Relevant bibliographies by topics / Pentraxina 3

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Academic literature on the topic 'Pentraxina 3'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Pentraxina 3"

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El Wakeel, Maged A., Rania N. Sabry, Ghada M. El-kassas, Shereen A. Abd El-Gaffar, Wael H. El batal, Essam M. Galal, Ashraf Azmy, and Eman Awadallah. "Pentraxin 3: A Potential Novel Predictor for Neonatal Pulmonary Hypertension." Open Access Macedonian Journal of Medical Sciences 7, no. 15 (August 14, 2019): 2424–27. http://dx.doi.org/10.3889/oamjms.2019.638.

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BACKGROUND: Persistent pulmonary hypertension of the newborn (PPHN) is a serious neonatal problem which has a high mortality rate even with advanced modes of mechanical ventilation. Pentraxin 3 is one of the long pentraxins, which plays an essential role in regulation of cell proliferation and angiogenesis. AIM: This study aims to assess serum pentraxin 3 levels in neonates with pulmonary arterial hypertension and compare them in those who have other congenital heart diseases and healthy neonates. Also, we intended to evaluate serum levels of CRP as a mediator of inflammation in the studied groups. METHODS: The study is a case-control study. Cases were recruited from El Galaa Teaching Hospital, classified into three groups; each group had thirty cases. The first one: cases with pulmonary hypertension (PHT), the second one: cases with congenital heart diseases (CHD) without pulmonary hypertension and the third group included healthy neonates. All participants were subjected to full history taking and full clinical examination. Diagnosis of congenital heart disease and pulmonary hypertension was made according to echocardiographic findings by pediatric cardiologist using echocardiography machine. Laboratory investigations included measurement of serum pentraxin 3, Routine CBC, CRP. RESULTS: This study found that the mean serum pentraxin 3 in PHT neonates was significantly higher than that of the control and CHD neonates (p ≤ 0.001, p = 0.02 respectively). Also, the mean Pentraxin3 of the CHD neonates was significantly higher than that of the control (p = 0.06). Also, the mean CRP of the PHT neonates was significantly higher than that of the control (p = 0.01). Regression analysis showed that Pentraxin3 was the main predictor of PAP (P = 0.01). CONCLUSION: Serum pentraxin 3 is significantly elevated in neonates with pulmonary hypertension, so measurement of pentraxin 3 levels in neonates may be valuable as a predictor for pulmonary hypertension in neonates.
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Kunes, P., Z. Holubcova, M. Kolackova, and J. Krejsek. "Pentraxin 3(PTX 3): An Endogenous Modulator of the Inflammatory Response." Mediators of Inflammation 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/920517.

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Inflammatory or anti-inflammatory? That is the question as far as the acute-phase response and its mediators, the pentraxins, are concerned. Only some ten years ago, the classical or short pentraxin C-reactive protein and the newly discovered long pentraxin PTX3 were considered to exert most of the detrimental effects of acute inflammation, whether microbial or sterile in origin. However, accumulating evidence suggests an at least dichotomous, context-dependent outcome attributable to the pentraxins, if not a straightforward anti-inflammatory nature of the acute-phase response. This paper is focused on the inherent effects of pentraxin 3 in inflammatory responses, mainly in coronary artery disease and inAspergillus fumigatusinfection. Both are examples of inflammatory reactions in which PTX3 is substantially involved; the former sterile, the latter infectious in origin. Apart from different inducing noxae, similarities in the pathogenesis of the two are striking. All the same, the introductory question still persists: is the ultimate impact of PTX3 in these conditions inflammatory or anti-inflammatory, paradoxical as the latter might appear? We try to provide an answer such as it emerges in the light of recent findings.
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Alieva, Amina M., Natalia V. Teplova, Maxim A. Batov, Kira V. Voronkova, Ramiz K. Valiev, Lidia M. Shnakhova, Tatiana V. Pinchuk, Alik M. Rakhaev, Marina R. Kalova, and Igor G. Nikitin. "Pentraxin-3 – a promising biological marker in heart failure: literature review." Consilium Medicum 24, no. 1 (January 15, 2022): 53–59. http://dx.doi.org/10.26442/20751753.2022.1.201382.

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According to many studies, inflammation plays a very significant role in the pathogenesis of heart failure. Many studies have demonstrated an increase in circulating levels of inflammatory markers and cytokines such as C-reactive protein, tumor necrosis factor-a (TNF-a), and interleukins. C-reactive protein is produced in the liver in response to stimulation by various cytokines, mainly interleukin-6, and is a member of the pentraxin superfamily. Pentraxin-3, which is a long pentraxin, has a C-terminal domain of pentraxin similar to the classic short pentraxins, but differs from them in the presence of an unrelated long N-terminal domain. Various cell types can produce pentraxin-3 when exposed to primary inflammatory signals such as interleukin-1, tumor necrosis (TNF-a), oxidized low density lipoprotein, and microbial fragments (eg, lipopolysaccharide, lipoarabinomannans). Data in experimental animal models have demonstrated that pentraxin-3 can play cardioprotective and atheroprotective roles through its influence on the inflammatory process. Pentraxin-3 has been studied in several clinical protocols as a potential biomarker for cardiovascular disease.
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Lucarelli, G., G. S. Netti, F. Spadaccino, G. Castellano, M. Gigante, C. Divella, M. T. Rocchetti, et al. "La Pentraxina 3 (PTX3) Modula l’immunoflogosi nel microambiente tumorale ed è un fattore prognostico in pazienti con carcinoma renale a cellule chiare." European Urology Open Science 20 (October 2020): S63—S64. http://dx.doi.org/10.1016/s2666-1683(20)35398-2.

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Bonacina, Fabrizia, Andrea Baragetti, Alberico Luigi Catapano, and Giuseppe Danilo Norata. "Long Pentraxin 3: Experimental and Clinical Relevance in Cardiovascular Diseases." Mediators of Inflammation 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/725102.

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Pentraxin 3 (PTX3) is an essential component of the humoral arm of innate immunity and belongs, together with the C-reactive protein (CRP) and other acute phase proteins, to the pentraxins' superfamily: soluble, multifunctional, pattern recognition proteins. Pentraxins share a common C-terminal pentraxin domain, which in the case of PTX3 is coupled to an unrelated long N-terminal domain. PTX3 in humans, like CRP, correlates with surrogate markers of atherosclerosis and is independently associated with the risk of developing vascular events. Studies addressing the potential physiopathological role of CRP in the cardiovascular system were so far inconclusive and have been limited by the fact that the sequence and regulation have not been conserved during evolution between mouse and man. On the contrary, the conservation of sequence, gene organization, and regulation of PTX3 supports the translation of animal model findings in humans. While PTX3 deficiency is associated with increased inflammation, cardiac damage, and atherosclerosis, the overexpression limits carotid restenosis after angioplasty. These observations point to a cardiovascular protective effect of PTX3 potentially associated with the ability of tuning inflammation and favor the hypothesis that the increased levels of PTX3 in subjects with cardiovascular diseases may reflect a protective physiological mechanism, which correlates with the immunoinflammatory response observed in several cardiovascular disorders.
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Introna, M., VV Alles, M. Castellano, G. Picardi, L. De Gioia, B. Bottazzai, G. Peri, et al. "Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites." Blood 87, no. 5 (March 1, 1996): 1862–72. http://dx.doi.org/10.1182/blood.v87.5.1862.1862.

