Search results for "PCS"

showing 10 items of 94 documents

PCSK9-D374Y mediated LDL-R degradation can be functionally inhibited by EGF-A and truncated EGF-A peptides: An in vitro study.

2019

Abstract Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low density lipoprotein receptor (LDLR) through the LDLR epidermal growth factor-like repeat A (EGF-A) domain and induces receptor internalization and degradation. PCSK9 has emerged as a novel therapeutic target for hypercholesterolemia. Clinical studies with PCSK9 inhibiting antibodies have demonstrated strong LDL-c lowering effects, but other therapeutic approaches using small molecule inhibitors for targeting PCSK9 functions may offer supplementary therapeutic options. The aim of our study was to evaluate the effect of synthetic EGF-A analogs on mutated (D374Y) PCSK9-D374Y mediated LDLR degradatio…

0301 basic medicineSmall peptidesmedia_common.quotation_subject030204 cardiovascular system & hematologyDecoy strategyPCSK903 medical and health sciences0302 clinical medicineHumansInternalizationCells Culturedmedia_commonExpression vectorEpidermal Growth FactorChemistryPCSK9PCSK9 InhibitorsTransfectionProprotein convertasePCSK9 inhibitionIn vitroCell biologyEGF-A domain030104 developmental biologyLDLRReceptors LDLLDL receptorMutationKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
researchProduct

Cellular Response to Spinal Cord Injury in Regenerative and Non-Regenerative Stages in Xenopus Laevis

2020

Abstract Background The efficient regenerative abilities at larvae stages followed by a non-regenerative response after metamorphosis in froglets makes Xenopus an ideal model organism to understand the cellular responses leading to spinal cord regeneration. Methods We compared the cellular response to spinal cord injury between the regenerative and non-regenerative stages of Xenopus laevis. For this analysis, we used electron microscopy, immunofluorescence and histological staining of the extracellular matrix. We generated two transgenic lines: i) the reporter line with the zebrafish GFAP regulatory regions driving the expression of EGFP, and ii) a cell specific inducible ablation line with…

0301 basic medicineSpinal Cord RegenerationGfapXenopusNeurogenesislcsh:RC346-429Glial scarGlial scar03 medical and health sciencesXenopus laevis0302 clinical medicineDevelopmental NeuroscienceNeural Stem CellsmedicineAnimalsRegenerationsox2Progenitor cellSpinal cord injuryZebrafishSpinal Cord RegenerationSpinal Cord InjuriesZebrafishlcsh:Neurology. Diseases of the nervous systemSpinal cordbiologyRegeneration (biology)NeurogenesisSpinal cordmedicine.diseasebiology.organism_classificationCell biology030104 developmental biologymedicine.anatomical_structureNSPCsnervous system030217 neurology & neurosurgeryResearch Article
researchProduct

Practical guidance for combination lipid-modifying therapy in high- and very-high-risk patients: A statement from a European Atherosclerosis Society …

2021

International audience; Background and aimsThis European Atherosclerosis Society (EAS) Task Force provides practical guidance for combination therapy for elevated low-density lipoprotein cholesterol (LDL-C) and/or triglycerides (TG) in high-risk and very-high-risk patients.MethodsEvidence-based review.ResultsStatin-ezetimibe combination treatment is the first choice for managing elevated LDL-C and should be given upfront in very-high-risk patients with high LDL-C unlikely to reach goal with a statin, and in primary prevention familial hypercholesterolaemia patients. A proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor may be added if LDL-C levels remain high. In high and very-h…

