WALCY PAGANELLI ROSOLIA TEODORO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina
LIM/17 - Laboratório de Investigação em Reumatologia, Hospital das Clínicas, Faculdade de Medicina
LIM/02 - Laboratório de Anatomia Médico-Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/17 - Laboratório de Investigação em Reumatologia, Hospital das Clínicas, Faculdade de Medicina
LIM/02 - Laboratório de Anatomia Médico-Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
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conferenceObject Pathophysiological features of lung and skin in human SSc and collagen V/C57LB6 mouse model(2018) TEODORO, W. Paganelli Rosolia; VELOSA, A. P. Pereira; QUEIROZ, Z. A. de Jesus; SANTOS, L. Araujo dos; CATANOZI, S.; SANTOS FILHO, A. dos; BUENO, C.; VENDRAMINI, M. Borges Galhardo; FERNEZLIAN, S. de Moraes; EHER, E. Miristene; LOPES, F. Degobbi T. Q. S.; CAPELOZZI, V. L.conferenceObject Collagen V Maintains Experimental Pulmonary Fibrosis In Il17-dependent And -Independent Pathways(2013) FABRO, A. T.; SILVA, P. Q.; ZOCOLARO, W. S.; ALMEIDA, M. S.; MINATEL, I. O.; PRANDO, E. C.; RAINHO, C. A.; VELOSA, A. P.; TEODORO, W. R.; PARRA-CUENTAS, E. R.; POPPER, H. H.; CAPELOZZI, V. L.- Modeling pulmonary fibrosis by abnormal expression of telomerase/apoptosis/collagen V in experimental usual interstitial pneumonia(2014) PARRA, E. R.; PINCELLI, M. S.; TEODORO, W. R.; VELOSA, A. P. P.; MARTINS, V.; RANGEL, M. P.; BARBAS-FILHO, J. V.; CAPELOZZI, V. L.Limitations on tissue proliferation capacity determined by telomerase/apoptosis balance have been implicated in pathogenesis of idiopathic pulmonary fibrosis. In addition, collagen V shows promise as an inductor of apoptosis. We evaluated the quantitative relationship between the telomerase/apoptosis index, collagen V synthesis, and epithelial/fibroblast replication in mice exposed to butylated hydroxytoluene (BHT) at high oxygen concentration. Two groups of mice were analyzed: 20 mice received BHT, and 10 control mice received corn oil. Telomerase expression, apoptosis, collagen I, III, and V fibers, and hydroxyproline were evaluated by immunohistochemistry, in situ detection of apoptosis, electron microscopy, immunofluorescence, and histomorphometry. Electron microscopy confirmed the presence of increased alveolar epithelial cells type 1 (AEC1) in apoptosis. Immunostaining showed increased nuclear expression of telomerase in AEC type 2 (AEC2) between normal and chronic scarring areas of usual interstitial pneumonia (UIP). Control lungs and normal areas from UIP lungs showed weak green birefringence of type I and III collagens in the alveolar wall and type V collagen in the basement membrane of alveolar capillaries. The increase in collagen V was greater than collagens I and III in scarring areas of UIP. A significant direct association was found between collagen V and AEC2 apoptosis. We concluded that telomerase, collagen V fiber density, and apoptosis evaluation in experimental UIP offers the potential to control reepithelization of alveolar septa and fibroblast proliferation. Strategies aimed at preventing high rates of collagen V synthesis, or local responses to high rates of cell apoptosis, may have a significant impact in pulmonary fibrosis.
conferenceObject PULMONARY FIBROSIS INDUCED BY BLEOMYCIN IS DRIVEN BY HIGH COLLAGEN V AND TGF-< BETA > SYNTHESIS(2014) MARTINS, V.; LOPES, D. B.; ANTUNES, M.; VELOSA, A. P. P.; TEODORO, W. R.; PARRA, E. R.; CAPELOZZI, V. L.conferenceObject Fibrogenesis failure of type V collagen observed in pulmonary and cutaneous fibroblast culture reinforce the pathogenic participation of this collagen in the pathway of systemic sclerosis(2012) TEODORO, W. R.; MORAIS, J.; MARTIN, P.; VELOSA, A. P. P.; CARRASCO, S.; SOUZA, R. B. C.; KATAYAMA, M. L.; GOLDEINSTEIN-SCHAINBERG, C.; PARRA, E. R.; CAPELOZZI, V. L.; YOSHINARI, N. H.Introduction: Unusual type V collagen (COLV) accumulation was demonstrated in systemic sclerosis (SSc) by our group. In this regard, this study analyzed tridimensional reconstruction (3D), biochemical and molecular profile of COLVα1 and COLVα2 chains in pulmonary and cutaneous fibroblasts culture from patients with SSc. Materials and Methods: Pulmonary and cutaneous fibroblasts for culture were obtained from 7 patients with SSc and from six controls respectively. COLV 3D reconstruction was performed by confocal microscopy. COLVα1 and COLVα2 gene expression was performed by RT-PCR and COLV protein expression by immunoblotting. Results: COL V 3D reconstruction showed distorted and strongly thickened fibers with irregular bundles resulting in a dense network in lung and skin fibroblast cultures from SSc patients compared to the thin fibers from fibroblast controls. Collagen quantification showed significant increased COLV fiber expression in SSc