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[PMID]:28453844
[Au] Autor:Suwarto S; Sasmono RT; Sinto R; Ibrahim E; Suryamin M
[Ad] Endereço:Division of Tropical and Infectious Diseases, Department of Internal Medicine, Faculty of Medicine, Universitas Indonesia, Cipto Mangunkusumo National Hospital, Jakarta, Indonesia.
[Ti] Título:Association of Endothelial Glycocalyx and Tight and Adherens Junctions With Severity of Plasma Leakage in Dengue Infection.
[So] Source:J Infect Dis;215(6):992-999, 2017 03 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: The role of vascular endothelial (VE) components in dengue infection with plasma leakage is unknown. Therefore, we conducted a study to determine the adjusted association of the endothelial glycocalyx layer (EGL) and tight and adherens junction markers with plasma leakage. Methods: A prospective observational study was conducted at Cipto Mangunkusumo Hospital and Persahabatan Hospital, Jakarta, Indonesia. Adult dengue patients admitted to the hospital on the third day of fever from November 2013 through August 2015 were included in the study. Multiple regression analysis was used to determine the adjusted association of the VE biomarkers with the severity of the plasma leakage. Results: A total of 103 dengue-infected patients participated in the study. In the critical phase, levels of syndecan-1 (odds ratio [OR] = 1.004; 95% confidence interval [CI] = 1.001-1.007) and chondroitin sulfate (OR = 1.157; 95% CI = 1.025-1.307) had an adjusted association with plasma leakage, whereas levels of syndecan-1 (OR = 1.004; 95% CI = 1.000-1.008) and claudin-5 (OR = 1.038; 95% CI = 1.004-1.074) had an adjusted association with severe plasma leakage. Conclusions: In dengue-infected patients, elevated levels of syndecan-1 and chondroitin sulfate are strongly associated with plasma leakage, and elevated levels of syndecan-1 and claudin-5 are strongly associated with severe plasma leakage.
[Mh] Termos MeSH primário: Sulfatos de Condroitina/sangue
Claudina-5/sangue
Dengue/sangue
Glicocálix/metabolismo
Sindecana-1/sangue
Junções Íntimas/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Biomarcadores/sangue
Permeabilidade Capilar
Quimiocinas/sangue
Endotélio Vascular/metabolismo
Feminino
Febre
Seres Humanos
Indonésia
Masculino
Razão de Chances
Estudos Prospectivos
Análise de Regressão
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Chemokines); 0 (Claudin-5); 0 (Syndecan-1); 9007-28-7 (Chondroitin Sulfates)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix041


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[PMID]:28453727
[Au] Autor:Lukasz A; Hillgruber C; Oberleithner H; Kusche-Vihrog K; Pavenstädt H; Rovas A; Hesse B; Goerge T; Kümpers P
[Ad] Endereço:Department of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Campus 1, 48149 Münster, Germany.
[Ti] Título:Endothelial glycocalyx breakdown is mediated by angiopoietin-2.
[So] Source:Cardiovasc Res;113(6):671-680, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: The endothelial glycocalyx (eGC), a carbohydrate-rich layer lining the luminal surface of the endothelium, provides a first vasoprotective barrier against vascular leakage and adhesion in sepsis and vessel inflammation. Angiopoietin-2 (Angpt-2), an antagonist of the endothelium-stabilizing receptor Tie2 secreted by endothelial cells, promotes vascular permeability through cellular contraction and junctional disintegration. We hypothesized that Angpt-2 might also mediate the breakdown of the eGC. Methods and results: Using confocal and atomic force microscopy, we show that exogenous Angpt-2 induces a rapid loss of the eGC in endothelial cells in vitro. Glycocalyx deterioration involves the specific loss of its main constituent heparan sulphate, paralleled by the secretion of the heparan sulphate-specific heparanase from late endosomal/lysosomal stores. Corresponding in vivo experiments revealed that exogenous Angpt-2 leads to heparanase-dependent eGC breakdown, which contributes to plasma leakage and leukocyte recruitment in vivo. Conclusion: Our data indicate that eGC breakdown is mediated by Angpt-2 in a non-redundant manner.