0301 basic medicinemedicine.medical_specialtyStatinSettore MED/09 - Medicina InternaCombination therapymedicine.drug_classHigh-risk2019 ESC/EAS Dyslipidaemia GuidelineLipid goal030204 cardiovascular system & hematologyTriglyceride03 medical and health sciences0302 clinical medicineCombined treatmentcardiovascular diseaseInternal medicinemedicineHumanstriglycerides2019 ESC/EAS Dyslipidaemia Guidelines; combination treatment; LDL cholesterol; triglycerides; lipid goals; high-risk; cardiovascular diseaselipid goalsbusiness.industryTask forceAnticholesteremic AgentsPCSK9Cholesterol LDL[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismAtherosclerosis2019 ESC/EAS Dyslipidaemia Guidelines3. Good health030104 developmental biologyDiabetes Mellitus Type 2Combination treatmentAtherosclerosiLDL cholesterolEuropean atherosclerosis societyKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Hydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicinebusinessVery high risk
researchProduct

Homozygous familial hypercholesterolemia in Italy: Clinical and molecular features

2020

Abstract Background and aims Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disorder characterized by extremely elevated plasma levels of low density lipoprotein cholesterol (LDL-C) and high risk of premature atherosclerotic cardiovascular disease (ASCVD). HoFH is caused by pathogenic variants in several genes, such as LDLR, APOB and PCSK9, responsible for autosomal dominant hypercholesterolemia (ADH), and LDLRAP1 responsible for autosomal recessive hypercholesterolemia (ARH). Aim of this study was the review of the clinical and molecular features of patients with HoFH identified in Italy from 1989 to 2019. Methods Data were collected from lipid clinics and laboratories, …

Adult0301 basic medicinemedicine.medical_specialtyCandidate geneCandidate geneGenotype-phenotype correlationApolipoprotein BCandidate genes; Genotype-phenotype correlations; Homozygous familial hypercholesterolemia; Pathogenic variantsHomozygous familial hypercholesterolemiaGenotype-phenotype correlationsFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosityCandidate genesHyperlipoproteinemia Type II03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansbiologybusiness.industryPCSK9HomozygoteGenetic disorderPathogenic variantsCandidate genes; Genotype-phenotype correlations; Homozygous familial hypercholesterolemia; Pathogenic variants;medicine.diseasePhenotype030104 developmental biologyEndocrinologyItalyReceptors LDLAutosomal Recessive HypercholesterolemiaMutationLDL receptorbiology.proteinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular Medicinebusiness
researchProduct

Hepatic and circulating levels of PCSK9 in morbidly obese patients: Relation with severity of liver steatosis

2020

Non-alcoholic fatty liver disease (NAFLD) is becoming the main cause of liver disease in Western countries, especially in morbidly obese patients (MOPs). The proprotein convertase subtilisin/kexin type 9 (PCSK9) has been recently studied because of its possible involvement in the pathogenesis of NAFLD, but its role, at least in MOPs, is still controversial. The aim of this study was to clarify the correlation between the circulating levels of the PCSK9 protein (cPCSK9) and its hepatic expression with the severity of liver damage in a population of MOPs with NAFLD undergoing bariatric surgery. PCSK9 mRNA was positively correlated with FASN, PPARγ and PPARα mRNAs, while no significant differe…

AdultMale0301 basic medicinemedicine.medical_specialtySettore MED/06 - Oncologia MedicaPopulationBariatric SurgeryInflammation030204 cardiovascular system & hematologySeverity of Illness IndexPathogenesisNon-alcoholic fatty liver disease (NAFLD)03 medical and health sciencesBallooning degenerationLiver disease0302 clinical medicineInternal medicinemedicineHumansMorbidly obese patients (MOPs)educationMolecular Biologyeducation.field_of_studybusiness.industryPCSK9Fatty liverCell BiologyMiddle AgedLipid Metabolismmedicine.diseaseObesity MorbidFatty LiverProprotein convertase subtilisin/kexin type 9 (PCSK9)030104 developmental biologyEndocrinologyLiverFemaleProprotein Convertase 9medicine.symptomSteatosisbusiness
researchProduct

Homozygous familial hypercholesterolemia with severe involvement of the aortic valve—A sibling‐controlled case study on the efficacy of lipoprotein a…

