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[PMID]:28137735
[Au] Autor:Kim N; Gu JY; Yoo HJ; Han SE; Kim YI; Nam-Goong IS; Kim ES; Kim HK
[Ad] Endereço:Department of Laboratory Medicine and Cancer Research InstituteSeoul National University College of Medicine, Seoul, Korea.
[Ti] Título:Contact system activation and high thrombin generation in hyperthyroidism.
[So] Source:Eur J Endocrinol;176(5):583-589, 2017 May.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hyperthyroidism is associated with increased thrombotic risk. As contact system activation through formation of neutrophil extracellular traps (NET) has emerged as an important trigger of thrombosis, we hypothesized that the contact system is activated along with active NET formation in hyperthyroidism and that their markers correlate with disease severity. SUBJECTS AND METHODS: In 61 patients with hyperthyroidism and 40 normal controls, the levels of coagulation factors (fibrinogen, and factor VII, VIII, IX, XI and XII), D-dimer, thrombin generation assay (TGA) markers, NET formation markers (histone-DNA complex, double-stranded DNA and neutrophil elastase) and contact system markers (activated factor XII (XIIa), high-molecular-weight kininogen (HMWK), prekallikrein and bradykinin) were measured. RESULTS: Patients with hyperthyroidism showed higher levels of fibrinogen (median (interquartile range), 315 (280-344) vs 262 (223-300), = 0.001), D-dimer (103.8 (64.8-151.5) vs 50.7 (37.4-76.0), < 0.001), peak thrombin (131.9 (102.2-159.4) vs 31.6 (14.8-83.7), < 0.001) and endogenous thrombin potential (649 (538-736) vs 367 (197-1147), = 0.021) in TGA with 1 pM tissue factor, neutrophil elastase (1.10 (0.39-2.18) vs 0.23 (0.20-0.35), < 0.001), factor XIIa (66.9 (52.8-87.0) vs 73.0 (57.1-86.6), < 0.001), HMWK (6.11 (4.95-7.98) vs 3.83 (2.60-5.68), < 0.001), prekallikrein (2.15 (1.00-6.36) vs 1.41 (0.63-2.22), = 0.026) and bradykinin (152.4 (137.6-180.4) vs 118.3 (97.1-137.9), < 0.001) than did normal controls. In age- and sex-adjusted logistic regression analysis, fibrinogen, factor VIII, IX and XIIa, D-dimer, peak thrombin, neutrophil elastase, HMWK and bradykinin showed significant odds ratios representing hyperthyroidism's contribution to coagulation and contact system activation. Free T4 was significantly correlated with factors VIII and IX, D-dimer, double-stranded DNA and bradykinin. CONCLUSION: This study demonstrated that contact system activation and abundant NET formation occurred in the high thrombin generation state in hyperthyroidism and were correlated with free T4 level.
[Mh] Termos MeSH primário: Armadilhas Extracelulares/fisiologia
Hipertireoidismo/metabolismo
Trombina/biossíntese
[Mh] Termos MeSH secundário: Adulto
Coagulação Sanguínea
Fatores de Coagulação Sanguínea/análise
Bradicinina/sangue
DNA/sangue
DNA/metabolismo
Fator XIIa/análise
Feminino
Histonas/sangue
Histonas/metabolismo
Seres Humanos
Cininogênio de Alto Peso Molecular/sangue
Elastase de Leucócito/sangue
Masculino
Meia-Idade
Pré-Calicreína/análise
Tiroxina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Coagulation Factors); 0 (Histones); 0 (Kininogen, High-Molecular-Weight); 9007-49-2 (DNA); 9055-02-1 (Prekallikrein); EC 3.4.21.37 (Leukocyte Elastase); EC 3.4.21.38 (Factor XIIa); EC 3.4.21.5 (Thrombin); Q51BO43MG4 (Thyroxine); S8TIM42R2W (Bradykinin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-16-0835


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[PMID]:27826093
[Au] Autor:Joseph K; Tholanikunnel BG; Kaplan AP
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC. Electronic address: josephk@musc.edu.
[Ti] Título:Cytokine and estrogen stimulation of endothelial cells augments activation of the prekallikrein-high molecular weight kininogen complex: Implications for hereditary angioedema.