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Abstract Pentraxins, which include C reactive protein (CRP) and serum amyloid P component (SAP), are prototypic acute phase reactants that serve as indicators of inflammatory reactions. Here we report genomic and cDNA cloning of mouse ptx3 (mptx3), a member of the pentraxin gene family and characterize its extrahepatic expression in vitro and in vivo. mptx3 is organized into three exons on chromosome 3: the first (43 aa) and second exon (175 aa) code for the signal peptide and for a protein portion with no high similarity to known sequences the third (203 aa) for a domain related to classical pentraxins, which contains the “pentraxin family signature.” Analysis of the N terminal portion predicts a predominantly alpha helical structure, while the pentraxin domain of ptx3 is accommodated comfortably in the tertiary structure fold of SAP. Normal and transformed fibroblasts, undifferentiated and differentiated myoblasts, normal endothelial cells, and mononuclear phagocytes express mptx3 mRNA and release the protein in vitro on exposure to interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)alpha. mptx3 was induced by bacterial lipopolysaccharide in vivo in a variety of organs and, most strongly, in the vascular endothelium of skeletal muscle and heart. Thus, mptx3 shows a distinct pattern of in vivo expression indicative of a significant role in cardiovascular and inflammatory pathology.
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Introna, M., VV Alles, M. Castellano, G. Picardi, L. De Gioia, B. Bottazzai, G. Peri, et al. "Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites." Blood 87, no. 5 (March 1, 1996): 1862–72. http://dx.doi.org/10.1182/blood.v87.5.1862.bloodjournal8751862.

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Pentraxins, which include C reactive protein (CRP) and serum amyloid P component (SAP), are prototypic acute phase reactants that serve as indicators of inflammatory reactions. Here we report genomic and cDNA cloning of mouse ptx3 (mptx3), a member of the pentraxin gene family and characterize its extrahepatic expression in vitro and in vivo. mptx3 is organized into three exons on chromosome 3: the first (43 aa) and second exon (175 aa) code for the signal peptide and for a protein portion with no high similarity to known sequences the third (203 aa) for a domain related to classical pentraxins, which contains the “pentraxin family signature.” Analysis of the N terminal portion predicts a predominantly alpha helical structure, while the pentraxin domain of ptx3 is accommodated comfortably in the tertiary structure fold of SAP. Normal and transformed fibroblasts, undifferentiated and differentiated myoblasts, normal endothelial cells, and mononuclear phagocytes express mptx3 mRNA and release the protein in vitro on exposure to interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)alpha. mptx3 was induced by bacterial lipopolysaccharide in vivo in a variety of organs and, most strongly, in the vascular endothelium of skeletal muscle and heart. Thus, mptx3 shows a distinct pattern of in vivo expression indicative of a significant role in cardiovascular and inflammatory pathology.
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Nagai, Kei, Atsushi Ueda, Chie Saito, Asako Zempo-Miyaki, and Kunihiro Yamagata. "Annual Decline in Pentraxin 3 Is a Risk of Vascular Access Troubles in Hemodialysis Patients." International Journal of Nephrology 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/297954.

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Pentraxin 3 (PTX3), a multifunctional modulator of the innate immunoinflammatory response, is higher in patients undergoing hemodialysis than healthy control. Our study focused on annual change in PTX3 levels in patients with chronic hemodialysis, because regularly undergoing hemodialysis for many years modifies vascular inflammatory status. To demonstrate whether annual change in PTX3 is associated with vascular events, we measured blood levels of pentraxins (PTX3 and high-sensitivity C-reactive protein (hsCRP)) at baseline and in the next year in 76 hemodialysis patients and observed 20 patients with vascular access troubles during follow-up years. The annual decline in PTX3, but not hsCRP, is a significant risk of the incidence of vascular access trouble that is a critical and specific complication for hemodialysis patients (hazard ratio; 0.732 per +1 ng/mL/year in PTX3,*P=0.039). This study is the first to focus on the annual change of pentraxins in a hemodialysis cohort.
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Lech, M., C. Rommele, and H. J. Anders. "Pentraxins in nephrology: C-reactive protein, serum amyloid P and pentraxin-3." Nephrology Dialysis Transplantation 28, no. 4 (December 14, 2012): 803–11. http://dx.doi.org/10.1093/ndt/gfs448.

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Szymkowiak, Martyna, Piotr Surmiak, and Małgorzata Baumert. "Pentraxin 3 – possible uses in neonatology and paediatrics." Pediatria i Medycyna Rodzinna 16, no. 3 (October 30, 2020): 247–50. http://dx.doi.org/10.15557/pimr.2020.0045.

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Pentraxin 3 (PTX3) is a multifunctional acute phase protein belonging to the family of long pentraxins, which is synthesised in numerous cells of the body under the influence of proinflammatory factors and locally at the site of inflammation. Under physiological conditions, PTX3 is stored in neutrophil granules, where there is a constant pool of glycoproteins. Increased pentraxin 3 levels in blood serum are observed as early as 1 hour after a damaging stimulus. Elevation of PTX3 serum levels can be used to diagnose fertility disorders in women as well as in pregnancy pathology, women at risk of pre-eclampsia, gestational diabetes, premature rupture of membrane and preterm delivery. The biological function of PTX3 is not fully understood, especially in the population of newborns and children. So far, no reference values for PTX3 levels in newborns and children have been developed. This protein can be used as a marker of pulmonary hypertension in newborns as well as to assess the degree of respiratory failure in premature infants. In older children, it is useful in the assessment of the severity of meningococcal disease and sepsis as well as in the treatment of childhood asthma. There are studies available in which blood levels of PTX3 significantly correlate with the severity of kidney damage in Henoch–Schönlein macular degeneration in children, and the evaluation of this protein in urine is used to detect renal parenchymal destruction after pyelonephritis.
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Dissertations / Theses on the topic "Pentraxina 3"

