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| 001 | 14547 | ||
| 005 | 20200402210006.0 | ||
| 024 | 7 | _ | |2 pmid |a pmid:21164077 |
| 024 | 7 | _ | |2 DOI |a 10.1161/ATVBAHA.110.219105 |
| 024 | 7 | _ | |2 WOS |a WOS:000287409900023 |
| 037 | _ | _ | |a PreJuSER-14547 |
| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 610 |
| 084 | _ | _ | |2 WoS |a Hematology |
| 084 | _ | _ | |2 WoS |a Peripheral Vascular Disease |
| 100 | 1 | _ | |0 P:(DE-HGF)0 |a Dangwal, S. |b 0 |
| 245 | _ | _ | |a High glucose enhances thrombin responses via protease-activated receptor-4 in human vascular smooth muscle cells |
| 260 | _ | _ | |a Philadelphia, Pa. |b Lippincott, Williams & Wilkins |c 2011 |
| 300 | _ | _ | |a 624 - 633 |
| 336 | 7 | _ | |a Journal Article |0 PUB:(DE-HGF)16 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a article |2 DRIVER |
| 440 | _ | 0 | |0 23721 |a Arteriosclerosis, Thrombosis, and Vascular Biology |v 31 |x 1079-5642 |y 3 |
| 500 | _ | _ | |a This study was supported in part by the Deutsche Forschungsgemeinschaft (SFB 612, Project B11), the Anna Wunderlich-Ernst Juhling Stiftung (Dusseldorf, Germany), and the Forschungsgruppe Herz-Kreislauf eV (Monheim, Germany). |
| 520 | _ | _ | |a Diabetes is associated with vascular remodeling and increased thrombin generation. Thrombin promotes vascular smooth muscle cell (SMC) mitogenesis and migration via protease-activated receptors (PAR)-1, PAR-3, and PAR-4. We investigated the effect of high glucose on expression and function of vascular thrombin receptors.In human vascular SMCs, high glucose (25 versus 5.5 mmol/L) induced a rapid and sustained increase in PAR-4 mRNA, protein, and cell surface expression. PAR-1 and PAR-3 expression were not changed. High glucose pretreatment (48 hours) enhanced thrombin or PAR-4-activating peptide but not PAR-1-activating peptide evoked intracellular calcium mobilization, migration, and tumor necrosis factor α gene expression. This enhancement of thrombin-stimulated migration and gene expression by high glucose was abolished by endogenous PAR-4 knockdown. PAR-4 regulation was prevented by inhibition of protein kinase (PK)C-β and -δ isoforms or nuclear factor (NF)κB. Nuclear translocation of NFκB in high glucose-stimulated SMCs led to PKC-dependent NFκB binding to the PAR-4 promoter in a chromatin immunoprecipitation assay. Furthermore, in situ hybridization and immunohistochemistry confirmed high abundance of PAR-4 in human diabetic vessels as compared with nondiabetic vessels.High glucose enhances SMC responsiveness to thrombin through transcriptional upregulation of PAR-4, mediated via PKC-β, -δ, and NFκB. This may play an important role in the vascular complications of diabetes. |
| 536 | _ | _ | |0 G:(DE-Juel1)FUEK505 |2 G:(DE-HGF) |a BioSoft: Makromolekulare Systeme und biologische Informationsverarbeitung |c P45 |x 0 |
| 588 | _ | _ | |a Dataset connected to Web of Science, Pubmed |
| 650 | _ | 2 | |2 MeSH |a Binding Sites |
| 650 | _ | 2 | |2 MeSH |a Calcium: metabolism |
| 650 | _ | 2 | |2 MeSH |a Calcium Signaling |
| 650 | _ | 2 | |2 MeSH |a Cell Movement |
| 650 | _ | 2 | |2 MeSH |a Cells, Cultured |
| 650 | _ | 2 | |2 MeSH |a Chromatin Immunoprecipitation |
| 650 | _ | 2 | |2 MeSH |a Diabetic Angiopathies: genetics |
| 650 | _ | 2 | |2 MeSH |a Diabetic Angiopathies: metabolism |
| 650 | _ | 2 | |2 MeSH |a Glucose: metabolism |
| 650 | _ | 2 | |2 MeSH |a Humans |
| 650 | _ | 2 | |2 MeSH |a Immunohistochemistry |
| 650 | _ | 2 | |2 MeSH |a In Situ Hybridization |
| 650 | _ | 2 | |2 MeSH |a Muscle, Smooth, Vascular: metabolism |
| 650 | _ | 2 | |2 MeSH |a Myocytes, Smooth Muscle: metabolism |
| 650 | _ | 2 | |2 MeSH |a NF-kappa B: metabolism |
| 650 | _ | 2 | |2 MeSH |a Promoter Regions, Genetic |
| 650 | _ | 2 | |2 MeSH |a Protein Kinase C: antagonists & inhibitors |
| 650 | _ | 2 | |2 MeSH |a Protein Kinase C: metabolism |