[So] Source:J Allergy Clin Immunol;140(1):170-176, 2017 Jul.
[Is] ISSN:1097-6825
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: When the prekallikrein-high molecular weight kininogen complex is bound to endothelial cells, prekallikrein is stoichiometrically converted to kallikrein because of release of heat shock protein-90 (Hsp90). Although bradykinin formation is typically initiated by factor XII autoactivation, it is also possible to activate factor XII either by kallikrein, thus formed, or by plasmin. OBJECTIVE: Because attacks of hereditary angioedema can be related to infection and/or exposure to estrogen, we questioned whether estrogen or cytokine stimulation of endothelial cells could augment release of Hsp90 and prekallikrein activation. We also tested release of profibrinolytic enzymes, urokinase, and tissue plasminogen activator (TPA) as a source for plasmin formation. METHODS: Cells were stimulated with agonists, and secretion of Hsp90, urokinase, and TPA was measured in the culture supernatants by ELISA. Activation of the prekallikrein-HK complex was measured by using pro-phe-arg-p-nitroanilide reflecting kallikrein formation. RESULTS: Hsp90 release was stimulated with optimal doses of estradiol, IL-1, and TNF-α (10 ng/mL) from 15 minutes to 120 minutes. TPA release was not augmented by any of the agonists tested but urokinase was released by IL-1, TNF-α, and thrombin (positive control), but not estrogen. Augmented activation of the prekallikrein-HK complex to generate kallikrein was seen with each agonist that releases Hsp90. Addition of 0.1% factor XII relative to prekallikrein-HK leads to rapid formation of kallikrein; factor XII alone does not autoactivate. CONCLUSIONS: IL-1, TNF-α, and estrogen stimulate release of Hsp90 and augment activation of the prekallikrein-HK complex to generate kallikrein and bradykinin. IL-1 and TNF-α stimulate release of urokinase, which can convert plasminogen to plasmin and represents a possible source for plasmin generation in all types of hereditary angioedema, but particularly hereditary angioedema with normal C1 inhibitor with a factor XII mutation. Both kallikrein and plasmin activate factor XII; kallikrein is 20 times more potent on a molar basis.
[Mh] Termos MeSH primário: Estradiol/farmacologia
Estrogênios/farmacologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Interleucina-1/farmacologia
Cininogênio de Alto Peso Molecular/metabolismo
Pré-Calicreína/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Angioedemas Hereditários/metabolismo
Células Cultivadas
Fator XII/metabolismo
Proteínas de Choque Térmico HSP90/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Ativador de Plasminogênio Tecidual/metabolismo
Ativador de Plasminogênio Tipo Uroquinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogens); 0 (HSP90 Heat-Shock Proteins); 0 (Interleukin-1); 0 (Kininogen, High-Molecular-Weight); 0 (Tumor Necrosis Factor-alpha); 4TI98Z838E (Estradiol); 9001-30-3 (Factor XII); 9055-02-1 (Prekallikrein); EC 3.4.21.68 (Tissue Plasminogen Activator); EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161110
[St] Status:MEDLINE


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[PMID]:27585864
[Au] Autor:Zheng S; Just S; Brighton T
[Ad] Endereço:Haematology Department and SEALS Pathology, Prince of Wales Hospital, Randwick, NSW, Australia. Electronic address: silviazh2006@gmail.com.
[Ti] Título:Prekallikrein deficiency.
[So] Source:Pathology;48(6):634-7, 2016 Oct.
[Is] ISSN:1465-3931
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Transtornos da Coagulação Sanguínea/diagnóstico
Pré-Calicreína/deficiência
[Mh] Termos MeSH secundário: Idoso
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
9055-02-1 (Prekallikrein)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170405
[Lr] Data última revisão:
170405
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160903
[St] Status:MEDLINE


  4 / 1218 MEDLINE  
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[PMID]:27581227
[Au] Autor:Ghulam QM; Bredahl KK; Gram JB; Lönn L; Goetze JP; Sillesen HH; Eiberg JP
[Ad] Endereço:Department of Vascular Surgery, Rigshospitalet, Blegdamsvej, Copenhagen, Denmark Faculty of Health and Medical Science, University of Copenhagen, Denmark qasam.mohammed.ghulam@regionh.dk.