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Gifoni, Markus Andret Cavalcante. "Envolvimento da pentraxina 3 (PTX3) na patogÃnese da cistite hemorrÃgica induzida por ifosfamida em camundongos." Universidade Federal do CearÃ, 2008. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=1245.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
A cistite hemorrÃgica (CH) à um fenÃmeno inflamatÃrio frequentemente associado à quimioterapia com oxazafosforinas. Trata-se de uma resposta inflamatÃria inata à aÃÃo da AcroleÃna (ACR), metabÃlito hepÃtico comum à Ifosfamida (IFO) e à ciclofosfamida (CTX). O papel da resposta ao recrutamento de receptores toll-like (TLR) e do estÃmulo por TNF-α e IL-1β com envolvimentto de iNOS e COX-2 tem sido demonstrado neste fenÃmeno. Estudos recentes demonstram que a Pentraxina 3 (PTX3) assume papel de mediador inflamatÃrio em modelos de resposta inflamatÃria inata in vivo, sobretudo relacionada ao recrutamento de TLR. Desta forma, o presente estudo pretende investigar o possÃvel envolvimento de PTX3 na patogÃnese da CH induzida por ifosfamida em camundongos. Para isso, foi realizada quantificaÃÃo de RNAm por RT-PCR para PTX3 e IL-1β em camundongos C57/ BL6 tratados com ifosfamida e salina. Em seguida, o modelo experimental da CH induzida por ifosfamida foi reproduzido em grupos de camundongos com hiperexpressÃo e nocauteados para PTX3 em comparaÃÃo com os respectivos controles do tipo selvagem e com grupos controle tratados com salina para posterior obtenÃÃo dos pesos vesicais Ãmidos (PVU), realizaÃÃo de anÃlise histomorfomÃtrica, imunohistoquÃmica e quantificaÃÃo de RNAm por RT-PCR para PTX3, IL-1β, TNF-α e iNOS. Os animais transgÃnicos e seus controles foram sacrificados com tempos de 3h e 12h apÃs o tratamento, enquanto os nocauteados e seus controles foram sacrificados com 12 horas do tratamento. Finalmente, a CH em animais C57/ BL6 foi modulada com o prÃ-tratamento com Talidomida, Pentoxifilina, MESNA, Amifostina e Aminoguanidina para a posterior marcaÃÃo imunohistoquÃmica com PTX3, IL-1β, TNF-α e iNOS. Observou-se que o RNAm de PTX3 està cerca de 70 vezes mais expresso em animais com CH, contra uma razÃo de expressÃo de 10 para IL-1β. Animais trangÃnicos para PTX3 tÃm reduÃÃo inicial da resposta inflamatÃria com expressÃo inferior de PTX3 e TNF-α e expressÃo aumentada de iNOS e intensificaÃÃo da inflamaÃÃo ao tempo de 12 horas, com expressÃo superior dos mediadores. NÃo houve diferenÃas significativas de intensidade da CH em animais KO em relaÃÃo aos controles. A modulaÃÃo da CH por talidomida e MESNA produziu reduÃÃo importante sobre a expressÃo de PTX3, enquanto a inibiÃÃo da CH por amifostina nÃo teve reduÃÃo expressiva da pentraxina. Em conjunto, estes dados apontam para um envolvimento inequÃvoco de PTX3 na fisiopatologia da inflamaÃÃo inata em modelo de CH murino com Ãntima relaÃÃo coma expressÃo de TNF-α
The Hemorrhagic Cystitis (HC) is an inflammatory reaction usually associated with Cancer Chemotherapy with Oxazaphosphorines. It is an innate inflammatory response to vesical irritation by Acrolein, an hepatic metabolite of the treatment with Iphosphamide and Cyclophosphamide. The role of toll-like receptor (TLR) engagement and TNF-α and IL-1β expression and the involvement of iNOS and COX-2 in the pathogenesis has been well demonstrated in a murine model of HC. Recent data configure pentraxin 3 (PTX3) as an inflammatory mediator in several experimental models of innate immune response in vivo, with a straight relation with TLR engagement. Because of that, this study looks at the involvement of PTX3 in the pathogenesis of iphosphamideâinduced HC in mice. For this purpose, the mRNA to PTX3 and IL-1β t was quantified by RT-PCR in groups of C57BL6 mice treated with Iphosphamide or Saline. After that, groups of transgenic and Knock-Out mice to PTX3 and its respectives wild-type controls were treated with Iphosphamide or saline with intention to measure the Bladder Wet Weight (BWW), histomorphometric scores and Immunohistochemistry and RT-PCR to PTX3, IL-1β, TNF-α e iNOS analysis. The transgenic mice and its controls were killed in 3h and 12h after the treatment, while the PTX3 KO and its controls were killed after 12 hours. Finally, the experimental HC was modulated by pretreatment with Talidomide, Pentoxiphiline, MESNA, Amifostine and Aminoguanidine and the bladders submitted to immunohistochemistry assay (PTX3, TNF-α, IL-1β and iNOS). By RT-PCR quantification, mRNA for PTX3 was expressed 70 times more in mice treated with iphosphamide than in controls, while IL-1β RNAm had an expression rate of 10 times. PTX3 transgenic mice had initial reduction of the inflammatory response with less expression of PTX3 and TNF-α and greater expression of iNOS. In the other hand, after 12 hours, the PTX3 transgenic mice had more inflammatory signs with superior expression of all the mediators. There was no difference between the PTX3 KO mice and its controls in the HC intensity although differences between groups were seen in cytokines expression. Talidomide and MESNA produced substantial reduction on the PTX3 expression, the same was seen to TNF-α, while the amifostine marked inhibition of HC had low effect on PTX3 expression. These data as a whole, point to an unequivocal involvement of PTX3 in the pathogenesis of innate inflammatory response of HC in mice with close relation with TNF-α engagement
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Rodrigues, Priscila Fabiana. "Avaliação do efeito da proteína Pentraxina 3 em células tumorais murinas." Universidade Federal de Minas Gerais, 2014. http://hdl.handle.net/1843/BUOS-9MKKQ3.

