THAIS FERNANDA DE ALMEIDA GALATRO

(Fonte: Lattes)
Índice h a partir de 2011
8
Projetos de Pesquisa
Unidades Organizacionais
LIM/15 - Laboratório de Investigação em Neurologia, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 4 de 4
  • article 460 Citação(ões) na Scopus
    Transcriptomic analysis of purified human cortical microglia reveals age-associated changes
    (2017) GALATRO, Thais F.; HOLTMAN, Inge R.; LERARIO, Antonio M.; VAINCHTEIN, Ilia D.; BROUWER, Nieske; SOLA, Paula R.; VERAS, Mariana M.; PEREIRA, Tulio F.; LEITE, Renata E. P.; MOLLER, Thomas; WES, Paul D.; SOGAYAR, Mari C.; LAMAN, Jon D.; DUNNEN, Wilfred den; PASQUALUCCI, Carlos A.; OBA-SHINJO, Sueli M.; BODDEKE, Erik W. G. M.; MARIE, Suely K. N.; EGGEN, Bart J. L.
    Microglia are essential for CNS homeostasis and innate neuroimmune function, and play important roles in neurodegeneration and brain aging. Here we present gene expression profiles of purified microglia isolated at autopsy from the parietal cortex of 39 human subjects with intact cognition. Overall, genes expressed by human microglia were similar to those in mouse, including established microglial genes CX3CR1, P2RY12 and ITGAM (CD11B). However, a number of immune genes, not identified as part of the mouse microglial signature, were abundantly expressed in human microglia, including TLR, F-c gamma and SIGLEC receptors, as well as TAL1 and IFI16, regulators of proliferation and cell cycle. Age-associated changes in human microglia were enriched for genes involved in cell adhesion, axonal guidance, cell surface receptor expression and actin (dis)assembly. Limited overlap was observed in microglial genes regulated during aging between mice and humans, indicating that human and mouse microglia age differently.
  • conferenceObject
    Toll-like receptors 1, 2, 4 and 6 expression levels in diffusely infiltrative astrocytomas
    (2016) MORETTI, Isabele F.; FRANCO, Daiane Gil; SILVA, Roseli; GALATRO, Thais F.; OBA-SHINJO, Sueli M.; MARIE, Suely K. N.
  • conferenceObject
    Microglia/macrophages activation status in diffuse gliomas
    (2016) GALATRO, Thais F.; SOLA, Paula; OBA-SHINJO, Sueli M.; EGGEN, Bart J.; MARIE, Suely K.
  • article 20 Citação(ões) na Scopus
    Serum amyloid A1 is upregulated in human glioblastoma
    (2017) KNEBEL, Franciele Hinterholz; UNO, Miyuki; GALATRO, Thais F.; BELLE, Luziane Potrich; OBA-SHINJO, Sueli Mieko; MARIE, Suely Kazue N.; CAMPA, Ana
    Serum amyloid A1 (SAA1) is a sensitive acute phase reactant primarily produced by the liver in response to acute inflammation. We have recently shown that SAA affects proliferation, migration, and invasion of glioblastoma cell lines, which suggest its participation in the malignant process. Consistently, levels of SAA have been used as a non-invasive biomarker for the prognosis of many cancers. In this study, we aimed to investigate SAA serum levels and expression of SAA genes in human astrocytomas tissues. Serum and tissue samples were obtained from patients with astrocytoma grades I to III and glioblastoma (GBM or grade IV). Levels of circulating SAA were significantly higher in the serum of patients with AGII-IV when compared to non-neoplastic samples derived from non-neoplastic patients (NN) (p > 0.0001). Quantitative real time PCR (qRT-PCR) of 148 astrocytomas samples (grades I-IV) showed that SAA1 mRNA was significantly higher in GBM when compared to AGI-III and NN samples (p < 0.0001). Immunohistochemistry analysis revealed cytoplasmic positivity for SAA in GBM. There was no correlation of SAA1 with clinical end-point of overall survival among GBM patients. However, it was found a positive correlation between SAA1 and genes involved in tumor progression, such as: HIF1A (r = 0.50; p < 0.00001), CD163 (r = 0.52; p < 0.00001), CXCR4 (r = 0.42; p < 0.00001) and CXCR7 (r = 0.33; p = 0.002). In conclusions, we show that astrocytoma patients have increased levels of serum SAA and SAA1 is expressed and secreted in GBM, and its co-expression with tumor-related genes supports its involvement in GBM angiogenesis and progression.