Avaliação de microRNAs na Periodontite Crônica

• Ano de defesa: 2015
• Autor(a) principal: Telma Cristina Arão
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais
• Palavras-chave em Português: Morfologia; MicroRNAs; Periodontite; Patogênese Homeopática; Patogênese
• Link de acesso: https://hdl.handle.net/1843/59725

MicroRNAs (miRNAs) are short RNA molecules that negatively regulate gene expression by degrading target mRNA or inhibit the translation of protein. Recently, many reports have shown the altered miRNA expression in various diseases. However, there are few reports about miRNA expression on periodontitis. Initially, this study aimed to compare the expression of 84 miRNAs in gingival tissues from individuals without (n=4) and with chronic periodontitis (n=6). Eight miRNAs miR148a-3p, miR142-3p, miR29b, miR138-5p, miR142 5p, miR150-5p, miR191-5p and miR223-3p were significantly increased in the samples of chronic periodontitis (CP). Among the increased miRNAs, miRNA 148a-3p expression was higher in CP compared to C group. The miRNA-148a gene expression was confirmed by RT-qPCR (n=17). Media miRNA-148a relative quantification (RQ) was 17.24 while control group was 14.05. Through in situ hybridization (ISH), it was observed positive staining for miRNA-148a predominantly in connective tissue of gingival fragment with CP. Target of the miRNA-148a-3p, v-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB), a regulatory molecule of osteoclastogenesis, was evaluated and its result did not was statistically significant. The in vitro experiment showed increase miRNA-148a expression when stimulated with P. gingivalis LPS and A. actinomycetemcomitans LPS in PBMC cultivated for 4 hour. In conclusion, these data highlight the possibility of miR-148a involvement in chronic periodontitis pathogenesis. More studies are necessary to demonstrate a causal relationship between these miRNA and their target in periodontal diseases, as well as its role in the pathogenesis and severity of disease.