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Pentraxin 3 (PTX3) is an inflammatory protein that plays important role in innate immunity, matrix deposition and female fertility. Moreover, it is a natural antagonist of fibroblast growth factor 2 (FGF2) that inhibit the cellular proliferation and angiogenesis promoted by this factor. PTX3 binds to FGF2 in the site of interaction with its receptor (FGFR) preventing the activation of FGF2/FGFR signaling pathway and, as a consequence, inhibiting the expression of genes related to cell proliferation, migration, differentiation, survival and angiogenesis. Neoplasms are among the leading causes of death worldwide and the estimatives point to an increase in incidence of this type of disease. The FGF signaling pathway is crucial in tumor biology by regulating essential processes in tumorigenesis, as cell proliferation and angiogenesis. The identification of inhibitors of this pathway is important for the understanding of the biology of cancer and for the development of therapeutic approaches aimed at controlling growth and tumor progression. The objective of this study was to evaluate the biological effect of PTX3 in murine tumor cell lines derived from melanocytic melanoma (B16F10 and B16F1), amelanocytic melanoma (K1735 and K1735 M2) and fibrosarcoma (MC-TGS17-51 and Sal/N). The morphology of the cells was assessed by optical phase contrast microscopy and the structure of the actin cytoskeleton by immunofluorescence. Cell proliferation was evaluated by MTT assay and gene expression profile was measured by RT-PCR. Under our experimental conditions, PTX3 did not promote morphological changes or in the pattern of organization of actin in the cells K1735 M2 and B16F1. A higher number of viable cells compared to control was observed in response to the treatment with PTX3 in all types of cells. The expression of the FGF receptors (FGFR) 1, 3 and 4 was verified in all cells but the expression of FGFR2 was detected only in the lineage of fibrosarcoma Sal/N. Ptx3 was expressed by almost all cell lines but not by K1735 melanoma. No FGF2 basal expression was observed in B16F1 melanoma. Our data corroborate the findings of lack of expression of FGFR2 in tumors, particularly melanomas. We show here, for the first time, the expression of PTX3 in murine fibrosarcomas and melanomas. The results presented here contribute to the functional characterization of PTX3 and point out the need for studies aiming the evaluation of its role in the tumor microenvironment and the potencial usage of PTX3 as a biomarker for the diagnosis and prognosis of tumors.
Pentraxina 3 (PTX3) é uma importante proteína inflamatória, componente essencial da resposta imune inata, com função também na deposição de matriz e fertilidade feminina. Além disso, ela também é capaz de se ligar ao fator de crescimento de fibroblasto 2 (FGF2) e inibir as atividades biológicas de indução da proliferação celular e angiogênese promovidas por esse fator. PTX3 se liga a FGF2 no sítio de interação com o seu receptor (FGFR) e impede que a ligação FGF2/FGFR ocorra e, consequentemente, vias de sinalização que ativam genes ligados à proliferação celular, migração, diferenciação, sobrevivência e angiogênese não são ativadas. As neoplasias figuram entre as principais causas de morte mundiais e as estimativas apontam para um aumento de sua incidência no mundo todo. A via de sinalização de FGF é importante na biologia dos tumores por regular a proliferação celular e a angiogênese, processos essenciais para o crescimento e desenvolvimento tumoral. A identificação de inibidores desta via é importante para o entendimento da biologia do câncer e para o desenvolvimento de abordagens terapêuticas visando controlar o crescimento e a progressão tumoral. PTX3 é um antagonista natural de FGF2 que, além de inibir a proliferação celular e a angiogênese induzidas por esse fator, também é capaz de diminuir o crescimento e volume tumoral in vivo. O objetivo deste trabalho foi avaliar o efeito biológico de Ptx3 em linhagens de células tumorais murinas derivadas de melanoma melanocítico (B16F10 e B16F1), melanoma amelanocítico (K1735 e K1735 M2) e fibrosarcoma (MC-TGS17-51 e Sal/N). A morfologia das células foi avaliada por microscopia óptica de contraste de fase e a estrutura do citoesqueleto de actina por imunofluorescência. A proliferação celular foi analisada pelo método MTT e o padrão de expressão de genes por RT-PCR. Nas condições dos nossos ensaios, o tratamento com Ptx3 não promoveu mudanças morfológicas nas células ou no padrão de organização da actina nas linhagens K1735 M2 e B16F1. Um maior número de células viáveis em comparação com o controle foi observado nas células tratadas com Ptx3. Foi verificado que todas as linhagens expressam os receptores Fgfr1, 3 e 4. Já a expressão do receptor Fgfr2 foi observada apenas na linhagem de fibrosarcoma Sal/N. Somente a linhagem de melanoma K1735 não apresentou expressão basal de Ptx3 e a linhagem B16F1 a expressão de Fgf2. Nossos dados corroboram os achados de ausência de expressão de Fgfr2 nos tumores, especialmente nos melanomas, e mostram de forma inédita a expressão de Ptx3 em linhagens murinas de fibrosarcomas e melanomas. Os resultados aqui apresentados contribuem para a caracterização funcional de PTX3, e apontam a necessidade de estudos buscando avaliar o seu papel no microambiente tumoral e a possibilidade do seu uso como biomarcador no diagnóstico diferencial e prognóstico de tumores.
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Carizzo, Albino. "La Pentraxina 3: un potenziale marcatore di danno endoteliale nell’ipertensione arteriosa." Doctoral thesis, Universita degli studi di Salerno, 2016. http://hdl.handle.net/10556/2195.

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2014 - 2015
Background - The pentraxin 3 (PTX3) is a protein of the acute phase of inflammation which represents the prototype of the long pentraxins. In the last years, numerous studies have correlated the elevated plasma levels of PTX3 with cardio- and cerebrovascular diseases and recently with high blood pressure. To date, there are no studies showing whether PTX3 is able to exert a direct action on the vascular component. Methods and Results - Through in vitro experiments of vascular reactivity and ultrastructural analysis, we have shown that PTX3 induces, per se, dysfunction and morphological changes in the endothelial layer through the the complex P-selectin / metalloproteinase-1 (MMP1). In vivo studies have shown that the administration of PTX3 in wild-type mice induces endothelial dysfunction and increased blood pressure, an effect which is absent in the P-selectin knockout mice. Finally, by ELISA technique, we demonstrated that hypertensive patients (n = 31) have higher plasma levels of PTX3, P-selectin and MMP1 compared to normotensive patients (n = 22). Conclusion - Our data show, for the first time, the direct role of PTX3 on vascular function and blood pressure homeostasis, identifying the molecular mechanisms involved. The results obtained in humans, suggest that PTX3, P-selectin and MMP-1 may be new biomarkers to predict the onset of vascular dysfunction in hypertensive patients. [edited by author]
XIV n.s.
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SCARCHILLI, LAURA. "Caratterizzazione e interazione di pentraxina 3 e inter -alpha-trypsin-inhibitor nella matrice del cumulo ooforo." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2006. http://hdl.handle.net/2108/208526.

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E' stato precedentemente dimostrato che la sintesi di PTX3 è stimolata nelle cellule del cumulo durante il periodo preovulatorio ed è essenziale per l'organizzazione dell'acido ialuronico e l'espansione del complesso ovocito-cellule del cumulo (COC). Il presente studio mostra che, sebbene tumor necrosis factor α and interleukin-1β siano capaci di indurre PTX3 in molti tipi cellulari e sebbene queste citochine siano prodotte nel follicolo, la prima non ha nessun effetto sulla sintesi di PTX3 e sull'espansione di COC coltivati in vitro e la seconda è soltanto parzialmente efficace, suggerendo un ruolo marginale di queste citochine in vivo. Inoltre questa ricerca mostra che il dominio N terminale di PTX3 ricombinante, così come la molecola intera, è capace di organizzare l'HA nella matrice e ripristinare la normale espansione in cumuli PTX3 -/-, mentre il dominio C terminale è completamente inefficace nello svolgere tale funzione. Abbiamo anche dimostrato che un anticorpo monoclonale che riconosce il dominio N terminale di PTX3 neutralizza l'azione dell'intera molecola ricombinante in cumuli PTX3 -/-. Questi risultati evidenziano che la funzione strutturale di PTX3 nella matrice del cumulo dipende esclusivamente dalla regione N terminale, che non è correlata a nessun altra proteina conosciuta. Noi avevamo precedentemente riportato che PTX3 è in grado di legare TSG6, una proteina sintetizzata dalle cellule del cumulo, capace di legare l'HA. Attraverso esperimenti di coimmunoprecipitazione abbiamo dimostrato che PTX3 lega anche le catene pesanti dell'IαI, che sono covalentemente legate all'HA. I risultati suggeriscono che queste molecole cooperino nello stabilizzare la matrice formando dei ponti trasversali tra le catene di HA.
It has been shown that PTX3 synthesis is stimulated in cumulus cell during the preovulatory period and is essential for hyaluronan (HA) organization and expansion by cumulus cell-oocyte complexes (COC). In the present study we show that, although tumor necrosis factor- and interleukin-1 are able to induce PTX3 in several cell types and these cytochines are produced in the follicle, the former is ineffective and the latter is a poor inducer of PTX3 synthesis and expansion in COC cultured in vitro, suggesting a marginal role of these cytochines in vivo. We also show that recombinant N terminal PTX3 domain, as the full length molecule, is able to organize HA in the matrix and restore normal expansion in PTX3 -/- COC culture, while recombinant C terminal PTX3 domain is not. In addition, an anti-PTX3 monoclonal antibody binding to N terminal region neutralizes the action of full length recombinant PTX3 in PTX3 -/- COC culture. These results demonstrate that the matrix structural function of PTX3 is exclusively dependent on the N terminal region, that is unrelated to other known proteins. We have previously reported that PTX3 is able to bind TSG-6, an HA binding protein synthesized by cumulus cells. By coimmunoprecipation studies and binding assay we now show that PTX3 also binds to I heavy chains, which are covalently linked to HA. These findings suggest a cooperative effect of these molecules on matrix stability by the formation of cross linking among HA strains.
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Nunes, João Paulo Silva. "Avaliação do efeito biológico da pentraxina 3 em linhagens de células tumorais humanas." Universidade Federal de Minas Gerais, 2014. http://hdl.handle.net/1843/BUOS-9KWJP6.