[Mh] Termos MeSH primário: Angiopoietina-2/metabolismo
Glicocálix/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Pele/irrigação sanguínea
[Mh] Termos MeSH secundário: Animais
Permeabilidade Capilar
Linhagem Celular
Glucuronidase/metabolismo
Heparitina Sulfato/metabolismo
Seres Humanos
Camundongos Endogâmicos C57BL
Microscopia de Força Atômica
Microscopia Confocal
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANGPT2 protein, human); 0 (Angiopoietin-2); 9050-30-0 (Heparitin Sulfate); EC 3.2.1.- (heparanase); EC 3.2.1.31 (Glucuronidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx023


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[PMID]:29023478
[Au] Autor:Mensah SA; Cheng MJ; Homayoni H; Plouffe BD; Coury AJ; Ebong EE
[Ad] Endereço:Department of Bioengineering, Northeastern University, Boston, Massachusetts, United States of America.
[Ti] Título:Regeneration of glycocalyx by heparan sulfate and sphingosine 1-phosphate restores inter-endothelial communication.
[So] Source:PLoS One;12(10):e0186116, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vasculoprotective endothelium glycocalyx (GCX) shedding plays a critical role in vascular disease. Previous work demonstrated that GCX degradation disrupts endothelial cell (EC) gap junction connexin (Cx) proteins, likely blocking interendothelial molecular transport that maintains EC and vascular tissue homeostasis to resist disease. Here, we focused on GCX regeneration and tested the hypothesis that vasculoprotective EC function can be stimulated via replacement of GCX when it is shed. We used EC with [i] intact heparan sulfate (HS), the most abundant GCX component; [ii] degraded HS; or [iii] HS that was restored after enzyme degradation, by cellular self-recovery or artificially. Artificial HS restoration was achieved via treatment with exogenous HS, with or without the GCX regenerator and protector sphingosine 1- phosphate (S1P). In these cells we immunocytochemically examined expression of Cx isotype 43 (Cx43) at EC borders and characterized Cx-containing gap junction activity by measuring interendothelial spread of gap junction permeable Lucifer Yellow dye. With intact HS, 60% of EC borders expressed Cx43 and dye spread to 2.88 ± 0.09 neighboring cells. HS degradation decreased Cx43 expression to 30% and reduced dye spread to 1.87± 0.06 cells. Cellular self-recovery of HS restored baseline levels of Cx43 and dye transfer. Artificial HS recovery with exogenous HS partially restored Cx43 expression to 46% and yielded dye spread to only 1.03 ± 0.07 cells. Treatment with both HS and S1P, recovered HS and restored Cx43 to 56% with significant dye transfer to 3.96 ± 0.23 cells. This is the first evidence of GCX regeneration in a manner that effectively restores vasculoprotective EC communication.
[Mh] Termos MeSH primário: Comunicação Celular
Células Endoteliais/citologia
Glicocálix/metabolismo
Heparitina Sulfato/metabolismo
Lisofosfolipídeos/metabolismo
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Conexina 43/metabolismo
Células Endoteliais/metabolismo
Junções Comunicantes/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Ratos
Esfingosina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (GJA1 protein, mouse); 0 (Lysophospholipids); 26993-30-6 (sphingosine 1-phosphate); 9050-30-0 (Heparitin Sulfate); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186116


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[PMID]:28832958
[Au] Autor:Li X; Ma X
[Ad] Endereço:Department of Intensive Care Unit, the First Affiliated Hospital, China Medical University, Shenyang, Liaoning Province, China.
[Ti] Título:The role of heparin in sepsis: much more than just an anticoagulant.
[So] Source:Br J Haematol;179(3):389-398, 2017 Nov.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Despite progress in antibiotic treatment, mechanical ventilation, fluid resuscitation and blood glucose maintenance, sepsis remains a cause of high mortality in the intensive care unit to date, there are no proven treatment strategies for the routine management of septic patients. The extensive interaction between inflammation and coagulation contributes to the basic pathophysiology of sepsis. Thus, the agents that attenuate the activation of both inflammation and coagulation may improve the outcome in sepsis. Apart from the well-known anticoagulant effects of heparin, it also possesses various immunomodulatory properties and protects glycocalyx from shedding. Hence, heparin seems to be such an agent. Immunothrombosis plays an important role in early host defence against bacterial dissemination, thus the proper timing for anticoagulant therapy should be determined. We review the available experimental and clinical data supporting the use of heparin in sepsis. At this time the use of heparin in the treatment of sepsis is conflicting. Future trials of heparin therapy for sepsis should concentrate on the very severely ill patients, in whom benefit is most likely to be demonstrated.