[Ti] Título:von Willebrand Factor and Prekallikrein in Plasma Are Associated With Thrombus Volume in Abdominal Aortic Aneurysms.
[So] Source:Vasc Endovascular Surg;50(6):391-7, 2016 Aug.
[Is] ISSN:1938-9116
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Disruption of the endothelial lining may be one of the events linking intraluminal thrombus and abdominal aortic aneurysm growth. In the present study, we examined whether von Willebrand factor activity in plasma, contact proteins of blood coagulation, and inflammatory biomarkers may be associated with intraluminal thrombus volume in search of a biochemical marker of endothelial damage and thrombus size. DESIGN: Prospective study, correlating potential endothelial biomarkers and intraluminal thrombus volume acquired by computed tomography angiography. MATERIALS AND METHODS: Plasma was consecutively obtained from 38 patients with asymptomatic infrarenal abdominal aortic aneurysm. von Willebrand factor activity, thrombin generation time, factor XII, and prekallikrein concentration were measured in plasma on automated and in-house platforms. In total, 8 patients were excluded due to ongoing anticoagulant therapy, renal impairment, or nonappearance, thus leaving 30 patients for further analysis. All patients had computed tomography angiography, and intraluminal volume was quantified off-line by OsiriX 6.5. RESULTS: Median intraluminal thrombus volume was 42.7 mL. Spearman correlation analysis revealed a positive correlation between thrombus volume, von Willebrand factor activity (ρ = 0.56, P = .0013), and prekallikrein concentration in plasma (ρ = 0.54, P = .002). CONCLUSION: von Willebrand factor activity and concentration of prekallikrein may both be of importance regarding the evolution of thrombus in abdominal aortic aneurysm and possible biomarkers for aneurysm growth.
[Mh] Termos MeSH primário: Aneurisma da Aorta Abdominal/sangue
Pré-Calicreína/análise
Trombose/sangue
Fator de von Willebrand/análise
[Mh] Termos MeSH secundário: Idoso
Aneurisma da Aorta Abdominal/diagnóstico por imagem
Aortografia/métodos
Doenças Assintomáticas
Biomarcadores/sangue
Coagulação Sanguínea
Angiografia por Tomografia Computadorizada
Feminino
Seres Humanos
Masculino
Tomografia Computadorizada Multidetectores
Valor Preditivo dos Testes
Prognóstico
Estudos Prospectivos
Tempo de Trombina
Trombose/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (von Willebrand Factor); 9055-02-1 (Prekallikrein)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170221
[Lr] Data última revisão:
170221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160902
[St] Status:MEDLINE
[do] DOI:10.1177/1538574416666224


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[PMID]:27380557
[Au] Autor:Schmaier AH
[Ad] Endereço:Division of Hematology and Oncology, Department of Medicine, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA.
[Ti] Título:Antithrombotic potential of the contact activation pathway.
[So] Source:Curr Opin Hematol;23(5):445-52, 2016 Sep.
[Is] ISSN:1531-7048
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: This report examines the mechanism(s) by which each protein of the contact activation system - factor XII (FXII), high-molecular-weight kininogen, and prekallikrein - influences thrombosis risk. RECENT FINDINGS: FXII generates thrombin through contact activation via interaction with artificial surfaces as on medical instruments such as indwelling catheters, mechanical valves, stents, and ventricular assist devices. Inhibition of FXIIa-mediated contact activation prevents thrombosis under contact activation circumstances without affecting hemostasis. Current studies suggest that high-molecular-weight kininogen deficiency parallels that of FXII and inhibits contact activation. Prekallikrein inhibition contributes to thrombosis prevention by contact activation inhibition in the nylon monofilament model of transient middle cerebral artery occlusion. However, in arterial thrombosis models where reactive oxygen species are generated, prekallikrein deficiency results in downregulation of vessel wall tissue factor generation with reduced thrombin generation. Exploiting this latter prekallikrein pathway for thrombosis risk reduction provides a general, overall reduced tissue factor, antithrombotic pathway without risk for bleeding. SUMMARY: These investigations indicate that the proteins of the contact activation and kallikrein/kinin systems influence thrombosis risk by several mechanisms and understanding of these pathway provides insight into several novel targets to prevent thrombosis without increase in bleeding risk.