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The pentraxin 3 is an acute phase glycoprotein expressed in a wide variety of cells and plays a myriad of roles in biological processes including female fertility, innate immunity and angiogenesis. PTX3 interacts selectively and specifically to fibroblast growth factors (FGFs) preventing the engagement of these factors with their specific tyrosine kinase receptors (FGFRs). The FGF/FGFR system plays important roles in many processes such as migration, differentiation, survival and cell proliferation, and in angiogenesis. Angiogenesis contributes to the development and progression of a variety of physiological and pathological conditions. In cancer, the formation of new vascular channels favors the proliferation of tumor cells, local invasion and metastasis. The possibility of modulating angiogenesis by altering the balance between pro- and anti-angiogenic factors therefore has great therapeutic potential. In this sense, studies aiming the identification and functional characterization of molecules such as PTX3, which is a natural antagonist of FGF/FGFR system, are very important. The objectives of this study were to characterize the expression of PTX3 in human cells derived from sarcoma (HT 1080, SAOS 2), colon (HCT 116, CACO 2 and SW 480) and melanoma (SK-MEL 37 and SK-MEL 188) and to evaluate its effect on cell proliferation and expression of genes related to inflammatory response and angiogenesis. Gene expression profile was investigated by RT-PCR and cell proliferation assessed by MTT assay and by counting cells stained with Trypan Blue dye. Morphology was observed by contrast phase optical microscopy and immunofluorescence using rhodamine-phalloidin conjugated to TRITC to assess F-actin filaments. We found that tumor cell lines HT 1080, HCT 116, SK-MEL 37 and SK-MEL 188 express FGF 2 and all the FGF receptors investigated (FGFR 1-4). None of the cells expressed FGF8. PTX3 basal expression was observed in HT 1080, HCT 116, SK-MEL 188 e CACO 2 lines. Preliminary results indicate that PTX3 impair the proliferation of human fibrosarcoma HT 1080 cells. By immunofluorescence, we found that PTX3 seems to interfere with the structure of actin filaments, and reduces the number of filopodia in HT 1080 cells and human colorectal adenocarcinoma HCT 116 cells. These results indicate the need for further investigation of the role of PTX3 in FGF -dependent human tumor cells migration and proliferation as well as for the evaluation of the therapeutic potential of PTX3 as an anti - angiogenic tool.
A pentraxina 3 é uma glicoproteína de fase aguda expressa em uma grande variedade de células e que desempenha uma miríade de funções em processos biológicos associados a fertilidade feminina, imunidade inata e angiogênese. PTX3 interage seletivamente e especificamente aos fatores de crescimento de fibroblastos (FGFs) impedindo a interação desses fatores com seus receptores específicos do tipo tirosina quinase (FGFR) presentes na membrana das células. O sistema FGF/FGFR desempenha papéis importantes em inúmeros processos tais como migração, diferenciação, sobrevivência e proliferação celulares, sendo um relevante agente pro-angiogênico que contribui para o desenvolvimento e progressão de uma variedade de condições fisiológicas e patológicas. No que se refere ao câncer, a angiogênese favorece a proliferação das células tumorais, invasão local e metástase hematogênica. A possibilidade de modular a angiogênese alterando o equilíbrio entre o balanço pró e anti-antiangiogênico tem, portanto, grande potencial terapêutico. Neste sentido, são relevantes as pesquisas buscando a identificação e caracterização funcional de moléculas, como PTX3, que é um antagonista natural do sistema FGF/FGFR. O objetivo deste estudo foi caracterizar a expressão de PTX3 em linhagens humanas derivadas de sarcoma (HT 1080, SAOS 2), cólon (HCT 116, CACO 2 e SW 480) e melanoma (SK-MEL 37 e SK-MEL 188) bem como avaliar o seu efeito sobre a proliferação celular e perfil de expressão de genes relacionados à resposta inflamatória e angiogênese nestas células. A expressão gênica foi avaliada por RT-PCR e a proliferação celular analisada pelo método MTT e por contagem de células coradas pelo Azul de Tripan. Os aspectos relacionados à morfologia foram investigados por microscopia de contraste de fase e por imunofluorescência utilizando faloidina-rodamina conjugada com TRITC para identificação da estrutura de actina-F nas células. As linhagens tumorais HT 1080, HCT 116, SK-MEL 37 e SK-MEL 188 apresentaram expressão basal tanto de FGF 2 quanto de todos os receptores para FGF (FGFR 1-4) investigados. Nenhuma das linhagens apresentou expressão basal de FGF8. Níveis basais de PTX3 foram detectados nas células HT 1080, HCT 116, SW 480 e SK-MEL 188. Resultados preliminares indicaram que PTX3 parece interferir negativamente na proliferação da linhagem de fibrosarcoma humano HT 1080. Os resultados obtidos através da análise, por imunofluorescência, sugerem que PTX3 promove alterações no citoesqueleto das células HT 1080 e HCT 116. Nas primeiras, uma aparente diminuição da abundância de filopódios foi detectada, e nas últimas, parece haver uma diminuição no número de filamentos transcelulares. Esses resultados preliminares suscitam a necessidade de aprofundamento dos estudos buscando a elucidação do papel de PTX3 nos mecanismos relacionados à migração e à proliferação celular dependentes de FGF em células tumorais humanas bem como a avaliação do potencial terapêutico de PTX3 como agente anti-angiogênico.
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6

Vietta, Giovanna Grünewald. "Caracterização dos níveis da pentraxina-3 (PTX-3) em amostra de pacientes com cardiopatia isquêmica estável na população brasileira." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/17435.

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Introdução: A Pentraxina-3 (PTX-3), produzida principalmente por macrófagos e células da vasculatura endotelial em resposta aos primeiros sinais pró-inflamatórios, tem sido apontada como um novo marcador de eventos coronarianos. Este estudo objetiva caracterizar os níveis plasmáticos de PTX-3 em pacientes com doença arterial coronariana estável em uma população brasileira, bem como sua relação com outros marcadores de risco cardiovascular e manifestação clínica de doença arterial coronariana (DAC). Métodos: Caracterização dos fatores de risco cardiovascular clássicos, e determinação dos níveis plasmáticos de PTX-3, proteína C reativa ultra-sensível (PCRus), interleucinas 18 (IL-18) e 10 (IL-10) foram realizadas numa coorte de 132 pacientes com doença arterial coronariana documentada, estáveis clinicamente. A determinação dos níveis plasmáticos de PTX-3, PCRus, IL-18 e IL-10 foi realizada pela técnica de ELISA utilizando-se kits comercialmente disponíveis. Os resultados dos valores dos marcadores inflamatórios foram comparados entre participantes que tiveram eventos clínicos ou não durante o seguimento médio de 47 meses. Resultados: Os níveis de PTX-3 e PCR-us coletados na primeira e segunda amostra foram semelhantes 3,45 e 3,84 ng/mL, e 4,89 e 4,72 mg/dL, respectivamente. A correlação de Pearson entre a primeira e segunda amostra foi maior para a dosagem de PCR-us que para o PTX3 (r=0,603 e r=0,356; p<0,001). Os níveis médios de PTX-3 em pacientes sem eventos foram 3,49±1,94ng/mL e nos pacientes que desenvolveram eventos 3,48±2,33ng/mL (p= 0,982). Para PCR, os valores foram de 5,07±8,26mg/mL e 4,60±4,66mg/dL (p= 0,737), respectivamente. Não foi encontrada associação entre níveis de PTX-3 e fatores de risco cardiovascular. Valores de PCRus foram associados com níveis séricos de LDL e a fração de ejeção do ventrículo esquerdo, não havendo relação com outros fatores de risco. Conclusões: Nesta amostra de indivíduos com DAC estável os níveis de PTX- 3 e PCR foram mais elevados do que em outras populações. Não identificamos fatores de risco relacionados com níveis aumentados de PTX-3 ou sua relação com eventos em médio prazo.
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Gifoni, Markus Andret Cavalcante. "Envolvimento da pentraxina 3 (PTX3) na patogênese da cistite hemorrágica induzida por ifosfamida em camundongos." reponame:Repositório Institucional da UFC, 2008. http://www.repositorio.ufc.br/handle/riufc/2592.

