0000000000855366

AUTHOR

Irina Grechowa

showing 2 related works from this author

Human neutrophil elastase induces endothelial cell apoptosis by activating the PERK‐CHOP branch of the unfolded protein response

2017

Human neutrophil elastase impacts on atherosclerotic plaque stability by inducing apoptosis in endothelial cells. Our aim was to investigate the proapoptotic mechanism of elastase on endothelial cells and to evaluate the presence of elastase in human plaque material. Human endothelial cells were treated with purified human neutrophil elastase. Apoptosis was assayed by capsase-3/7 activation, TUNEL, and sub-G1 assay. Activation of unfolded protein response (UPR) effector molecules binding Ig protein, soluble X-binding protein-1, protein kinase RNA-like ER kinase (PERK), and C/EBP-homologous protein (CHOP) was analyzed by RT-PCR, immunocytochemistry, and Western blot. Genetic silencing of CHO…

0301 basic medicineSmall interfering RNACell SurvivalApoptosisCHOPBiochemistryGene Expression Regulation EnzymologicCell LineeIF-2 Kinase03 medical and health sciencesGeneticsHumansReceptor PAR-2Receptor PAR-1Protein kinase AMolecular BiologyCaspase 7Caspase 3KinaseChemistryElastaseEndothelial CellsAtherosclerosisMolecular biologyEndothelial stem cellCarotid Arteries030104 developmental biologyApoptosisUnfolded Protein ResponseUnfolded protein responseLeukocyte ElastaseTranscription Factor CHOPBiotechnologyThe FASEB Journal
researchProduct

Activation of the Proapoptotic Unfolded Protein Response in Plaques of the Human Carotid Artery

2014

Objective To analyze expression of keystone markers of apoptosis and the proapoptotic signaling pathway “unfolded protein response” (UPR) in rupture-prone plaques of the human carotid artery. Methods Plaque specimens were obtained during endarterectomy for high-grade carotid stenosis, and were formalin-fixed. Ten specimens were identified that exhibited criteria of advanced rupture-prone atherosclerotic plaques, and histological and immunohistological analysis of markers of apoptosis (cleaved Caspase-3, TUNEL) and UPR (KDEL, ATF3, CHOP, CHAC-1) was performed. In addition, co-localization of apoptosis and UPR-activation was assessed by double-immunohistochemistry. Results The mean size of th…

MalePathologymedicine.medical_specialtyReceptors PeptideArteriosclerosisKDELmedicine.medical_treatmentApoptosisCHOPImmunoenzyme TechniquesRisk FactorsIn Situ Nick-End LabelingMedicineHumansCarotid StenosisEndarterectomyAgedAtherosclerotic plaqueAged 80 and overMedicine(all)Endarterectomy CarotidTUNEL assayActivating Transcription Factor 3business.industryCaspase 3MacrophagesFibrous capMiddle AgedImmunohistochemistrymedicine.anatomical_structureCarotid ArteriesApoptosisUnfolded protein responseUnfolded Protein ResponseImmunohistochemistrySurgeryFemalebusinessCardiology and Cardiovascular MedicineBiomarkersTranscription Factor CHOPSignal TransductionEuropean Journal of Vascular and Endovascular Surgery
researchProduct