadian rhythmTriiodothyroninePulse (signal processing)ThyroidGeneral MedicineMiddle AgedCircadian RhythmThyroxineEndocrinologymedicine.anatomical_structurePulsatile FlowTriiodothyronineFemaleHormoneEuropean Journal of Endocrinology
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Stimulatory TSH-Receptor Antibodies and Oxidative Stress in Graves Disease

2018

CONTEXT: We hypothesized that TSH-receptor (TSHR) stimulating antibodies (TSAbs) are involved in oxidative stress mechanisms in patients with Graves disease (GD). METHODS: Nicotinamide adenine dinucleotide phosphate oxidase, isoform 2 (NOX2); oxidative parameters; and oxidative burst were measured in serum, urine, and whole blood from patients with GD and control subjects. Superoxide production was investigated in human embryonic kidney (HEK)-293 cells stably overexpressing the TSHR. Lipid peroxidation was determined by immunodot-blot analysis for protein-bound 4-hydroxy-2-nonenal (4-HNE) in human primary thyrocytes and HEK-293–TSHR cells. RESULTS: Serum NOX2 levels were markedly higher in …

AdultMale0301 basic medicineendocrine systemmedicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and MetabolismGraves' diseaseClinical Biochemistry030209 endocrinology & metabolismContext (language use)medicine.disease_causeBiochemistryLipid peroxidation03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyInternal medicinemedicineHumansEuthyroidClinical Research ArticlesTriiodothyroninebusiness.industryBiochemistry (medical)Toxic nodular goiterReceptors ThyrotropinMiddle AgedPrognosismedicine.diseaseGraves DiseaseRespiratory burstOxidative StressHEK293 Cells030104 developmental biologyEndocrinologychemistryFemaleLipid PeroxidationbusinessBiomarkershormones hormone substitutes and hormone antagonistsOxidative stressFollow-Up StudiesImmunoglobulins Thyroid-StimulatingThe Journal of Clinical Endocrinology & Metabolism
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