| 650 | _ | 2 | |2 MeSH |a Protein Kinase C-delta: genetics |
| 650 | _ | 2 | |2 MeSH |a Protein Kinase C-delta: metabolism |
| 650 | _ | 2 | |2 MeSH |a Protein Kinase Inhibitors: pharmacology |
| 650 | _ | 2 | |2 MeSH |a RNA Interference |
| 650 | _ | 2 | |2 MeSH |a RNA, Messenger: metabolism |
| 650 | _ | 2 | |2 MeSH |a Receptor, PAR-1: metabolism |
| 650 | _ | 2 | |2 MeSH |a Receptors, Thrombin: genetics |
| 650 | _ | 2 | |2 MeSH |a Receptors, Thrombin: metabolism |
| 650 | _ | 2 | |2 MeSH |a Thrombin: metabolism |
| 650 | _ | 2 | |2 MeSH |a Time Factors |
| 650 | _ | 2 | |2 MeSH |a Transcriptional Activation |
| 650 | _ | 2 | |2 MeSH |a Tumor Necrosis Factor-alpha: genetics |
| 650 | _ | 2 | |2 MeSH |a Up-Regulation |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a NF-kappa B |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a Protein Kinase Inhibitors |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a RNA, Messenger |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a Receptor, PAR-1 |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a Receptors, Thrombin |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a Tumor Necrosis Factor-alpha |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a protease-activated receptor 3 |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a protease-activated receptor 4 |
| 650 | _ | 7 | |0 50-99-7 |2 NLM Chemicals |a Glucose |
| 650 | _ | 7 | |0 7440-70-2 |2 NLM Chemicals |a Calcium |
| 650 | _ | 7 | |0 EC 2.7.1.- |2 NLM Chemicals |a protein kinase C beta |
| 650 | _ | 7 | |0 EC 2.7.11.13 |2 NLM Chemicals |a PRKCD protein, human |
| 650 | _ | 7 | |0 EC 2.7.11.13 |2 NLM Chemicals |a Protein Kinase C |
| 650 | _ | 7 | |0 EC 2.7.11.13 |2 NLM Chemicals |a Protein Kinase C-delta |
| 650 | _ | 7 | |0 EC 3.4.21.5 |2 NLM Chemicals |a Thrombin |
| 650 | _ | 7 | |2 WoSType |a J |
| 653 | 2 | 0 | |2 Author |a diabetes mellitus |
| 653 | 2 | 0 | |2 Author |a thrombin |
| 653 | 2 | 0 | |2 Author |a vascular muscle |
| 653 | 2 | 0 | |2 Author |a protease-activated receptors |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Rauch, B.H. |b 1 |
| 700 | 1 | _ | |0 P:(DE-Juel1)131924 |a Gensch, T. |b 2 |u FZJ |
| 700 | 1 | _ | |0 P:(DE-Juel1)VDB57287 |a Dai, L. |b 3 |u FZJ |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Bretschneider, E. |b 4 |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Vogelaar, C.F. |b 5 |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Schrör, K. |b 6 |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Rosenkranz, A.C. |b 7 |
| 773 | _ | _ | |0 PERI:(DE-600)1494427-3 |a 10.1161/ATVBAHA.110.219105 |g Vol. 31, p. 624 - 633 |p 624 - 633 |q 31<624 - 633 |t Arteriosclerosis, thrombosis, and vascular biology |v 31 |x 1079-5642 |y 2011 |
| 856 | 7 | _ | |u http://dx.doi.org/10.1161/ATVBAHA.110.219105 |
| 909 | C | O | |o oai:juser.fz-juelich.de:14547 |p VDB |
| 913 | 1 | _ | |0 G:(DE-Juel1)FUEK505 |a DE-HGF |b Schlüsseltechnologien |k P45 |l Biologische Informationsverarbeitung |v BioSoft: Makromolekulare Systeme und biologische Informationsverarbeitung |x 0 |
| 913 | 2 | _ | |0 G:(DE-HGF)POF3-552 |1 G:(DE-HGF)POF3-550 |2 G:(DE-HGF)POF3-500 |a DE-HGF |b Key Technologies |l BioSoft Fundamentals for future Technologies in the fields of Soft Matter and Life Sciences |v Engineering Cell Function |x 0 |
| 914 | 1 | _ | |y 2011 |
| 915 | _ | _ | |0 StatID:(DE-HGF)0020 |a No peer review |
| 920 | 1 | _ | |0 I:(DE-Juel1)VDB922 |g ISB |k ISB-1 |l Zelluläre Biophysik |x 0 |
| 970 | _ | _ | |a VDB:(DE-Juel1)126730 |
| 980 | _ | _ | |a VDB |
| 980 | _ | _ | |a ConvertedRecord |
| 980 | _ | _ | |a journal |
| 980 | _ | _ | |a I:(DE-Juel1)ICS-4-20110106 |
| 980 | _ | _ | |a UNRESTRICTED |
| 981 | _ | _ | |a I:(DE-Juel1)IBI-1-20200312 |
| 981 | _ | _ | |a I:(DE-Juel1)ICS-4-20110106 |
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