Influência dos níveis de ferritina sérica, das mutações no gene da beta globina e dos valores das enzimas de detoxificação Catalase e Glutationa S -Transferase na expressão fenotípica de Beta Talassemia Heterozigota

Pós-graduação em Genética - IBILCE

Participação da glia nas alterações morfológicas do cérebro e na produção de beta-quimiocinas na encefalite experimental pelo vírus da estomatite vesicular em camundongos

Pós-graduação em Medicina Veterinária - FCAV

Efeitos da combinação do fator de crescimento de fibroblastos básico e fator de transformação de crescimento beta na proliferação, expressão de genes para colágeno tipos I e III, metaloproteases-1 e -2 e TIMPs 1,2 e 3, e na modulação da síntese destes próprios fatores de crescimento pelas células do ligamento periodontal de humanos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Estresse e imuno modulação por beta-glucano em Pacu (Piaractus mesopotamicus)

Pós-graduação em Aquicultura - FCAV

Efeitos do diabetes gestacional moderado e da reposição com insulina na lactação sobre a próstata ventral do rato Wistar

Pós-graduação em Biologia Geral e Aplicada - IBB

Effect of Qualea multiflora on Macrophages and Tumour Cells

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Recombinant disintegrin targets alpha(v) beta(3) integrin and leads to mediator production

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Erythrina mulungu Alkaloids Are Potent Inhibitors of Neuronal Nicotinic Receptor Currents in Mammalian Cells

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Thyroid Hormone Stimulates the Proliferation of Sertoli Cells and Single Type A Spermatogonia in Adult Zebrafish (Danio rerio) Testis

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Differential expression of aromatase, estrogen receptor alpha and 17 beta-HSD associated with the processes of total testicular regression and recrudescence in the bat Myotis nigricans (Chiroptera: Vespertilionidae)

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

CD4+FOXP3+cells produce IL-10 in the spleens of dogs with visceral leishmaniasis

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Macrophage Cell Activation with Acute Apical Abscess Contents Determined by Interleukin-1 Beta and Tumor Necrosis Factor Alpha Production

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Complexes of platinum and palladium with beta-diketones and DMSO: Synthesis, characterization, molecular modeling, and biological studies

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Green tea extract and its major constituent, epigallocatechin-3-gallate, induce epithelial beta-defensin secretion and prevent beta-defensin degradation by Porphyromonas gingivalis

Background and Objective: Antimicrobial peptides, such as beta-defensins, secreted by gingival epithelial cells, are thought to play a major role in preventing periodontal diseases. In the present study, we investigated the ability of green tea polyphenols to induce human beta-defensin (hBD) secretion in gingival epithelial cells and to protect hBDs from proteolytic degradation by Porphyromonas gingivalis.Material and Methods: Gingival epithelial cells were treated with various amounts (25-200 mu g/mL) of green tea extract or epigallocatechin-3-gallate (EGCG). The secretion of hBD1 and hBD2 was measured using ELISAs, and gene expression was quantified by real-time PCR. The treatments were also carried out in the presence of specific kinase inhibitors to identify the signaling pathways involved in hBD secretion. The ability of green tea extract and EGCG to prevent hBD degradation by proteases of P. gingivalis present in a bacterial culture supernatant was evaluated by ELISA.Results: The secretion of hBD1 and hBD2 was up-regulated, in a dose-dependent manner, following the stimulation of gingival epithelial cells with a green tea extract or EGCG. Expression of the hBD gene in gingival epithelial cells treated with green tea polyphenols was also increased. EGCG-induced secretion of hBD1 and hBD2 appeared to involve extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase. Lastly, green tea extract and EGCG prevented the degradation of recombinant hBD1 and hBD2 by a culture supernatant of P. gingivalis.Conclusion: Green tea extract and EGCG, through their ability to induce hBD secretion by epithelial cells and to protect hBDs from proteolytic degradation by P. gingivalis, have the potential to strengthen the epithelial antimicrobial barrier. Future clinical studies will indicate whether these polyphenols represent a valuable therapeutic agent for treating/preventing periodontal diseases.

Leptin Effects on the Regenerative Capacity of Human Periodontal Cells

Obesity is increasing throughout the globe and characterized by excess adipose tissue, which represents a complex endocrine organ. Adipose tissue secrets bioactivemolecules called adipokines, which act at endocrine, paracrine, and autocrine levels. Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing. Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link. The objective of this study was to examine the impact of leptin on the regenerative capacity of human periodontal ligament (PDL) cells and also to study the local leptin production by these cells. Leptin caused a significant downregulation of growth (TGF beta 1, and VEGFA) and transcription (RUNX2) factors as well as matrix molecules (collagen, and periostin) and inhibited SMAD signaling under regenerative conditions. Moreover, the local expression of leptin and its full-length receptor was significantly downregulated by inflammatory, microbial, and biomechanical signals. This study demonstrates that the hormone leptin negatively interferes with the regenerative capacity of PDL cells, suggesting leptin as a pathomechanistic link between obesity and compromised periodontal healing.