Expressão Imuno-histoquímica de COX-2, EMMPRIN, HIF-1α e GLUT-1 no tecido gengival normal e inflamado

The aim of this study was determine whether an association exists in the gum tissue between the expression of markers of tissue hypoxia (HIF-1α and GLUT-1) with a marker of inflammatory activity (COX-2) and a marker of collagen degradation (EMMPRIN). Was performed immunohistochemistry with antibodies specific for these markers on 60 samples of gingival tissue divided into two groups: gums (n = 26) and gingivitis (n = 34) and expression was analyzed in the epithelial tissue and connective tissue . The reactivity epithelial for COX-2 was observed in only two cases as the HIF-1α, GLUT-1 and EMMPRIN was strongly expressed in the epithelial basal layer and the immunostaining was gradually decreased as the cells away from this layer, and negative in the region suprabasal in most specimens. In connective tissue, and HIF-1α EMMPRIN were strongly positive for most cases analyzed as GLUT-1 was negative in most cases. Immunostaining for COX-2 showed an association with gingival inflammatory infiltrate. The expression of EMMPRIN, HIF-1α and GLUT-1 in normal gums confirms the physiological role of these markers, however there was no association with tissue inflammation. Given the findings we can conclude that the inflammatory changes installed in frames of chronic gingivitis may not be sufficient to activate the factors of hypoxia to levels that can be quantified by immunohistochemical analysis, in addition, the findings are not conclusive in relationship to involvement of EMMPRIN in the secretion of MMPs to degrade collagen in the frames of gingivitis. We suggest the use of technical analysis and quantification of RNA of EMMPRIN and MMPs in order to determine whether collagen degradation observed in gingivitis suffers or not, significant influence of EMMPRIN for secretion and activation of MMPs

Effect of Helicobacter pylori infection on IL-8, IL-1 and COX-2 expression in patients with chronic gastritis and gastric cancer

Objective. Helicobacter pylori infection is related to gastric cancer development, and chronic inflammation is presumed to be the main cause. The aim of the present study was to evaluate the influence of H. pylori cagA, vacA, iceA, and babA genotypes on COX-2, IL-1, and IL-8 expression. Material and methods. of the 217 patients included in the study, 26 were uninfected, 127 had chronic gastritis and were H. pylori-positive, and 64 had gastric cancer. Bacterial genotypes were evaluated by polymerase chain reaction (PCR), and the expression values were determined by quantitative real-time PCR and immunohistochemistry. Results. An association was found between the infection with cagA, vacA s1m1 strains and gastric cancer development. Regarding the 3' region of the cagA gene, we also found an association between the infection with cagA EPIYA-ABCCC strains and clinical outcome. Higher levels of IL-8, IL-1, and COX-2 were detected in gastric mucosa from infected patients with chronic gastritis, and they were also associated with the infection by cagA, vacA s1m1 strains. The IL-8 and IL-1 levels decrease significantly from chronic gastritis to gastric cancer, while the relative expression remained unaltered when COX-2 expression was analyzed among patients with gastritis and cancer. Conclusions. Since inflammatory response to H. pylori infection plays an important role in cellular proliferation and gastric mucosal damage, the up-regulation of IL-1, IL-8, and COX-2 in patients with chronic gastritis has an important clinical implication in gastric carcinogenesis.

Inactivation of COX-2, HMLH1 and CDKN2A Gene by Promoter Methylation in Gastric Cancer: Relationship with Histological Subtype, Tumor Location and Helicobacter pylori Genotype