[Mh] Termos MeSH primário: Coagulação Sanguínea
Transdução de Sinais
Trombose/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Ativação Enzimática
Fator XII/antagonistas & inibidores
Fator XII/genética
Fator XII/metabolismo
Seres Humanos
Cininogênio de Alto Peso Molecular/genética
Cininogênio de Alto Peso Molecular/metabolismo
Leucócitos/metabolismo
Pré-Calicreína/genética
Pré-Calicreína/metabolismo
Ligação Proteica
Trombose/sangue
Trombose/genética
Trombose/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Kininogen, High-Molecular-Weight); 9001-30-3 (Factor XII); 9055-02-1 (Prekallikrein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160706
[St] Status:MEDLINE
[do] DOI:10.1097/MOH.0000000000000271


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[PMID]:27273087
[Au] Autor:Kaplan AP; Joseph K
[Ad] Endereço:Medical University of South Carolina, Charleston, SC, USA. kaplana@musc.edu.
[Ti] Título:Complement, Kinins, and Hereditary Angioedema: Mechanisms of Plasma Instability when C1 Inhibitor is Absent.
[So] Source:Clin Rev Allergy Immunol;51(2):207-15, 2016 Oct.
[Is] ISSN:1559-0267
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plasma of patients with types I and II hereditary angioedema is unstable if incubated in a plastic (i.e., inert) vessel at 37 °C manifested by progressively increasing formation of bradykinin. There is also a persistent low level of C4 in 95 % of patients even when they are symptomatic. These phenomena are due to the properties of the C1r subcomponent of C1, factor XII, and the bimolecular complex of prekallikrein with high molecular weight kininogen (HK). Purified C1r auto-activates in physiologic buffers, activates C1s, which in turn depletes C4. This occurs when C1 inhibitor is deficient. The complex of prekallikrein-HK acquires an inducible active site not present in prekallikrein which in Tris-type buffers cleaves HK stoichiometrically to release bradykinin, or in phosphate buffer auto-activates to generate kallikrein and bradykinin. Thus immunologic depletion of C1 inhibitor from factor XII-deficient plasma (phosphate is the natural buffer) auto-activates on incubation to release bradykinin. Normal C1 inhibitor prevents this from occurring. During attacks of angioedema, if factor XII auto-activates on surfaces, the initial factor XIIa formed converts prekallikrein to kallikrein, and kallikrein cleaves HK to release bradykinin. Kallikrein also rapidly activates most remaining factor XII to factor XIIa. Additional cleavages convert factor XIIa to factor XIIf and factor XIIf activates C1r enzymatically so that C4 levels approach zero, and C2 is depleted. There is also a possibility that kallikrein is generated first as a result of activation of the prekallikrein-HK complex by heat shock protein 90 released from endothelial cells, followed by kallikrein activation of factor XII.
[Mh] Termos MeSH primário: Angioedemas Hereditários/etiologia
Angioedemas Hereditários/metabolismo
Proteínas do Sistema Complemento/imunologia
Cininas/metabolismo
[Mh] Termos MeSH secundário: Angioedemas Hereditários/diagnóstico
Bradicinina/metabolismo
Ativação do Complemento/imunologia
Proteína Inibidora do Complemento C1/genética
Proteína Inibidora do Complemento C1/metabolismo
Proteínas do Sistema Complemento/metabolismo
Ativação Enzimática
Fator XII/metabolismo
Angioedema Hereditário Tipos I e II/diagnóstico
Angioedema Hereditário Tipos I e II/etiologia
Angioedema Hereditário Tipos I e II/metabolismo
Seres Humanos
Cininogênio de Alto Peso Molecular/metabolismo
Pré-Calicreína/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Complement C1 Inhibitor Protein); 0 (Kininogen, High-Molecular-Weight); 0 (Kinins); 9001-30-3 (Factor XII); 9007-36-7 (Complement System Proteins); 9055-02-1 (Prekallikrein); S8TIM42R2W (Bradykinin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160609
[St] Status:MEDLINE
[do] DOI:10.1007/s12016-016-8555-6


  7 / 1218 MEDLINE  
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[PMID]:26969407
[Au] Autor:Biswas N; Maihofer AX; Mir SA; Rao F; Zhang K; Khandrika S; Mahata M; Friese RS; Hightower CM; Mahata SK; Baker DG; Nievergelt CM; Vaingankar SM; O'Connor DT
[Ad] Endereço:Departments of Medicine, University of California at San Diego, 9500 Gilman Drive, La Jolla, 92093-0838, USA. nbiswas33@gmail.com.
