Examinando por Autor "Riedel, Claudia"

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    Correction for Echeverría et al., "Endotoxin-Induced Endothelial Fibrosis Is Dependent on Expression of Transforming Growth Factors β1 and β2" [Infect Immun., Volume 82, no. 9, p. 3678-3686, 2014]
    (American Society for Microbiology, 2015) Echeverría, César; Montorfano, Ignacio; Tapia, Pablo; Riedel, Claudia; Cabello-Verrugio, Claudio; Simon, Felipe a
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    Differential expression profile of CXCR3 splicing variants is associated with thyroid neoplasia. Potential role in papillary thyroid carcinoma oncogenesis?
    (Impact Journals LLC, 2018) Gamboa, Soledad Urra; Fischer, Martin C.; Martínez, José R.; Véliz, Loreto; Orellana, Paulina; Solar, Antonieta; Bohmwald, Karen; Kalergis, Alexis; Riedel, Claudia; Corvalán, Alejandro H.; Roa, Juan C.; Fuentealba, Rodrigo; Cáceres, C. Joaquín; López-Lastra, Marcelo; León, Augusto; Droppelmann, Nicolás; González, Hernán E.
    Papillary thyroid cancer (PTC) is the most prevalent endocrine neoplasia. The increased incidence of PTC in patients with thyroiditis and the frequent immune infiltrate found in PTC suggest that inflammation might be a risk factor for PTC development. The CXCR3-ligand system is involved in thyroid inflammation and CXCR3 has been found upregulated in many tumors, suggesting its pro-tumorigenic role under the inflammatory microenvironment. CXCR3 ligands (CXCL4, CXCL9, CXCL10 and CXCL11) trigger antagonistic responses partly due to the presence of two splice variants, CXCR3A and CXCR3B. Whereas CXCR3A promotes cell proliferation, CXCR3B induces apoptosis. However, the relation between CXCR3 variant expression with chronic inflammation and PTC development remains unknown. Here, we characterized the expression pattern of CXCR3 variants and their ligands in benign tumors and PTC. We found that CXCR3A and CXCL10 mRNA levels were increased in non-metastatic PTC when compared to non-neoplastic tissue. This increment was also observed in a PTC epithelial cell line (TPC-1). Although elevated protein levels of both isoforms were detected in benign and malignant tumors, the CXCR3A expression remained greater than CXCR3B and promoted proliferation in Nthy-ori-3-1 cells. In non-metastatic PTC, inflammation was conditioning for the CXCR3 ligands increased availability. Consistently, CXCL10 was strongly induced by interferon gamma in normal and tumor thyrocytes. Our results suggest that persistent inflammation upregulates CXCL10 expression favoring tumor development via enhanced CXCR3A-CXCL10 signaling. These findings may help to further understand the contribution of inflammation as a risk factor in PTC development and set the basis for potential therapeutic studies.
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    Endotoxin-induced endothelial fibrosis is dependent on expression of transforming growth factors β1 and β2
    (American Society for Microbiology, 2014) Echeverría, César; Montorfano, Ignacio; Tapia, Pablo; Riedel, Claudia; Cabello-Verrugio, Claudio; Simon, Felipe
    During endotoxemia-induced inflammatory disease, bacterial endotoxins circulate in the bloodstream and interact with endo thelial cells (ECs), inducing dysfunction of the ECs. We previously reported that endotoxins induce the conversion of ECs into activated fibroblasts. Through endotoxin-induced endothelial fibrosis, ECs change their morphology and their protein expres sion pattern, thereby suppressing endothelial markers and upregulating fibrotic proteins. The most commonly used fibrotic in ducers are transforming growth factor 1 (TGF- 1) and TGF- 2. However, whether TGF- 1 and TGF- 2 participate in endo toxin-induced endothelial fibrosis remains unknown. We have shown that the endotoxin-induced endothelial fibrosis process is dependent on the TGF- receptor, ALK5, and the activation of Smad3, a protein that is activated by ALK5 activation, thus sug gesting that endotoxin elicits TGF- production to mediate endotoxin-induced endothelial fibrosis. Therefore, we investigated the dependence of endotoxin-induced endothelial fibrosis on the expression of TGF- 1 and TGF- 2. Endotoxin-treated ECs induced the expression and secretion of TGF- 1 and TGF- 2. TGF- 1 and TGF- 2 downregulation inhibited the endotoxin induced changes in the endothelial marker VE-cadherin and in the fibrotic proteins -SMA and fibronectin. Thus, endotoxin in duces the production of TGF- 1 and TGF- 2 as a mechanism to promote endotoxin-induced endothelial fibrosis. To the best of our knowledge, this is the first report showing that endotoxin induces endothelial fibrosis via TGF- secretion, which represents an emerging source of vascular dysfunction. These findings contribute to understanding the molecular mechanism of endotox in-induced endothelial fibrosis, which could be useful in the treatment of inflammatory diseases
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    Evaluation of monoclonal antibodies that detect conserved proteins from Respiratory Syncytial Virus, Metapneumovirus and Adenovirus in human samples
    (Elsevier B.V., 2018-04) González, Liliana A.; Vázquez, Yaneisi; Mora, Jorge E.; Palavecino, Christian E.; Bertrand, Pablo; Ferrés, Marcela; Contreras, Ana M.; Beckhaus, Andrea A.; Riedel, Claudia; Bueno, Susan M.
    Human Respiratory Syncytial Virus (hRSV), human Metapneumovirus (hMPV) and Adenovirus (ADV), are three of the most prevalent viruses responsible for pneumonia and bronchiolitis in children and elderly worldwide, accounting for a high number of hospitalizations annually. Diagnosis of these viruses is required to take clinical actions that allow an appropriate patient management. Thereby, new strategies to design fast diagnostic methods are highly required. In the present work, six monoclonal antibodies (mAbs, two for each virus) specific for conserved proteins from hRSV, hMPV and ADV were generated and evaluated through different immunological techniques, based on detection of purified protein, viral particles and human samples. In vitro evaluation of these antibodies showed higher specificity and sensitivity than commercial antibodies tested in this study. These antibodies were used to design a sandwich ELISA tests that allowed the detection of hRSV, hMPV, and ADV in human nasopharyngeal swabs. We observed that hRSV and ADV were detected with sensitivity and specificity equivalent to a current Direct Fluorescence Assay (DFA) methodology. However, hMPV was detected with more sensitivity than DFA. Our data suggest that these new mAbs can efficiently identify infected samples and discriminate from patients infected with other respiratory pathogens. © 2018 The Authors