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- ItemAcesso aberto (Open Access)Células endoteliais circulantes em diferentes tipos de tratamentos da Anemia Falciforme(Universidade Federal de São Paulo (UNIFESP), 2020-12-15) Souza, Claudia Regina Lustosa [UNIFESP]; Figueiredo, Maria Stella [UNIFESP]; Universidade Federal de São PauloSickle cell anemia (SCA) is characterized by anemia and pain due to chronic hemolysis and recurrent episodes of ischemia, respectively. In the presence of hypoxia, the anomalous hemoglobin (Hb), HbS, triggers microvascular occlusion, a phenomenon enhanced by the adhesion of erythrocytes and leukocytes to the vascular endothelium. As a result, vasculopathy and inflammation characteristic of SCA are observed, with the endothelial cell playing an important role. The endothelium is a dynamic, balanced tissue, where the circulation compartment reflects both the lesion and the regeneration of the vascular tree. In this compartment, circulating endothelial cells (CECs) released from vascular injury and progenitor endothelial cells (PECs) involved in vascular regeneration are identified. However, the importance of these cells in SCA and their relationship with the type of treatment still needs further clarification. Objectives: To evaluate the endothelial phenotype of individuals with sickle cell anemia and determine whether the type of treatment influences this manifestation. Casuistic: 45 patients with SCA were analyzed, followed up at the Hemoglobinopathies Outpatient Clinic of Escola Paulista de Medicina (EPM / UNIFESP). According to the treatment, the following groups were distributed: a) SS (N = 11) - steady state without hydroxyurea (HU); b) SS-HU (N = 19) – in use of maximum tolerated dose of HU; c) SS-TF (N = 15) - chronic transfusion regimen. Control group (CN, N = 13) consisting of healthy individuals. Work approved by Ethical Comittee and participants signed an informed consent form. Exclusion criteria: pregnant and puerperal women, vaso-occlusive crisis in the last 3 months, chronic renal failure and active leg ulcer. In the SS and SS-HU groups, those who received red blood cell transfusion in the last 3 months were also excluded. Methods: Laboratory evaluation: complete blood count, hemolysis tests and C-reactive protein (CRP). Identification and quantification of CECs and PECs performed by Flow Cytometry (FACSCantoII®). Results: The SS group had a higher number of CECs (median: 2.73; range: 0 - 20.0) than the CN (0.39; 0 - 4.20) and the SS-TF (0.67 ; 0 - 2.99), p = 0.016 and 0.013 respectively. The SS-HU group showed higher PECs quantification (0; 0 - 6.62) than the SS and SS-TF groups (0; 0 - 0 in both groups), p <0.05. There was no relationship between determination of CECs and clinical manifestations, however patients with priapism showed higher values (2.28; 0.74 - 6.09) than those without this manifestation (0.68; 0 - 20.0) with p = 0.055. There was no significant correlation between PECs data and clinical manifestations. Discussion & Conclusion: Our results corroborate previous studies that associate the increase in CECs with endothelial complications of SCA. The presence of fewer PECs in groups SS and SS-TF when compared to SS-HU group suggests that HU can provide endothelial protection and raises the question of its indication for all SCA patients in order to prevent serious manifestations related to endothelial dysfunction.
- ItemSomente MetadadadosEstudo Da Ação Dos Inibidores Da 3-Hidroximetilglutaril Coa Redutase Sobre A Secreção De Citocinas Inflamatórias Em Células Endoteliais Estimuladas Com Soro Urêmico(Universidade Federal de São Paulo (UNIFESP), 2017-06-29) Carmona, Silmara De Melo [UNIFESP]; Batista, Marcelo Costa [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Introduction: Atherosclerosis, the anatomopathological basis of dyslipidemia, is associated with the occurrence of cardiovascular diseases (CVD), demonstrating a high prevalence in chronic renal disease (CKD). Non-traditional risk factors such as the uremic environment and inflammation promote metabolic alterations related with CVD. Uremic mileu has been considered preponderant issue for secretion of cytokines, as TNF-α and interleukins, which are associated with endothelial dysfunction. Statins, drugs that inhibit the enzyme 3-Hydroxymethylglutaryl CoA Reductase, preventing the formation of mevalonic acid and its precursors, have pleiotropic effects with potential benefit under such conditions of systemic inflammatory response. Objective: The aim of the present study was to characterize immortalized human umbilical vein cells by expressing constitutive and specific markers, as well as analyzing the impact of simvastatin on the secretion of TNF-α and IL-10 in endothelial cells stimulated with uremic serum. Methods: To validated the source of the cell line used as in vitro model in this study, cell culture was incubated with primary monoclonal antibodies and secondary antibodies conjugated to Allophycocyanin (APC) and Phycoerythrin (PE). After, the cells were submitted to flow cytometry and immunofluorescence methods to evaluate the expression of constitutive and specific markers. For the study of the impact of 3-Hydroxymethylglutaryl CoA reductase inhibitors on the expression and secretion of IL-10 and TNF-α, HUVEC cells were pretreated with simvastatin and insulted with uremic serum and serum from healthy subjects. Additionally, the cell supernatant was collected and analyzed by ELISA method. Results and Conclusions: Our findings confirm the endothelial origin of the cells used in this study by which expressing the constitutive markers CD31, CD146 and vWF, as well as the expression of the specific markers VCAM and ICAM in the cells incubated with TNF-α, mimicking the inflammatory scenario. We also demonstrate that 3-Hydroxymethylglutaryl CoA reductase inhibitors have a pleiotropic effect on endothelial tissue, reducing TNF-α secretion and increasing IL-10 secretion. These actions determine the partial reversal of the inflammatory response and consequently, the attenuation of endothelial dysfunction which is observed in the uremic environment. However, the elucidation of the mechanisms by which statins acts in the endothelium should be the object of future studies.
