SOLANGE CARRASCO

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Departamento de Clínica Médica, Faculdade de Medicina
LIM/17 - Laboratório de Investigação em Reumatologia, Hospital das Clínicas, Faculdade de Medicina

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Autor e Coautores FMUSP-HC Normalizados: WALCY PAGANELLI ROSOLIA TEODORO ×

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Agora exibindo 1 - 10 de 21
  • conferenceObject
    Increased decorin and type V collagen in SSc pulmonary fibrosis
    (2012) TEODORO, W.; VELOSA, A. P.; MARCELINO, A.; MARTIN, P.; CARRASCO, S.; GOLDENSTEIN-SCHAINBERG, C.; PARRA, E.; YOSHINARI, N.; CAPELOZZI, V.
    Objective: To evaluate COL V and decorin expression in pulmonary tissue and to characterize biochemical profile of COLV from lung fibroblasts culture from SSc patients. Method: We evaluated COL V and decorin expression and tridimensional reconstruction (3D) of 6 patients with SSc without pulmonary hypertension that underwent surgical lung biopsy and as control was obtained lung fragments from 6 normal individuals who died from trauma. COL V amount in lung sections was evaluated with immunofluorescence. To biochemical characterization of COL V from lung fibroblasts culture was used quantitative immunoblot. Results: It was found that the structure of COLV fibers was distorted and strongly thickened in lung tissue from SSc patients compared with thin fibers pattern in the healthy controls. Decorin was distributed around COL V fibrils in the bronchovascular interstitium and vascular walls. Histomorphometric analysis of SSc lung demonstrated increased expression of both COL V and decorin when compared to the control (p<0.01). The semiquantitative imunoblot detected an increased high molecular weight COLV fraction in patients when compared to the control. Conclusion: The over expression and unusual organization of COLV fibers with biochemical changes associated to increased decorin indicates that matrix signalization pathway is involved in COLV fibrillogenesis process in SSc pulmonary fibrosis.
  • conferenceObject
    COLLAGEN TYPE V FACILITATE THE DIFFERENTIATION OF RABBIT ADIPOSE TISSUE-DERIVED STEM CELLS INTO A CHONDROCYTE-LIKE PHENOTYPE ""IN VITRO""
    (2012) CRUZ, Isabele B.; GOLDENSTEIN-SCHAINBERG, C.; FULLER, R.; VELOSA, A. P.; CARRASCO, S.; CAPELOZZI, V.; YOSHINARI, N. H.; TEODORO, W. R.
  • conferenceObject
    Collagen V induces differentiation of rabbit adipose tissue-derived stem cells in chondrocyte-like phenotype
    (2012) TEODORO, W.; CRUZ, I. Brindo da; VELOSA, A. P.; CARRASCO, S.; GOLDENSTEIN-SCHAINBERG, C.; FULLER, R.; PARRA, E.; CAPELOZZI, V.
    Objective: Stimulated mesenchymal stem cells (MSCs) have capacity of differentiation in many cell types. It is being used in degenerative diseases treatment protocols. We evaluated the collagen V (COL V) and collagen XI (COL XI) influence in the differentiation of rabbits adipose tissue-derived MSCs in a chondrocyte-like cell phenotype. Method: MSCs isolated of New Zealand rabbits adipose-tissue were maintained in culture by 4 weeks. COLV, COLXI and COLV/XI (10μg/ml) were added to culture during 72 h. The cells aggregates were stained with Toluidine blue, Alcian blue and Picrosirius. Chondrocyte-like phenotype was confirmed by immunofluorescence to CD34, vimentin and collagens I, II and III. Results: MSCs stimulated with COLV expressed proteoglicans and collagen, when compared with COLXI and COLV/XI and control. In the presence of COLV, MSCs was capable to increase collagen II expression confirming its chondro-cyte-like cell phenotype. In contrast, MSCs cultured with COLXI and COLV/XI express collagen I and III. Conclusion: The data suggest that COLV may facilitate the differentiation of rabbit adipose tissue-derived stem cells into a chondrocyte-like phenotype. Further studies are urged in order to evaluate the influence of COLV in the ability of chondrocytes to remodel osteoarthritic joint surface at ultrastructural and molecular levels.
  • conferenceObject
    Unusual distribution of Type V collagen isoforms determines the cutaneous fibrosis in scleroderma
    (2016) TEODORO, W. Rosolia; MORAIS, J.; VELOSA, A. P. Pereira; MARTIN, P.; CARRASCO, S.; CAMARGO, L.; GOLDENSTEIN-SCHAINBERG, C.; CAPELOZZI, V.
  • 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
    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. Rosolia
  • article 4 Citação(ões) na Scopus
    Identification of Autoimmunity to Peptides of Collagen V alpha 1 Chain as Newly Biomarkers of Early Stage of Systemic Sclerosis
    (2021) VELOSA, Ana Paula Pereira; BRITO, Lais; QUEIROZ, Zelita Aparecida de Jesus; CARRASCO, Solange; MIRANDA, Jurandir Tomaz de; FARHAT, Cecilia; GOLDENSTEIN-SCHAINBERG, Claudia; PARRA, Edwin Roger; ANDRADE, Danieli Castro Oliveira de; SILVA, Pedro Leme; CAPELOZZI, Vera Luiza; TEODORO, Walcy Rosolia