[Ti] Título:Polymorphisms at the F12 and KLKB1 loci have significant trait association with activation of the renin-angiotensin system.
[So] Source:BMC Med Genet;17:21, 2016 Mar 11.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Plasma coagulation Factor XIIa (Hageman factor; encoded by F12) and kallikrein (KAL or Fletcher factor; encoded by KLKB1) are proteases of the kallikerin-kinin system involved in converting the inactive circulating prorenin to renin. Renin is a key enzyme in the formation of angiotensin II, which regulates blood pressure, fluid and electrolyte balance and is a biomarker for cardiovascular, metabolic and renal function. The renin-angiotensin system is implicated in extinction learning in posttraumatic stress disorder. METHODS & RESULTS: Active plasma renin was measured from two independent cohorts- civilian twins and siblings, as well as U.S. Marines, for a total of 1,180 subjects. Genotyping these subjects revealed that the carriers of the minor alleles at the two loci- F12 and KLKB1 had a significant association with reduced levels of active plasma renin. Meta-analyses confirmed the association across cohorts. In vitro studies verified digestion of human recombinant pro-renin by kallikrein (KAL) to generate active renin. Subsequently, the active renin was able to digest the synthetic substrate angiotensinogen to angiotensin-I. Examination of mouse juxtaglomerular cell line and mouse kidney sections showed co-localization of KAL with renin. Expression of either REN or KLKB1 was regulated in cell line and rodent models of hypertension in response to oxidative stress, interleukin or arterial blood pressure changes. CONCLUSIONS: The functional variants of KLKB1 (rs3733402) and F12 (rs1801020) disrupted the cascade of enzymatic events, resulting in diminished formation of active renin. Using genetic, cellular and molecular approaches we found that conversion of zymogen prorenin to renin was influenced by these polymorphisms. The study suggests that the variant version of protease factor XIIa due to the amino acid substitution had reduced ability to activate prekallikrein to KAL. As a result KAL has reduced efficacy in converting prorenin to renin and this step of the pathway leading to activation of renin affords a potential therapeutic target.
[Mh] Termos MeSH primário: Fator XIIa/genética
Calicreínas/genética
Polimorfismo de Nucleotídeo Único
Sistema Renina-Angiotensina/genética
Renina/sangue
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Alelos
Angiotensina I/sangue
Angiotensinogênio/sangue
Animais
Pressão Sanguínea
Linhagem Celular
Regulação da Expressão Gênica
Loci Gênicos
Estudo de Associação Genômica Ampla
Técnicas de Genotipagem
Seres Humanos
Hipertensão/genética
Sistema Justaglomerular/citologia
Calicreínas/sangue
Masculino
Camundongos
Meia-Idade
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Pré-Calicreína/metabolismo
Renina/genética
Serina Endopeptidases/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Kctd11 protein, mouse); 0 (Nerve Tissue Proteins); 11002-13-4 (Angiotensinogen); 9041-90-1 (Angiotensin I); 9055-02-1 (Prekallikrein); EC 3.4.21.- (Kallikreins); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.- (zymogen E); EC 3.4.21.38 (Factor XIIa); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160313
[St] Status:MEDLINE
[do] DOI:10.1186/s12881-016-0283-5


  8 / 1218 MEDLINE  
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[PMID]:26950760
[Au] Autor:Kokoye Y; Ivanov I; Cheng Q; Matafonov A; Dickeson SK; Mason S; Sexton DJ; Renné T; McCrae K; Feener EP; Gailani D
[Ad] Endereço:Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, TN, USA.