[Mh] Termos MeSH primário: Anticoagulantes/uso terapêutico
Heparina/uso terapêutico
Sepse/tratamento farmacológico
[Mh] Termos MeSH secundário: Anticoagulantes/farmacologia
Glicocálix/efeitos dos fármacos
Heparina/farmacologia
Seres Humanos
Fatores Imunológicos/farmacologia
Fatores Imunológicos/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto/métodos
Sepse/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Immunologic Factors); 9005-49-6 (Heparin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14885


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[PMID]:28700908
[Au] Autor:Bartosch AMW; Mathews R; Tarbell JM
[Ad] Endereço:Department of Biomedical Engineering, The City College of New York, New York, New York.
[Ti] Título:Endothelial Glycocalyx-Mediated Nitric Oxide Production in Response to Selective AFM Pulling.
[So] Source:Biophys J;113(1):101-108, 2017 Jul 11.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nitric oxide (NO) is a regulatory molecule in the vascular system and its inhibition due to endothelial injury contributes to cardiovascular disease. The glycocalyx is a thin layer of glycolipids, glycoproteins, and proteoglycans on the surface of mammalian epithelial cells. Extracellular forces are transmitted through the glycocalyx to initiate intracellular signaling pathways. In endothelial cells (ECs), previous studies have shown the glycocalyx to be a significant mediator of NO production; degradation of the endothelial glycocalyx layer (EGL) drastically reduces EC production of NO in response to fluid shear stress. However, the specific EGL components involved in this process are not well established. Recent work using short-hairpin RNA approaches in vitro suggest that the proteoglycan glypican-1, not syndecan-1, is the dominant core protein mediating shear-induced NO production. We utilized atomic force microscopy (AFM) to apply force selectively to components of the EGL of confluent rat fat pad ECs (RFPECs), including proteoglycans and glycosaminoglycans, to observe how each component individually contributes to force-induced production of NO. 4,5-diaminofluorescein diacetate, a cell-permeable fluorescent molecule, was used to detect changes in intracellular NO production. Antibody-coated AFM probes exhibited strong surface binding to RFPEC monolayers, with 100-300 pN mean adhesion forces. AFM pulling on glypican-1 and heparan sulfate for 10 min caused significantly increased NO production, whereas pulling on syndecan-1, CD44, hyaluronic acid, and with control probes did not. We conclude that AFM pulling can be used to activate EGL-mediated NO production and that the heparan sulfate proteoglycan glypican-1 is a primary mechanosensor for shear-induced NO production.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Glicocálix/metabolismo
Mecanotransdução Celular/fisiologia
Óxido Nítrico/metabolismo
Estresse Fisiológico/fisiologia
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Animais
Fluoresceína
Glipicanas/metabolismo
Heparitina Sulfato/metabolismo
Receptores de Hialuronatos/metabolismo
Ácido Hialurônico/metabolismo
Indicadores e Reagentes
Espaço Intracelular/metabolismo
Microscopia de Força Atômica
Ratos
Estresse Mecânico
Sindecana-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4,5-diaminofluorescein diacetate); 0 (Glypicans); 0 (Hyaluronan Receptors); 0 (Indicators and Reagents); 0 (Sdc1 protein, rat); 0 (Syndecan-1); 31C4KY9ESH (Nitric Oxide); 9004-61-9 (Hyaluronic Acid); 9050-30-0 (Heparitin Sulfate); TPY09G7XIR (Fluorescein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE


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[PMID]:28504989
[Au] Autor:Kataoka H; Ushiyama A; Akimoto Y; Matsubara S; Kawakami H; Iijima T
[Ad] Endereço:From the *Division of Anesthesiology, Department of Perioperative Medicine, Showa University, School of Dentistry, Tokyo, Japan; †Department of Environmental Health, National Institute of Public Health, Saitama, Japan; and ‡Department of Anatomy and §Laboratory for Electron Microscopy, Kyorin University School of Medicine, Tokyo, Japan.
