DARLAN DA SILVA CANDIDO

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LIM/19 - Laboratório de Histocompatibilidade e Imunidade Celular, Hospital das Clínicas, Faculdade de Medicina

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  • article 39 Citação(ões) na Scopus
    Myocardial Infarction-Associated Transcript, a Long Noncoding RNA, Is Overexpressed During Dilated Cardiomyopathy Due to Chronic Chagas Disease
    (2016) FRADE, Amanda Farage; LAUGIER, Laurie; FERREIRA, Ludmila Rodrigues Pinto; BARON, Monique Andrade; BENVENUTI, Luiz Alberto; TEIXEIRA, Priscila Camillo; NAVARRO, Isabela Cunha; CABANTOUS, Sandrine; FERREIRA, Frederico Moraes; CANDIDO, Darlan da Silva; GAIOTTO, Fabio Antonio; BACAL, Fernando; POMERANTZEFF, Pablo; SANTOS, Ronaldo Honorato Barros; KALIL, Jorge; CUNHA-NETO, Edecio; CHEVILLARD, Christophe
    Long noncoding RNAs (lncRNAs) modulate gene expression at the epigenetic, transcriptional, and posttranscriptional levels. Dysregulation of the lncRNA known as myocardial infarction-associated transcript (MIAT) has been associated with myocardial infarction. Chagas disease causes a severe inflammatory dilated chronic cardiomyopathy (CCC). We investigated the role of MIAT in CCC. A whole-transcriptome analysis of heart biopsy specimens and formalin-fixed, paraffin-embedded samples revealed that MIAT was overexpressed in patients with CCC, compared with subjects with noninflammatory dilated cardiomyopathy and controls. These results were confirmed in a mouse model. Results suggest that MIAT is a specific biomarker of CCC.
  • article 25 Citação(ões) na Scopus
    Blood Gene Signatures of Chagas Cardiomyopathy With or Without Ventricular Dysfunction
    (2017) FERREIRA, Ludmila Rodrigues Pinto; FERREIRA, Frederico Moraes; NAKAYA, Helder Imoto; DENG, Xutao; CNDIDO, Darlan da Silva; OLIVEIRA, Lea Campos de; BILLAUD, Jean-Noel; LANTERI, Marion C.; RIGAUD, Vagner Oliveira-Carvalho; SEIELSTAD, Mark; KALIL, Jorge; FERNANDES, Fabio; RIBEIRO, Antonio Luiz P.; SABINO, Ester Cerdeira; CUNHA-NETO, Edecio
    Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects 7 million people in Latin American areas of endemicity. About 30% of infected patients will develop chronic Chagas cardiomyopathy (CCC), an inflammatory cardiomyopathy characterized by hypertrophy, fibrosis, and myocarditis. Further studies are necessary to understand the molecular mechanisms of disease progression. Transcriptome analysis has been increasingly used to identify molecular changes associated with disease outcomes. We thus assessed the whole-blood transcriptome of patients with Chagas disease. Microarray analysis was performed on blood samples from 150 subjects, of whom 30 were uninfected control patients and 120 had Chagas disease (1 group had asymptomatic disease, and 2 groups had CCC with either a preserved or reduced left ventricular ejection fraction [LVEF]). Each Chagas disease group displayed distinct gene expression and functional pathway profiles. The most different expression patterns were between CCC groups with a preserved or reduced LVEF. A more stringent analysis indicated that 27 differentially expressed genes, particularly those related to natural killer (NK)/CD8(+) T-cell cytotoxicity, separated the 2 groups. NK/CD8(+) T-cell cytotoxicity could play a role in determining Chagas disease progression. Understanding genes associated with disease may lead to improved insight into CCC pathogenesis and the identification of prognostic factors for CCC progression.