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GIFONI, Markus Andret Cavalcante. Envolvimento da pentraxina 3 (PTX3) na patogênese da cistite hemorrágica induzida por ifosfamida em camundongos. 130 f. 2008. Dissertação (Mestrado em Farmacologia) - Universidade Federal do Ceará. Faculdade de Medicina, Fortaleza, 2008.
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The Hemorrhagic Cystitis (HC) is an inflammatory reaction usually associated with Cancer Chemotherapy with Oxazaphosphorines. It is an innate inflammatory response to vesical irritation by Acrolein, an hepatic metabolite of the treatment with Iphosphamide and Cyclophosphamide. The role of toll-like receptor (TLR) engagement and TNF-α and IL-1β expression and the involvement of iNOS and COX-2 in the pathogenesis has been well demonstrated in a murine model of HC. Recent data configure pentraxin 3 (PTX3) as an inflammatory mediator in several experimental models of innate immune response in vivo, with a straight relation with TLR engagement. Because of that, this study looks at the involvement of PTX3 in the pathogenesis of iphosphamide–induced HC in mice. For this purpose, the mRNA to PTX3 and IL-1β t was quantified by RT-PCR in groups of C57BL6 mice treated with Iphosphamide or Saline. After that, groups of transgenic and Knock-Out mice to PTX3 and its respectives wild-type controls were treated with Iphosphamide or saline with intention to measure the Bladder Wet Weight (BWW), histomorphometric scores and Immunohistochemistry and RT-PCR to PTX3, IL-1β, TNF-α e iNOS analysis. The transgenic mice and its controls were killed in 3h and 12h after the treatment, while the PTX3 KO and its controls were killed after 12 hours. Finally, the experimental HC was modulated by pretreatment with Talidomide, Pentoxiphiline, MESNA, Amifostine and Aminoguanidine and the bladders submitted to immunohistochemistry assay (PTX3, TNF-α, IL-1β and iNOS). By RT-PCR quantification, mRNA for PTX3 was expressed 70 times more in mice treated with iphosphamide than in controls, while IL-1β RNAm had an expression rate of 10 times. PTX3 transgenic mice had initial reduction of the inflammatory response with less expression of PTX3 and TNF-α and greater expression of iNOS. In the other hand, after 12 hours, the PTX3 transgenic mice had more inflammatory signs with superior expression of all the mediators. There was no difference between the PTX3 KO mice and its controls in the HC intensity although differences between groups were seen in cytokines expression. Talidomide and MESNA produced substantial reduction on the PTX3 expression, the same was seen to TNF-α, while the amifostine marked inhibition of HC had low effect on PTX3 expression. These data as a whole, point to an unequivocal involvement of PTX3 in the pathogenesis of innate inflammatory response of HC in mice with close relation with TNF-α engagement.
A cistite hemorrágica (CH) é um fenômeno inflamatório frequentemente associado à quimioterapia com oxazafosforinas. Trata-se de uma resposta inflamatória inata à ação da Acroleína (ACR), metabólito hepático comum à Ifosfamida (IFO) e à ciclofosfamida (CTX). O papel da resposta ao recrutamento de receptores toll-like (TLR) e do estímulo por TNF-α e IL-1β com envolvimentto de iNOS e COX-2 tem sido demonstrado neste fenômeno. Estudos recentes demonstram que a Pentraxina 3 (PTX3) assume papel de mediador inflamatório em modelos de resposta inflamatória inata in vivo, sobretudo relacionada ao recrutamento de TLR. Desta forma, o presente estudo pretende investigar o possível envolvimento de PTX3 na patogênese da CH induzida por ifosfamida em camundongos. Para isso, foi realizada quantificação de RNAm por RT-PCR para PTX3 e IL-1β em camundongos C57/ BL6 tratados com ifosfamida e salina. Em seguida, o modelo experimental da CH induzida por ifosfamida foi reproduzido em grupos de camundongos com hiperexpressão e nocauteados para PTX3 em comparação com os respectivos controles do tipo selvagem e com grupos controle tratados com salina para posterior obtenção dos pesos vesicais úmidos (PVU), realização de análise histomorfométrica, imunohistoquímica e quantificação de RNAm por RT-PCR para PTX3, IL-1β, TNF-α e iNOS. Os animais transgênicos e seus controles foram sacrificados com tempos de 3h e 12h após o tratamento, enquanto os nocauteados e seus controles foram sacrificados com 12 horas do tratamento. Finalmente, a CH em animais C57/ BL6 foi modulada com o pré-tratamento com Talidomida, Pentoxifilina, MESNA, Amifostina e Aminoguanidina para a posterior marcação imunohistoquímica com PTX3, IL-1β, TNF-α e iNOS. Observou-se que o RNAm de PTX3 está cerca de 70 vezes mais expresso em animais com CH, contra uma razão de expressão de 10 para IL-1β. Animais trangênicos para PTX3 têm redução inicial da resposta inflamatória com expressão inferior de PTX3 e TNF-α e expressão aumentada de iNOS e intensificação da inflamação ao tempo de 12 horas, com expressão superior dos mediadores. Não houve diferenças significativas de intensidade da CH em animais KO em relação aos controles. A modulação da CH por talidomida e MESNA produziu redução importante sobre a expressão de PTX3, enquanto a inibição da CH por amifostina não teve redução expressiva da pentraxina. Em conjunto, estes dados apontam para um envolvimento inequívoco de PTX3 na fisiopatologia da inflamação inata em modelo de CH murino com íntima relação coma expressão de TNF-α.
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Cozzi, V. "Pentraxina 3 come potenziale marcatore di danno endoteliale in gravidanze complicate da preeclampsia e ritardato accrescimento intrauterino." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/174026.