[Ti] Título:Structural Behavior of the Endothelial Glycocalyx Is Associated With Pathophysiologic Status in Septic Mice: An Integrated Approach to Analyzing the Behavior and Function of the Glycocalyx Using Both Electron and Fluorescence Intravital Microscopy.
[So] Source:Anesth Analg;125(3):874-883, 2017 Sep.
[Is] ISSN:1526-7598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The endothelial surface layer (ESL) regulates vascular permeability to maintain fluid homeostasis. The glycocalyx (GCX), which has a complex and fragile ultrastructure, is an important component of the ESL. Abnormalities of the GCX have been hypothesized to trigger pathological hyperpermeability. Here, we report an integrated in vivo analysis of the morphological and functional properties of the GCX in a vital organ. METHODS: We examined the behavior of the ESL and GCX, using both electron microscopy (EM) and intravital microscopy (IVM). We also compared morphological changes in the ESL of mouse skin in a glycosidase-treated and control group. Combined approaches were also used to examine both morphology and function in a lipopolysaccharide-induced septic model and the pathophysiological features of leukocyte-endothelial interactions and in vivo vascular permeability. RESULTS: Using IVM, we identified an illuminated part of the ESL as the GCX and confirmed our observation using morphological and biochemical means. In septic mice, we found that the GCX was thinner than in nonseptic controls in both an EM image analysis (0.98 ± 2.08 nm vs 70.68 ± 36.36 nm, P< .001) and an IVM image analysis (0.36 ± 0.15 µm vs 1.07 ± 0.39 µm, P< .001). Under septic conditions, syndecan-1, a representative core protein of the GCX, was released into the blood serum at a higher rate in septic animals (7.33 ± 3.46 ng/mL) when compared with controls (below the limit of detection, P< .001). Significant increases in leukocyte-endothelial interactions, defined as the numbers of rolling or firm-sticking leukocytes, and molecular hyperpermeability to the interstitium were also observed after GCX shedding in vivo. CONCLUSIONS: Using IVM, we visualized an illuminated part of the ESL layer that was subsequently confirmed as the GCX using EM. Severe sepsis induced morphological degradation of the GCX, accompanied by shedding of the syndecan-1 core protein and an increase in leukocyte-endothelial interactions affecting the vascular permeability. Our in vivo model describes a new approach to deciphering the relationship between structural and functional behaviors of the GCX.
[Mh] Termos MeSH primário: Endotélio/patologia
Endotélio/ultraestrutura
Glicocálix/patologia
Glicocálix/ultraestrutura
Microscopia Intravital/métodos
Sepse/patologia
[Mh] Termos MeSH secundário: Animais
Permeabilidade Capilar/fisiologia
Endotélio/metabolismo
Glicocálix/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Microscopia Eletrônica
Microscopia de Fluorescência/métodos
Sepse/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE
[do] DOI:10.1213/ANE.0000000000002057


  7 / 789 MEDLINE  
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[PMID]:28487369
[Au] Autor:Taniguchi T; Woodward AM; Magnelli P; McColgan NM; Lehoux S; Jacobo SMP; Mauris J; Argüeso P
[Ad] Endereço:From the Schepens Eye Research Institute and Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts 02114.
[Ti] Título:-Glycosylation affects the stability and barrier function of the MUC16 mucin.
[So] Source:J Biol Chem;292(26):11079-11090, 2017 Jun 30.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transmembrane mucins are highly -glycosylated glycoproteins that coat the apical glycocalyx on mucosal surfaces and represent the first line of cellular defense against infection and injury. Relatively low levels of -glycans are found on transmembrane mucins, and their structure and function remain poorly characterized. We previously reported that carbohydrate-dependent interactions of transmembrane mucins with galectin-3 contribute to maintenance of the epithelial barrier at the ocular surface. Now, using MALDI-TOF mass spectrometry, we report that transmembrane mucin -glycans in differentiated human corneal epithelial cells contain primarily complex-type structures with -acetyllactosamine, a preferred galectin ligand. In -glycosylation inhibition experiments, we find that treatment with tunicamycin and siRNA-mediated knockdown of the Golgi -acetylglucosaminyltransferase I gene ( ) induce partial loss of both total and cell-surface levels of the largest mucin, MUC16, and a concomitant reduction in glycocalyx barrier function. Moreover, we identified a distinct role for -glycans in promoting MUC16's binding affinity toward galectin-3 and in causing retention of the lectin on the epithelial cell surface. Taken together, these studies define a role for -linked oligosaccharides in supporting the stability and function of transmembrane mucins on mucosal surfaces.