cutaneous and pulmonary fibroblasts (P<0.01) compared with the respective controls. In the same way, molecular evaluation demonstrated an increased significance (P=0.05) of COLVα1 and COLVα2 mRNA expression in cutaneous and pulmonary fibroblasts from SSc patients to that of control groups. The immunoblotting analysis demonstrated the increased weight of the molecular COLV chains. Conclusion: COLV overexpression and an unusual organization of these fibers including molecular and biochemical changes, suggest an interference process of the COLV fibrillogenesis in patients with SSc, reinforcing the participation of this collagen in SSc pathogenesis and open new therapeutic perspectives for these patients.conferenceObject COLLAGEN V/C57BL6 MOUSE MODEL: A NOVEL PRECLINICAL MODEL TO STUDY PATHOPHYSIOLOGY AND THERAPEUTIC APPROACHES IN SYSTEMIC SCLEROSIS(2018) TEODORO, W. R.; VELOSA, A. P. P.; QUEIROZ, Z. A. de J.; SANTOS, L. A. dos; CATANOZI, S.; SANTOS FILHO, A. dos; BUENO, C.; VENDRAMINI, M.; FERNEZLIAN, S. M.; EHER, E. M.; LOPES, F. D. T. Q. S.; SAMPAIO-BARROS, P. D.; CAPELOZZI, V. L.conferenceObject INFLUENCE OF ALPHA 2 DO COLLAGEN V OVEREXPRESSION IN PHYSIOPHATOLOGY OF FIBROSIS SYSTEMIC SCLEROSIS PATIENTS(2014) MORAIS, J.; MARTIN, P.; VELOSA, A. P. P.; ANDRADE, P. C.; CRUZ, I. B.; MIRACCA, E. C.; FAC, F. A. C. Barrence; CARRASCO, S.; GOLDEINSTEIN-SCHAINBERG, C.; NAGAI, M. A.; PARRA, E. R.; CAPELOZZI, V. L.; TEODORO, W. R.conferenceObject Interstitial lung disease in systemic sclerosis is associated with autoimmunity to alpha 1(V) chain of type V collagen(2019) VELOSA, A. P. Pereira; BRITO, L.; QUEIROZ, Z. A.; CARRASCO, S.; MIRANDA, J. Tomaz de; GOLDENSTAIN-SCHAINBERG, C.; PARRA, E. Roger; CAPELOZZI, V. L.; TEODORO, W. RosoliaconferenceObject Vulvar lichen sclerosus: A misnomer for an entity with decreased fibrillar components and increased amorphous components in extracellular matrix remodeling(2012) PARRA, E.; GODOY, C. A. Pires de; FEITOSA, V. L. Correia; TEODORO, W.; VELOSA, A. P.; CAPELOZZI, V. L.Objective: The hyalinization of subepidermal skin is one of the histopathological characteristics of the vulvar lichen sclerosus (VLS). It was found that patients with VLS present autoantibodies against the extracellular matrix protein 1 (ECM-1) and the deficiency of this protein is responsible for the development of a different disease, the Lipoid Proteinosis. This disease shows a similar histology with VLS and has better characterized morphology. Method: We analyzed 20 VLS patients biopsies and the control group was composed by 20 vulva samples from authopsy. The biopsies and control samples were analysed by immunofluorescence for collagen I, III and V and th total collagen fibers by Picrosirius staining. The elastic fibers were stained with Verhoeff and the proteoglycans and glycosaminoglycans with Periodic Acid-Schiff and Alcian Blue. Collagen quantification was performed through image analysis. Results: It was observed a significant reduction in all studied collagens as well as in the elastic fibers. On the other hand, the proteoglycans were increased in the VLS biopsies. Conclusion: This study did not found an increase in collagen sclerosis that would justify the term used for the LS. It was observed a predominance of the edema area probably caused by the increase of glycoproteins as in lipoid proteinosis.- Effects of acute hypercapnia with and without acidosis on lung inflammation and apoptosis in experimental acute lung injury(2015) NARDELLI, L. M.; RZEZINSKI, A.; SILVA, J. D.; MARON-GUTIERREZ, T.; ORNELLAS, D. S.; HENRIQUES, I.; CAPELOZZI, V. L.; TEODORO, W.; MORALES, M. M.; SILVA, P. L.; PELOSI, P.; GARCIA, C. S. N. B.; ROCCO, P. R. M.We investigated the effects of acute hypercapnic acidosis and buffered hypercapnia on lung inflammation and apoptosis in experimental acute lung injury (ALI). Twenty-four hours after paraquat injection, 28 Wistar rats were randomized into four groups (n = 7/group): (1) normocapnia (NC, PaCO2 = 35-45 mmHg), ventilated with 0.03%CO2 + 21%O-2 + balanced N-2; (2) hypercapnic acidosis (HC, PaCO2 = 60-70 mmHg), ventilated with 5%CO2 + 21%O-2 + balanced N-2; and (3) buffered hypercapnic acidosis (BHC), ventilated with 5%CO2 + 21%O-2 + balanced N-2 and treated with sodium bicarbonate (8.4%). The remaining seven animals were not mechanically ventilated (NV). The mRNA expression of interleukin (IL)-6 (p = 0.003), IL-1 beta (p<0.001), and type III procollagen (PCIII) (p = 0.001) in lung tissue was more reduced in the HC group in comparison with NC, with no significant differences between HC and BHC. Lung and kidney cell apoptosis was reduced in HC and BHC in comparison with NC and NV. In conclusion, in this experimental ALI model, hypercapnia, regardless of acidosis, reduced lung inflammation and lung and kidney cell apoptosis.