[Ti] Título:A comparison of the effects of factor XII deficiency and prekallikrein deficiency on thrombus formation.
[So] Source:Thromb Res;140:118-124, 2016 Apr.
[Is] ISSN:1879-2472
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Studies with animal models implicate the plasma proteases factor XIIa (FXIIa) and α-kallikrein in arterial and venous thrombosis. As congenital deficiencies of factor XII (FXII) or prekallikrein (PK), the zymogens of FXIIa and α-kallikrein respectively, do not cause bleeding disorders, inhibition of these enzymes may have therapeutic benefit without compromising hemostasis. The relative contributions of FXIIa and α-kallikrein to thrombosis in animal models are not clear. We compared mice lacking FXII or PK to wild type mice in established models of arterial thrombosis. Wild type mice developed carotid artery occlusion when the vessel was exposed to a 3.5% solution of ferric chloride (FeCl3). FXII-deficient mice were resistant to occlusion at 5% FeCl3 and partially resistant at 10% FeCl3. PK-deficient mice were resistant at 3.5% FeCl3 and partially resistant at 5% FeCl3. Mice lacking high molecular weight kininogen, a cofactor for PK activation and activity, were also partially resistant to thrombosis at 5% FeCl3. Induction of carotid artery thrombosis with Rose Bengal was delayed in FXII-deficient mice compared to wild type or PK-deficient animals. In human plasma supplemented with silica, DNA or collagen to induce contact activation, an antibody to the FXIIa active site was more effective at preventing thrombin generation than an antibody to the α-kallikrein active site. Similarly, the FXIIa antibody was more effective at reducing fibrin formation in human blood flowing through collagen coated-tubes. The findings suggest that inhibitors of FXIIa will have more potent anti-thrombotic effects than inhibitors of α-kallikrein.
[Mh] Termos MeSH primário: Transtornos da Coagulação Sanguínea/complicações
Deficiência do Fator XII/complicações
Fator XII/genética
Pré-Calicreína/deficiência
Pré-Calicreína/genética
Trombose/etiologia
Trombose/genética
[Mh] Termos MeSH secundário: Animais
Coagulação Sanguínea/efeitos dos fármacos
Transtornos da Coagulação Sanguínea/genética
Fator XII/antagonistas & inibidores
Deficiência do Fator XII/genética
Deleção de Genes
Seres Humanos
Calicreínas/antagonistas & inibidores
Calicreínas/genética
Camundongos
Camundongos Endogâmicos C57BL
Pré-Calicreína/antagonistas & inibidores
Fatores de Proteção
Trombose/prevenção & controle
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
9001-30-3 (Factor XII); 9055-02-1 (Prekallikrein); EC 3.4.21.- (Kallikreins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160308
[St] Status:MEDLINE


  9 / 1218 MEDLINE  
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[PMID]:26603531
[Au] Autor:Jaffa MA; Luttrell D; Schmaier AH; Klein RL; Lopes-Virella M; Luttrell LM; Jaffa AA; DCCT/EDIC Research Group
[Ad] Endereço:Epidemiology and Population Health Department, Faculty of Health Sciences, American University of Beirut, Beirut, Lebanon.
[Ti] Título:Plasma Prekallikrein Is Associated With Carotid Intima-Media Thickness in Type 1 Diabetes.
[So] Source:Diabetes;65(2):498-502, 2016 Feb.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The hypothesis that plasma prekallikrein (PK) is a risk factor for the development of vascular complications was assessed in a study using the Diabetes Control and Complications Trial (DCCT)/Epidemiology and Diabetes Interventions and Complications (EDIC) cohort of subjects with type 1 diabetes. The circulating levels of plasma PK activity were measured in the plasma of 636 subjects with type 1 diabetes (EDIC years 3-5). Common and internal carotid intima-media thickness (IMT) were measured by B-mode ultrasonography in EDIC years 1 and 6. Plasma PK levels were positively and significantly associated with BMI, hemoglobin A1c, systolic blood pressure, total cholesterol, LDL cholesterol, and triglycerides but not with age, sex, duration of diabetes, or HDL cholesterol. Univariate and multivariable statistical models after controlling for other risk factors consistently demonstrated a positive association between plasma PK and progression of internal carotid IMT. Multivariate analysis using a general linear model showed plasma PK to be significantly associated with progression of both internal and combined IMT (Wilks Λ P value of 0.005). In addition, the mean internal carotid IMT levels were higher in subjects with plasma PK levels in the highest 10th percentile compared with subjects with plasma PK levels in the lower 10th percentile (P = 0.048). These novel findings implicate plasma PK as a risk factor for vascular disease in type 1 diabetes.