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Objectives: Endothelial dysfunction typical of preeeclampsia (PE) is the result of an excessive maternal inflammatory response to pregnancy. PE can occur alone or together with intrauterine growth restriction (IUGR). We investigated PTX3 in maternal, fetal and placental compartments in complicated pregnancies. Study design: Maternal blood samples were collected during the III trimester in 53 PE, 43 IUGR and 50 normal pregnancies. Fetal samples were collected from the umbilical vein in 26 PE, 23 IUGR and 26 normal pregnancies at elective cesarean section. PTX3 plasma levels were determined by ELISA. Pattern and site of expression of PTX3 was studied by immunohistochemistry (IHC) on placenta, decidual bed and maternal peritoneum. Results: PE and IUGR pregnancies showed significantly higher median maternal PTX3 levels vs normal pregnancies (24.8 and 9.9 vs 3.8 ng/ml; p<0.001). IUGR showed significantly lower levels than PE (p<0.001). Severe PE revealed higher levels (33.1 vs 17.1 ng/ml, p<0.001) than mild PE. Severe PE with HELLP presented significantly higher levels. IHC on placenta and decidual bed biopsies showed similar expression in pathologic compared to normal cases. Maternal peritoneum expressed a significantly higher signal in the endothelium of pathological vs normal pregnancies. PTX3 was detected in the fetal circulation with values significantly higher in IUGR thsn in normal fetuses with a trend towards higher values in correlation with IUGR severity. Conclusions: We report elevated maternal levels of PTX3 in PE and IUGR pregnancies. PTX3 levels correlated to clinical severity of disease with higher PTX3 levels in severe than in mild PE, IUGR without clinical PE were significantly different from both normal and PE pregnancies. PTX3 increase may represent the expression of endothelial systemic damage on the maternal side. Moreover, PTX3 is detected in fetal blood and is significantly incresased in IUGR fetuses likely reflecting endothelial damage.
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Junqueira, Ana FlÃvia Torquato de AraÃjo. "Estudo do efeito do inibidor da enzima adenosina desaminase, EHNA, sobre a enterite induzida pela toxina a do Clostridium difficile em alÃa ileal isolada de camundongos." Universidade Federal do CearÃ, 2008. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=1305.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico
O Clostridium difficile tem como principal fator de virulÃncia a toxina A (TxA), a qual provoca inflamaÃÃo e destruiÃÃo tecidual aguda em intestinos de animais experimentais e de pacientes com a doenÃa induzida por esta bactÃria. Em locais de injÃria tecidual, adenosina à produzida em altas concentraÃÃes, onde exerce uma sÃrie de efeitos antiinflamatÃrios, limitados por sua rÃpida degradaÃÃo pela enzima adenosina desaminase. O objetivo deste trabalho foi investigar o efeito da inibiÃÃo da enzima adenosina desaminase pelo EHNA (eritro-9-(2-hidrÃxi-3-nonil)-adenina) sobre a enterite induzida pela TxA do C. difficile em alÃa ileal de camundongos. Para isto, injetamos EHNA (90 μmol/kg) ou PBS i.p. 30 minutos antes da administraÃÃo de TxA (10 a 100 μg) ou PBS na alÃa ileal isolada. Os animais foram sacrificados 3 horas depois da induÃÃo da enterite e as alÃas foram retiradas para estudo. As razÃes peso/comprimento da alÃa e volume de secreÃÃo/comprimento da alÃa foram calculadas e amostras de tecido foram coletadas para histopatologia, dosagem de atividade de mieloperoxidase (MPO), dosagem de TNF-α, IL-1β e IL-10 por ELISA, imunohistoquÃmica para TNF-α, IL-1β, NOS induzÃvel e PTX3, e PCR para TNF-α, IL-1β e PTX3. A injeÃÃo de TxA (10 a 100 μg) nas alÃas ileais aumentou significativamente (p<0,05) as razÃes peso/comprimento da alÃa e volume de secreÃÃo/comprimento da alÃa com resultados consistentes a partir de 50 μg. A TxA promoveu significativa (p<0,05) destruiÃÃo tecidual, edema, infiltraÃÃo de cÃlulas inflamatÃrias, aumento das citocinas TNF-α e IL-1β, e elevaÃÃo de iNOS e PTX3. Todos esses parÃmetros foram significativamente revertidos com o uso do EHNA (p<0,05). Em adiÃÃo, a TxA nÃo alterou os nÃveis de IL-10 em relaÃÃo ao controle, mas o prÃ-tratamento com EHNA promoveu uma elevaÃÃo nos nÃveis desta citocina. Assim, concluÃmos que na enterite induzida pela TxA em camundongos o EHNA demonstrou um potente efeito antiinflamatÃrio, reduzindo consideravelmente a lesÃo tecidual, a migraÃÃo neutrofÃlica, a expressÃo e os nÃveis de citocinas prÃinflamatÃrias (TNF-α, IL-1β) e produzindo um aumento nos nÃveis de IL-10. AlÃm disso, a administraÃÃo de TxA induziu um aumento na expressÃo da proteÃna PTX3 e no nÃmero de cÃlulas imunomarcadas para iNOS no tecido ileal, ambos revertidos pelo EHNA
The main factor of virulence in Clostridium difficile is toxin A (TxA), which can induce inflammation and acute tissue injury in the bowels of animals and humans affected by this organism. The high concentration of adenosine generated upon injury produces a number of antiinflammatory effects limited by rapid degradation by adenosine deaminase. The objective of this study was to determine the effect of EHNA (erythro-9-(2-hydroxy-3-nonyl)-adenine) inhibition of adenosine deaminase upon TxA-induced ileal loop enteritis in mice. EHNA (90 μmol/kg) or PBS was injected i.p. 30 minutes prior to TxA (10-100 μg) or PBS instillation into the ligated ileal loop. The animals were euthanized 3 hours after enteritis induction and the ileal loops were retrieved for analysis. The weight/length ratio and the secretion volume/length ratio were calculated and tissue samples were submitted to histopathological study, myeloperoxidase assay (MPO), measurement of TNF-α, IL-1β and IL-10 levels with ELISA, immunohistochemical tests for TNF-α, IL-1β, inducible NOS and PTX3, and PCR assay for TNF-α, IL-1β and PTX3. The instillation of TxA (10-100 μg) into the ileal loop significantly increased (p<0.05) the weight/length ratio and the secretion volume/length ratio with consistent results above 50 μg. TxA induced a significant amount (p<0.05) of histological damage, edema and inflammatory cell infiltration and increased the production of TNF-α, IL-1β, iNOS and PTX3. All changes were significantly reverted by treatment with EHNA (p<0.05). Moreover, IL-10 levels remained unchanged in animals treated with TxA, but increased in animals receiving EHNA. In conclusion, in mice with TxA-induced enteritis EHNA produced considerable antiinflammatory effects, reducing tissue injury, neutrophil migration, the expression and levels of proinflammatory cytokines (TNF-α and IL-1β) and producing an increase in IL-10 levels. In addition, TxA instillation increased PTX3 expression and the number of cells immunolabeled for iNOS in the ileal tissue, both of which were reverted by EHNA
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Gullo, Jackson da Silva. "Associação entre os níveis séricos de pentraxina 3 e a mortalidade de pacientes vítimas de traumatismo crânio-encefálico grave." reponame:Repositório Institucional da UFSC, 2013. http://repositorio.ufsc.br/handle/123456789/103292.