[Mh] Termos MeSH primário: Antígeno Ca-125/metabolismo
Córnea/metabolismo
Células Epiteliais/metabolismo
Galectina 3/metabolismo
Glicocálix/metabolismo
Proteínas de Membrana/metabolismo
[Mh] Termos MeSH secundário: Antígeno Ca-125/genética
Linhagem Celular Transformada
Galectina 3/genética
Glicocálix/genética
Glicosilação
Seres Humanos
Proteínas de Membrana/genética
Estabilidade Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CA-125 Antigen); 0 (Galectin 3); 0 (MUC16 protein, human); 0 (Membrane Proteins); 0 (galectin-3, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170715
[Lr] Data última revisão:
170715
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.770123


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[PMID]:28486888
[Au] Autor:Pillinger NL; Kam P
[Ad] Endereço:Staff Specialist Anaesthetist, Department of Anaesthetics, Royal Prince Alfred Hospital, Sydney, New South Wales.
[Ti] Título:Endothelial glycocalyx: basic science and clinical implications.
[So] Source:Anaesth Intensive Care;45(3):295-307, 2017 05.
[Is] ISSN:0310-057X
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:The classic Starling principle proposed that microvascular fluid exchange was determined by a balance of hydrostatic and oncotic pressures relative to the vascular wall and this movement of water was regulated by gaps in the intercellular spaces. However, current literature on the endothelial glycocalyx (a jelly-like protective layer covering the luminal surface of the endothelium) has revised Starling's traditional concepts. This article aims to summarise the literature on the glycocalyx related to its basic science, clinical settings inciting injury, protective strategies and clinical perspectives. Perioperative damage to the glycocalyx structure can increase vascular permeability leading to interstitial fluid shifts, oedema, and increased surgical morbidity. Pathological shedding of the glycocalyx occurs in response to mechanical cellular stress, endotoxins, inflammatory mediators, atrial natriuretic peptide, ischaemia-reperfusion injury, free oxygen radicals and hyperglycaemia. Increased understanding of the endothelial glycocalyx may change perioperative fluid management, and therapeutic strategies aimed at its preservation may improve patient outcomes.
[Mh] Termos MeSH primário: Endotélio Vascular/citologia
Glicocálix/fisiologia
[Mh] Termos MeSH secundário: Animais
Glicemia/análise
Permeabilidade Capilar
Endotélio Vascular/fisiologia
Líquido Extracelular/metabolismo
Hidratação
Glicocálix/química
Seres Humanos
Mediadores da Inflamação/fisiologia
Mecanotransdução Celular/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Inflammation Mediators)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE


  9 / 789 MEDLINE  
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[PMID]:28365703
[Au] Autor:Yoon JH; Lee ES; Jeong Y
[Ad] Endereço:Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
[Ti] Título:In vivo Imaging of the Cerebral Endothelial Glycocalyx in Mice.
[So] Source:J Vasc Res;54(2):59-67, 2017.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Endothelial glycocalyx refers to the proteoglycan or glycoprotein layer of vessel walls and has critical physiological functions. Cerebral glycocalyx may have additional functions considering the blood-brain barrier and other features. However, the assessment of it has only been performed ex vivo, which includes processes presumably damaging the glycocalyx layer. Here we visualize and characterize the cerebral endothelial glycocalyx in vivo. METHODS: We visualized and quantified the cerebral endothelial glycocalyx in vivo under a 2-photon microscope by tagging glycocalyx and vessel lumen with wheat germ agglutinin lectin and dextran, respectively. The radial intensity was analyzed to measure the thickness of the cerebral endothelial glycocalyx in each vessel type. RESULTS: Cerebral arteries and capillaries have an intact endothelial glycocalyx, but veins and venules do not. The thickness of the glycocalyx layer in pial arteries, penetrating arteries, and capillaries was different; however, it was not correlated with the vessel diameter within each vessel type. CONCLUSION: We characterized the distribution of the cerebral endothelial glycocalyx in vivo. Compared to the results from ex vivo studies, the layer is thicker, indicating that the layer may be damaged in ex vivo systems. We also observed an inhomogeneous cerebral endothelial glycocalyx distribution that might reflect the functional heterogeneity of the vessel type.