- ItemSomente MetadadadosExpressão de glicosaminoglicanos e proteínas da matriz extracelular em células endoteliais(Universidade Federal de São Paulo (UNIFESP), 2008) Dominato, Juliana Augusta Albieri [UNIFESP]; Nader, Helena Bonciani [UNIFESP]
- ItemAcesso aberto (Open Access)Heparin modulates the expression of genes encoding pro and anti-apoptotic proteins in endothelial cells exposed to intestinal ischemia and reperfusion in rats(Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia, 2014-07-01) Taha, Murched Omar [UNIFESP]; Miranda-Ferreira, Regiane [UNIFESP]; Taha, Nabiha Saadi Abrahão [UNIFESP]; Monteiro, Hugo Pequeno [UNIFESP]; Caricati-Neto, Afonso [UNIFESP]; Fagundes, Djalma José [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)PURPOSE: To investigate if expression of genes encoding pro and anti-apoptotic proteins in the rat enteric endothelial cells stimulated by intestinal ischemia followed by reperfusion (IR) can be modified by treatment with heparin (HP).METHODS: Eighteen adult Wistar rats were divided in three groups: sham group submitted to laparotomy only (SG), ischemia followed by reperfusion group (IRG); ischemia followed by reperfusion plus pretreatment with HP 100 mg.kg-1 (IRG+HP). Ischemia was performed by clamping of the superior mesenteric artery. After 60 min of ischemia, metal clamps were removed for reperfusion for 120 min. Gene expression of encoding pro (Casp1, Casp6, Casp3, Cflar, Fas and Pgl) and anti-apoptotic (Bcl2, Bcl2l1 and Naip2) proteins in rat enteric endothelial cells was evaluated by PCR microarray method.RESULTS: Compared to rat endothelial cells of SG, the expression of pro-apoptotic genes was up-regulated in IRG while anti-apoptotic genes were down-regulated. In contrast, the expression of anti-apoptotic genes in IRG+HP was up-regulated while pro-apoptotic genes was down-regulated compared to SG.CONCLUSION: The attenuation by heparin of intestinal ischemia-reperfusion previously demonstrated in rodents could be related with ability of this drug to stimulate and reduce gene expression of encoding anti and pro-apoptotic proteins, respectively.
- ItemAcesso aberto (Open Access)Ischemic preconditioning and the gene expression of enteric endothelial cell biology of rats submitted to intestinal ischemia and reperfusion(Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia, 2013-03-01) Taha, Murched Omar [UNIFESP]; Miranda-Ferreira, Regiane [UNIFESP]; Taha, Nabiha Saadi Abrahão [UNIFESP]; Monteiro, Hugo Pequeno [UNIFESP]; Caricati-Neto, Afonso [UNIFESP]; Oliveira-Júnior, Itamar Souza [UNIFESP]; Fagundes, Djalma José [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)PURPOSE: To investigate the effects of ischemic preconditioning (IPC) on the expression of pro and anti-apoptotic genes in rat endothelial cells undergoing enteric ischemia (I) and reperfusion (R). METHODS: Thirty rats underwent clamping of the superior mesenteric vessels. Sham group (GS) laparotomy only; Ischemia (GI): intestinal ischemia (60 min); Ischemia and Reperfusion (GIR): ischemia (60 min) and reperfusion (120 min); Ischemia and intestinal ischemic preconditioning (GI + IPC) : 5 minutes of ischemia followed by 10 min of reperfusion before sustained ischemia (60 min) ischemia and reperfusion and IPC (GIR + IPC): 5 min ischemia followed by 10 min of reperfusion before sustained ischemia (60min) and reperfusion (120 min). Rat Endothelial Cell Biology (PCR array) to determine the expression of genes related to endothelial cell biology. RESULTS: Gene expression of pro-apoptotic markers (Casp1, Casp6, Cflar, Fas, and Pgl) was down regulated in GI+IPC and in GIR + IPC. In contrast, the expression of anti-apoptotic genes (Bcl2 and Naip2), was up-regulated in GI + IPC and in GIR + IPC. CONCLUSION: Ischemic preconditioning may protect against cell death caused by ischemia and reperfusion.