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Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências da Saúde, Programa de Pós-Graduação em Ciências Médicas, Florianópolis, 2010
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Introdução: O trauma cranioencefálico (TCE), é a umas das maiores causas de morbidade e mortalidade no mundo. Pentraxina 3 (PTX3) é um componente do sistema humoral de resposta imune inata que tem sido estudada como marcador para inflamação, infecções ou patologias cardiovasculares. Objetivos: Investigar a associação entre os níveis séricos de PTX3 e a mortalidade de pacientes com TCE grave. Métodos: A associação independente entre os níveis séricos de PTX3 após o TCE grave (Escala de Coma de Glasgow, ECG ? 8) e a mortalidade no momento da alta foi analisada em um estudo prospectivo de 83 pacientes consecutivos, por uma análise de regressão logística múltipla. Resultados: A média de idade dos pacientes foi de 35 anos e 85 porcento são homens. Os níveis séricos de PTX3 são determinados em 18.0 (DP ± 17.0) horas após o trauma. Pacientes que morreram apresentaram uma média no nível sérico de PTX3 de 9,95 ?gm / ml (DP ± 6,42) em comparação com 5,46 ?gm / ml (DP ± 4,87) no Grupo de sobreviventes (p = 0,007). Após a análise por regressão logística múltipla, níveis séricos de PTX3 maior que 10 ?gm/ml foi 3 vezes mais associado com à morte do que os níveis mais baixos (OR ajustado 3.38, IC 95% 1.10 - 10.45, p = 0.03). A idade avançada, anormalidades pupilares e menor pontuação na ECG também foram associadas independentemente à mortalidade. Conclusão: Níveis séricos de PTX3 após o TCE grave estão associados à maior mortalidade no momento da alta. Nossa descoberta sugere que PTX3 pode ser um marcador útil de TCE grave e seu prognóstico.
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Book chapters on the topic "Pentraxina 3"

1

Gressner, A. M., and O. A. Gressner. "Pentraxine." In Springer Reference Medizin, 1849. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2379.

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Jaillon, Sébastien, Antonio Inforzato, Barbara Bottazzi, and Cecilia Garlanda. "Pentraxins." In Compendium of Inflammatory Diseases, 1069–79. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_225.

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Gressner, A. M., and O. A. Gressner. "Pentraxine." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_2379-1.

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Jaillon, Sébastien, Antonio Inforzato, Barbara Bottazzi, and Cecilia Garlanda. "Pentraxins." In Encyclopedia of Inflammatory Diseases, 1–12. Basel: Springer Basel, 2015. http://dx.doi.org/10.1007/978-3-0348-0620-6_225-1.

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Yaman, Halil, Emin Ozgur Akgul, Yasemin Gulcan Kurt, and Erdinc Cakir. "Pentraxin 3 as Biomarker." In Biomarkers in Disease: Methods, Discoveries and Applications, 267–90. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7696-8_3.

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Yaman, Halil, Emin Ozgur Akgul, Yasemin Gulcan Kurt, and Erdinc Cakir. "Pentraxin 3 as Biomarker." In General Methods in Biomarker Research and their Applications, 1–20. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7740-8_3-1.

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Barbati, Elisa, Barbara Bottazzi, Alberico L. Catapano, Cecilia Garlanda, Roberto Latini, Alberto Mantovani, Giuseppe Danilo Norata, and Sonia Valentino. "Pentraxins and Atherosclerosis." In Inflammation and Atherosclerosis, 219–37. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0338-8_11.

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Mauri, T., B. Bottazzi, and A. Pesenti. "Pentraxin 3 (PTX3): Possible Role in Critical Care Medicine." In Annual Update in Intensive Care and Emergency Medicine 2011, 543–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-18081-1_49.

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Choi, Bongkun, and Eun-Ju Chang. "Pentraxin 3 (PTX3) as a Biomarker of Liver Disease." In Biomarkers in Disease: Methods, Discoveries and Applications, 603–21. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7675-3_32.

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Choi, Bongkun, and Eun-Ju Chang. "Pentraxin 3 (PTX3) as a Biomarker of Bone Disease." In Biomarkers in Bone Disease, 253–65. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7693-7_40.

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Conference papers on the topic "Pentraxina 3"

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Matarazzo, Sara, Laura Melocchi, Sara Rezzola, Elisabetta Grillo, Federica Maccarinelli, Arianna Giacomini, Sara Taranto, et al. "Abstract C121: Long Pentraxin-3 modulates bladder cancer progression." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-c121.

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Pizzichini, MM, T. Kleveston, EF Morato, JT Pinheiro, LJ Steidle, CC Rocha, CR Zimmerman, and E. Pizzichini. "Pentraxin 3 (PTX3): A New Marker To Study Airway Inflammation?." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2532.

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Bayler, R., S. Sarinc Ulasli, A. Batur, F. Tekin, G. Durhan, Z. G. Dikmen, S. Karahan, et al. "Diagnostic and prognostic value of pentraxin-3 in pulmonary thromboembolism." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3380.

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Stober, V., A. Mehta, A. Doni, C. Garlanda, and S. Garantziotis. "Pentraxin-3 Is Necessary for Hyaluronan-Induced Airway Inflammation and Hyperresponsiveness." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2954.

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Toledo, A., G. L. M. D. Assunção, E. P. Oliveira, H. Giardini, R. Pereira, and C. S. V. Barbas. "Anti Pentraxin 3 Autoantibodies in Brazilian Patients with Granulomatosis with Polyangiitis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6838.

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Van Pottelberge, Geert R. M., Ken R. Bracke, Nele S. Pauwels, Yannick M. van Durme, Geert M. Verleden, Frank E. Vermassen, Guy F. Joos, and Guy G. Brusselle. "Reduced Expression Of Pentraxin-3 In The Lungs Of Patients With COPD." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3887.

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Watt, Jennifer, Imran Siddique, Thomas Dowe, Tatjana Crnogorac-Jurcevic, Satyajit Bhattacharya, Paola Allavena, and Hemant M. Kocher. "Abstract A56: The role of Pentraxin 3 (PTX3) in pancreatic ductal adenocarcinoma." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-a56.

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Goulart, Michelle R., Jennifer Watt, Imran Siddique, Rita Lawor, Thomas Dowe, Satyajit Bhattacharya, Tatjana Crnogorac-Jurcevic, Paola Allavena, Aldo Scarpa, and Hemant M. Kocher. "Abstract 4892: Pentraxin 3: A stromal derived diagnostic biomarker for pancreatic ductal adenocarcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4892.

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Goulart, Michelle R., Jennifer Watt, Imran Siddique, Rita Lawor, Thomas Dowe, Satyajit Bhattacharya, Tatjana Crnogorac-Jurcevic, Paola Allavena, Aldo Scarpa, and Hemant M. Kocher. "Abstract 4892: Pentraxin 3: A stromal derived diagnostic biomarker for pancreatic ductal adenocarcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4892.

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Bekos, C., S. Dekan, S. Aust, E. Reiser, A. Reinthaller, and S. Polterauer. "Die Rolle von Pentraxin 3 als Biomarker für Tumorbiologie und Therapieansprechen im Ovarialkarzinom." In Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe – OEGGG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1648274.

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Reports on the topic "Pentraxina 3"

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Zhou, Zhongwei, Huixiang Ju, Hongmei Chen, Mingzhong Sun, Hao Jin, and Li Li. Pentraxin-3 is a Better Predictor of Adverse Clinical Events than C-reactive Protein in Chronic Kidney Disease: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0135.

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