2020

Background Homozygous familial hypercholesterolemia (hoFH) can cause severe atherosclerotic cardiovascular disease (ASCVD) in early infancy. Diagnosis and initiation of effective lipid-lowering therapy (LLT) are recommended as early as possible to prevent ASCVD-related morbidity and mortality. Methods The clinical courses of a pair of siblings with an identical hoFH genotype, who exhibited major similarities of their clinical phenotype were analyzed in a case-control fashion including the family. Results The older sibling was diagnosed with hoFH at the age of 4. Untreated LDL-cholesterol (LDL-C) was 17 mmol/L (660 mg/dL). LLT including lipoprotein apheresis (LA) was initiated and has been s…

AdultMaleAortic valvemedicine.medical_specialtyGenotypeBiopsyLipoproteinsFamilial hypercholesterolemia030204 cardiovascular system & hematologyHyperlipoproteinemia Type II03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEzetimibeInternal medicineXanthomatosisHumansMedicineSiblingChildAortaRetrospective StudiesFamily Healthbusiness.industryCholesterolSiblingsPCSK9HomozygoteMechanical Aortic ValveCholesterol LDLHematologyGeneral Medicinemedicine.diseaseLipidsPhenotypemedicine.anatomical_structurechemistryEchocardiographyAortic ValveCase-Control StudiesChild PreschoolAortic valve stenosisBlood Component RemovalFemalelipids (amino acids peptides and proteins)Proprotein Convertase 9business030215 immunologymedicine.drugJournal of Clinical Apheresis
researchProduct

Reduced penetrance of autosomal dominant hypercholesterolemia in a high percentage of families: importance of genetic testing in the entire family.

2011

Abstract Background Autosomal dominant hypercholesterolemias (ADHs) are characterised by increased plasma levels of total and LDL cholesterol, predisposing to premature atherosclerosis. ADHs comprise several diseases with undistinguishable phenotype, caused by mutations in different genes: LDLR, APOB and PCSK9. Genetic studies are usually performed in patients with altered cholesterol levels. However, some persons carrying pathogenic mutations are normocholesterolemic and there are no further studies about this subject. We have studied the frequency of families and individuals carrying ADH mutations who do not present the disease in Spanish population. Methods We have analysed genes known t…

AdultMaleApolipoprotein BAdolescentFamilial hypercholesterolemiaBiologymedicine.disease_causeHyperlipoproteinemia Type IIChlorocebus aethiopsmedicineAnimalsHumansGenetic TestingChildGeneGenetic testingAgedApolipoproteins BGeneticsFamily HealthMutationmedicine.diagnostic_testurogenital systemPCSK9Serine EndopeptidasesCholesterol LDLSequence Analysis DNAMiddle Agedmedicine.diseasePenetrancePhenotypePedigreePhenotypeMutagenesisSpainApolipoprotein B-100COS CellsMutationbiology.proteinFemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular Medicinehormones hormone substitutes and hormone antagonistsAtherosclerosis
researchProduct

Identifying genetic risk variants for coronary heart disease in familial hypercholesterolemia: an extreme genetics approach

2015

Mutations in the low-density lipoprotein receptor (LDLR) gene cause familial hypercholesterolemia (FH), a disorder characterized by coronary heart disease (CHD) at young age. We aimed to apply an extreme sampling method to enhance the statistical power to identify novel genetic risk variants for CHD in individuals with FH. We selected cases and controls with an extreme contrast in CHD risk from 17 000 FH patients from the Netherlands, whose functional LDLR mutation was unequivocally established. The genome-wide association (GWA) study was performed on 249 very young FH cases with CHD and 217 old FH controls without CHD (above 65 years for males and 70 years of age for females) using the Ill…