[Mh] Termos MeSH primário: Encéfalo/irrigação sanguínea
Capilares/química
Artérias Cerebrais/química
Veias Cerebrais/química
Células Endoteliais/química
Glicocálix/química
Microscopia de Fluorescência por Excitação Multifotônica/métodos
Vênulas/química
[Mh] Termos MeSH secundário: Animais
Capilares/ultraestrutura
Artérias Cerebrais/ultraestrutura
Veias Cerebrais/ultraestrutura
Células Endoteliais/ultraestrutura
Fluoresceína-5-Isotiocianato/análogos & derivados
Glicocálix/ultraestrutura
Masculino
Camundongos Endogâmicos C57BL
Vênulas/ultraestrutura
Aglutininas do Germe de Trigo
Xantenos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Wheat Germ Agglutinins); 0 (Xanthenes); 0 (fluorescein isothiocyanate-wheat germ agglutinin); 82354-19-6 (Texas red); I223NX31W9 (Fluorescein-5-isothiocyanate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170403
[St] Status:MEDLINE
[do] DOI:10.1159/000457799


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[PMID]:28337244
[Au] Autor:Díaz-Juárez JA; Hernández-Muñoz R
[Ad] Endereço:División de Ciencias Biológicas y de la Salud, Departamento de Atención a la Salud, Universidad Autónoma Metropolitana (UAM Xochimilco), 04960 Ciudad de México, Mexico.
[Ti] Título:Rat Liver Enzyme Release Depends on Blood Flow-Bearing Physical Forces Acting in Endothelium Glycocalyx rather than on Liver Damage.
[So] Source:Oxid Med Cell Longev;2017:1360565, 2017.
[Is] ISSN:1942-0994
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have found selective elevation of serum enzyme activities in rats subjected to partial hepatectomy (PH), apparently controlled by hemodynamic flow-bearing physical forces. Here, we assess the involvement of stretch-sensitive calcium channels and calcium mobilization in isolated livers, after chemical modifications of the endothelial glycocalyx and changing perfusion directionality. Inhibiting in vivo protein synthesis, we found that liver enzyme release is influenced by de novo synthesis of endothelial glycocalyx components, and released enzymes are confined into a liver "pool." Moreover, liver enzyme release depended on extracellular calcium entry possibly mediated by stretch-sensitive calcium channels, and this endothelial-mediated mechanotransduction in liver enzyme release was also evidenced by modifying the glycocalyx carbohydrate components, directionality of perfusing flow rate, and the participation of nitric oxide (NO) and malondialdehyde (MDA), leading to modifications in the intracellular distribution of these enzymes mainly as nuclear enrichment of "mitochondrial" enzymes. In conclusion, the flow-induced shear stress may provide fine-tuned control of released hepatic enzymes through mediation by the endothelium glycocalyx, which provides evidence of a biological role of the enzyme release rather to be merely a biomarker for evaluating hepatotoxicity and liver damage, actually positively influencing progression of liver regeneration in mammals.
[Mh] Termos MeSH primário: Endotélio Vascular/metabolismo
Glicocálix/metabolismo
Fígado/enzimologia
Fígado/cirurgia
Fluxo Sanguíneo Regional/fisiologia
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Aspartato Aminotransferases/sangue
Cálcio/metabolismo
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio/química
Canais de Cálcio/metabolismo
Glutamato Desidrogenase/sangue
Fígado/efeitos dos fármacos
Fígado/lesões
Malato Desidrogenase/sangue
Masculino
Malondialdeído/sangue
Mecanotransdução Celular/efeitos dos fármacos
Óxido Nítrico/sangue
Ratos
Ratos Wistar
Fluxo Sanguíneo Regional/efeitos dos fármacos
Resistência ao Cisalhamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Calcium Channels); 31C4KY9ESH (Nitric Oxide); 4Y8F71G49Q (Malondialdehyde); EC 1.1.1.37 (Malate Dehydrogenase); EC 1.4.1.2 (Glutamate Dehydrogenase); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1155/2017/1360565



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