    Patients with Systemic sclerosis (SSc) presents immune dysregulation, vasculopathy, and fibrosis of the skin and various internal organs. Pulmonary fibrosis leads to SSc-associated interstitial lung disease (ILD), which is the main cause of morbidity and mortality in SSc. Recently autoimmunity to type V collagen (Col V) has been characterized in idiopathic pulmonary fibrosis and show promise to be related to the development in SSc. Our aim was to evaluate autoimmunity to Col V alpha 1(V) and alpha 2(V) chains and to the antigenic peptides of these Col V chains in early-SSc sera employing lung tissue of SSc-ILD, as antigen source. We found that sera samples from patients with early-SSc were reactive to Col V (41.18%) and presented immunoreactivity for Col5A1(1.049) and Col5A1(1.439) peptides. The IgG isolated from early-SSc patients-anti-Col V positive sera (anti-ColV IgG) was adsorbed with alpha 1(V) chain (anti-ColV IgG/ads-alpha 1(V)) and alpha 2(V) chain (anti-ColV IgG/ads-alpha 2(V)) and biotinylated to evaluate the spectrum of reactivity in SSc-ILD patients lung biopsies by immunofluorescence. The SSc-ILD lung tissue samples immunostained with anti-ColV IgG showed increased green fluorescence in the vascular basement membrane, bronchiolar smooth muscle, and adventitial layer, contrasting with the tenue immunostaining in control lungs. Col V protein expression in these pulmonary compartments immunostained with early-SSc anti-ColV IgG was confirmed by immune colocalization assays with commercial anti-human Col V antibodies. In addition, SSc-ILD lung tissues immunostained with anti-ColV IgG/ads-alpha 1(V) (sample in which Col V alpha 1 chain-specific antibodies were removed) showed decreased green fluorescence compared to anti-ColV IgG and anti-ColV IgG/ads-alpha 2(V). Our data show that autoimmunity to Col V in early-SSc was related to peptides of the alpha 1(V) chain, suggesting that these antibodies could be biomarkers of SSc stages and potential target of immunotherapy with Col V immunogenic peptides.
  • conferenceObject
    DYNAMIC COLLAGEN V REMODELING IS RELATED TO SKIN THICKENING IN SSc
    (2012) MARTIN, P.; TEODORO, W. R.; VELOSA, A. P.; CARRASCO, S.; MORAIS, J. de; CHRISTMANN, R. B.; PARRAS, E. R.; CAPELOZZI, V. L.; YOSHINARI, N. H.
    Background. Normal physiological properties of skin, one of the primary organs affected in SSc, depends on collagen Types I (COL I), III (COLIII) and V (COLV) assembly forming heterotypic fibres. COLV regulates fibril diameter and loss of this function could result in tissue fibrosis. In this way, our aim was to evaluate the histological and molecular profiles of COLI, COLIII and COLV in SSc skin and its correlation with skin thickening and disease activity. Methods. Skin biopsies of 18 patients (5 at early and 13 at late disease stage) and 10 healthy controls were studied. Assessment of skin thickening was performed using the modified Rodnan skin score (MRSS) and disease activity was calculated by Valentini Disease Activity Index. Quantification of COLI, COLIII and COLV was evaluated by histomorphometry in dermis and quantitative RT–PCR in dermal fibroblast culture. Results. A higher expression of abnormal COLV was observed in dermis of patients with early disease when compared with control group and late disease. The COLIII content was also higher in early SSc when compared with healthy controls and late SSc. On the other hand, the amount of COLI was higher in late disease when compared with control and early SSc. A positive correlation between COLV and MRSS (r = 0.42, P = 0.04) as well as disease activity (r = 0.45, P = 0.03) was observed, but there was no correlation between COLI and COLIII expression and these parameters. COLV α-1 and COLV α-2, as well as COLI α-1 and COLIII α-1 mRNA expression were higher in SSc when compared with control group. Conclusion. We found increased COLIII and COLV deposition in early SSc and increased COLI expression in late SSc indicating that collagen remodelling in SSc is a dynamic process. The fact that abnormal COLV expression decreases in later disease stages could explain why skin thickening sometimes improves spontaneously with time. Besides, COLV is correlated to MRSS and disease activity. These findings include COLV as an important regulator of cutaneous thickness in SSc and may add this protein as a new target for future treatments.
  • conferenceObject
    COLVa2 a Biomarker of Vasculopathy in Scleroderma?
    (2013) MORAIS, J.; MARTIN, P.; CAMARGO, I. C.; KATAYAMA, M. L.; CARRASCO, S.; GOLDEINSTEIN-SCHAINBERG, C.; PARRAS, E. R.; BARRENCE, F.; VELOSA, A. P.; CAPELOZZI, V. L.; TEODORA, W. R.