AdultMaleRiskSettore MED/09 - Medicina InternaGenotypePopulationCoronary DiseaseSingle-nucleotide polymorphismGenome-wide association studyComorbidityFamilial hypercholesterolemiaQuantitative trait locusBiologymedicine.disease_causePolymorphism Single NucleotideArticleHyperlipoproteinemia Type IIYoung Adultsymbols.namesakeGene FrequencyRisk FactorsOdds RatioGeneticsmedicineHumansGenetic Predisposition to DiseaseeducationAllelesGenetics (clinical)AgedAged 80 and overGeneticsMutationeducation.field_of_studyfamilial hypercholesterolemiaPCSK9familial hypercholesterolemia; genetic risk factorgenetic risk factorGenetic VariationMiddle Agedmedicine.diseaseBonferroni correctionReceptors LDLCase-Control StudiesMutationsymbolsFemaleGenome-Wide Association StudyEuropean journal of human genetics
researchProduct

Plasma PCSK9 is a late biomarker of severity in patients with severe trauma injury.

2013

PCSK9 (proprotein convertase subtilisin kexin type 9) is a secreted protease that modulates cholesterol homeostasis by decreasing low-density lipoprotein receptor expression. Low levels of plasma lipoproteins are related to severity of illness and survival in patients of intensive care units (ICU).The aim of the study was to investigate the regulation of plasma PCSK9 and its association with plasma lipid parameters and clinical markers of severity during critical illness.The plasma biobank from the previously published HYPOLYTE prospective study was used to measure PCSK9 concentrations by ELISA at days 0 and 8 in 111 patients admitted to surgical ICU for severe multiple trauma. Patients wer…

AdultMalemedicine.medical_specialtyHydrocortisoneEndocrinology Diabetes and MetabolismReceptor expressionCritical IllnessClinical BiochemistryContext (language use)PlaceboBiochemistryGastroenterologySeverity of Illness IndexPlacebosEndocrinologyIntensive careInternal medicineSeverity of illnessmedicineHumansProspective cohort studyInfusion PumpsHydrocortisoneTrauma Severity Indicesbusiness.industryPCSK9Biochemistry (medical)Serine EndopeptidasesCholesterol LDLPrognosisIntensive Care UnitsEndocrinologyImmunologyWounds and InjuriesFemaleProprotein ConvertasesProprotein Convertase 9businessBiomarkersmedicine.drugThe Journal of clinical endocrinology and metabolism
researchProduct

A Novel Loss of Function Mutation of PCSK9 Gene in White Subjects With Low-Plasma Low-Density Lipoprotein Cholesterol

2007

Objectives— The PCSK9 gene, encoding a pro-protein convertase involved in posttranslational degradation of low-density lipoprotein receptor, has emerged as a key regulator of plasma low-density lipoprotein cholesterol. In African-Americans two nonsense mutations resulting in loss of function of PCSK9 are associated with a 30% to 40% reduction of plasma low-density lipoprotein cholesterol. The aim of this study was to assess whether loss of function mutations of PCSK9 were a cause of familial hypobetalipoproteinemia and a determinant of low-plasma low-density lipoprotein cholesterol in whites. Methods and Results— We sequenced PCSK9 gene in 18 familial hypobetalipoproteinemia subjects and i…

AdultMalemedicine.medical_specialtyNonsense mutationBiologymedicine.disease_causePolymorphism Single NucleotideRisk AssessmentSensitivity and SpecificityStatistics NonparametricWhite Peopleloss of function mutationHypobetalipoproteinemiaschemistry.chemical_compoundPCSK9 GeneGene FrequencyInternal medicinemedicineHumansGenetic Predisposition to DiseaseMutationhypocholesterolemiaCholesterolIncidencePCSK9Serine EndopeptidasesCholesterol LDLmedicine.diseaseHypocholesterolemiaEndocrinologyfamilial hypobetalipoproteinemiachemistryCodon NonsensePCSK9 geneCase-Control Studiesfamilial hypobetalipoproteinemia hypocholesterolemia loss of function mutation PCSK9 genefamilial hypobetalipoproteinemia; hypocholesterolemia; loss of function mutation; PCSK9 gene.FemaleProprotein ConvertasesHypobetalipoproteinemiaProprotein Convertase 9Cardiology and Cardiovascular MedicineLipoprotein
researchProduct