Objective: We aimed to evaluate the inactivation of COX-2, HMLH1 and CDKN2A by promoter methylation and its relationship with the infection by different Helicobacter pylori strains in gastric cancer. Methods: DNA extracted from 76 H. pylori-positive gastric tumor samples was available for promoter methylation identification by methylation-specific PCR and H. pylori subtyping by PCR. Immunohistochemistry was used to determine COX-2, p16(INK4A) and HMLH1 expression. Results: A strong negative correlation was found between the expression of these markers and the presence of promoter methylation in their genes. Among cardia tumors, negativity of p16(INK4A) was a significant finding. on the other hand, in noncardia tumors, the histological subtypes had different gene expression patterns. In the intestinal subtype, a significant finding was HMLH1 inactivation by methylation, while in the diffuse subtype, CDKN2A inactivation by methylation was the significant finding. Tumors with methylated COX-2 and HMLH1 genes were associated with H. pylori vac A s1 (p = 0.025 and 0.047, respectively), and the nonmethylated tumors were associated with the presence of the gene flaA. Conclusions: These data suggest that the inactivation of these genes by methylation occurs by distinct pathways according to the histological subtype and tumor location and depends on the H. pylori genotype. Copyright (C) 2011 S. Karger AG, Basel

COX-2 and TGF-β expression in proliferative disorders of canine prostate

COX-2 and TGF-β expression was determined in order to correlate non-neoplastic lesions, preneoplastic lesions and carcinoma in the prostate of dogs. The results show that neoplastic and preneoplastic lesions express more COX-2 and TGF-β when compared to carcinomas, which suggests these proteins may cooperate in the process of prostate tumorigenesis.

Imunomarcação de COX-2 e TGF-beta nas lesòes proliferativas da próstata do cão

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

Uso de antiinflamatórios COX-2 seletivos em ratos (Rattus novergicus) Wistar

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

Imunomarcação de COX-2, PGE-2, VEGF e CASPASE-3 em mastocitomas cutâneos caninos

Pós-graduação em Medicina Veterinária - FMVZ

Prostaglandina E2 em cães portadores de linfoma multicêntrico submetidos ao protocolo quimioterápico de Madison-Wisconsin associado ou não a um inibidor de COX-2

Pós-graduação em Medicina Veterinária - FCAV

Expressão gênica de MMP-2 e 9, TIMP-1 e 2, ATM, TP53, VEGF, COX-2 e CDH-1 no TVT canino

Pós-graduação em Medicina Veterinária - FCAV

Expressão gênica e proteica da cox-2 e c-Kit em neoplasias mamárias de cadelas

Pós-graduação em Medicina Veterinária - FCAV

Efeitos da inibição da cox-2 no sistema cardiovascular de cães

Os anti-inflamatórios não esteroidais (AINEs) estão entre os medicamentos mais prescritos em todo o mundo, tanto na medicina humana, como na medicina veterinária. Atualmente os AINEs são classificados em não seletivos (convencionais ou clássicos), que são os mais antigos, e seletivos para COX-2 ou coxibes. Alguns estudos constataram uma possível relação entre os inibidores COX-2 seletivos e os efeitos adversos no sistema cardiovascular. Devido a isso, objetivou-se realizar um levantamento de pesquisas que comprovem os efeitos cardiovasculares ocasionados por essa classe farmacológica utilizando livros e artigos das bases de dados PubMed, Periódicos da Capes e SciELO que respondessem à pergunta: a inibição da COX-2 acarreta efeitos adversos para o sistema cardiovascular?. Do total de resultados encontrados, foram utilizados 16 artigos. Os trabalhos mostraram que o uso de inibidores da COX-2 alterou o perfil de coagulação para uma tendência trombótica, além de diminuir a resposta vasodilatadora gerada na resposta inflamatória. Diante dos resultados obtidos através desses estudos, conclui-se que a COX-2 desempenha papel fisiológico no sistema cardiovascular, facilitando a não formação de trombos nos vasos sanguíneos, e, portanto, que sua inibição favorece a coagulação. Assim, os fármacos que inibem a COX-2 devem ser prescritos com cautela, levando-se em consideração o perfil de coagulação do paciente

Expressão imuno-histoquímica de KI-67, COX-2, MMP-9 e P53 nos tumores testiculares caninos

Pós-graduação em Ciência Animal - FMVA