[Mh] Termos MeSH primário: Espessura Intima-Media Carotídea
Diabetes Mellitus Tipo 1/sangue
Angiopatias Diabéticas/etiologia
Pré-Calicreína/análise
[Mh] Termos MeSH secundário: Adolescente
Adulto
Pressão Sanguínea
Índice de Massa Corporal
Colesterol/sangue
Diabetes Mellitus Tipo 1/complicações
Diabetes Mellitus Tipo 1/diagnóstico por imagem
Feminino
Hemoglobina A Glicada/análise
Seres Humanos
Modelos Lineares
Masculino
Análise Multivariada
Fatores de Risco
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; OBSERVATIONAL STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Glycated Hemoglobin A); 0 (hemoglobin A1c protein, human); 9055-02-1 (Prekallikrein); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:151126
[St] Status:MEDLINE
[do] DOI:10.2337/db15-0930


  10 / 1218 MEDLINE  
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[PMID]:26565070
[Au] Autor:Schmaier AH
[Ad] Endereço:Department of Medicine, Case Western Reserve University, Cleveland, OH, USA.
[Ti] Título:The contact activation and kallikrein/kinin systems: pathophysiologic and physiologic activities.
[So] Source:J Thromb Haemost;14(1):28-39, 2016 Jan.
[Is] ISSN:1538-7836
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The contact activation system (CAS) and kallikrein/kinin system (KKS) are older recognized biochemical pathways that include several proteins that skirt the fringes of the blood coagulation, fibrinolytic, complement and renin-angiotensin fields. These proteins initially were proposed as part of the hemostatic pathways because their deficiencies are associated with prolonged clinical assays. However, the absence of bleeding states with deficiencies of factor XII (FXII), prekallikrein (PK) and high-molecular-weight kininogen indicates that the CAS and KKS do not contribute to hemostasis. Since the discovery of the Hageman factor 60 years ago much has been learned about the biochemistry, cell biology and animal physiology of these proteins. The CAS is a pathophysiologic surface defense mechanism against foreign proteins, organisms and artificial materials. The KKS is an inflammatory response mechanism. Targeting their activation through FXIIa or plasma kallikrein inhibition when blood interacts with the artificial surfaces of modern interventional medicine or in acute attacks of hereditary angioedema restores vascular homeostasis. FXII/FXIIa and products that arise with PK deficiency also offer novel ways to reduce arterial and venous thrombosis without an effect on hemostasis. In summary, there is revived interest in the CAS and KKS due to better understanding of their activities. The new appreciation of these systems will lead to several new therapies for a variety of medical disorders.
[Mh] Termos MeSH primário: Transtornos da Coagulação Sanguínea/imunologia
Sistema Calicreína-Cinina
Pré-Calicreína/deficiência
[Mh] Termos MeSH secundário: Animais
Coagulação Sanguínea
Bradicinina/metabolismo
Fator XII/metabolismo
Fator XIIa/metabolismo
Hemostasia
Homeostase
Seres Humanos
Inflamação
Cininogênio de Alto Peso Molecular/metabolismo
Camundongos
Calicreína Plasmática/metabolismo
Pré-Calicreína/imunologia
Pré-Calicreína/metabolismo
Receptores da Bradicinina/metabolismo
Trombose/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Kininogen, High-Molecular-Weight); 0 (Receptors, Bradykinin); 9001-30-3 (Factor XII); 9055-02-1 (Prekallikrein); EC 3.4.21.34 (Plasma Kallikrein); EC 3.4.21.38 (Factor XIIa); S8TIM42R2W (Bradykinin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151114
[St] Status:MEDLINE
[do] DOI:10.1111/jth.13194



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