| Autor: |
de Carvalho Fraga, Carlos Alberto, Alves, Lucas Rodrigues, Marques-Silva, Luciano, de Sousa, Adriana Alkmim, Jorge, Antonio Sérgio Barcala, de Jesus, Sabrina Ferreira, Vilela, Daniel Nogueira, Pinheiro, Ugo Borges, Jones, Kimberly Marie, de Paula, Alfredo Maurício Batista, Guimarães, André Luiz Sena |
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| Zdroj: |
Clinical Oral Investigations; Dec2013, Vol. 17 Issue 9, p2011-2015, 5p, 2 Charts |
| Abstrakt: |
Objective: The aim of this study is to assess whether C1772T and G1790A hypoxia-inducible factor-1 (HIF-1)α polymorphisms are associated with risk of oral lichen planus (OLP). Material and methods: Restriction fragment length polymorphism analysis was used to investigate HIF-1α C1779T and G1790A polymorphisms in 32 OLP and 88 individuals without OLP. Results: The frequency of the CC, TT, GA, and AA genotypes was higher in patients with OLP. Notably, individuals carrying the C and A, and T and A haplotypes showed a significant association OLP risk. Conclusions: Our study demonstrated that the C1772T and G1790A polymorphisms of HIF-1α gene increased the risk of OLP. C1772T and G1790A polymorphisms of HIF-1α gene had differing patterns of allelic imbalance in the normal samples and subsequent chronic lesions. Further studies are necessary to elucidate the HIF-1α pathway in OLP, which would facilitate the development of novel therapeutic strategies for the prevention and treatment of OLP. Clinical relevance: These results, in conjunction with previous studies, suggest that HIF-1α may play important roles in the chronicity of oral mucosa lesions of OLP patients. Taken together, we suggest that HIF-1α polymorphisms enhance its target genes, thereby altering the microenvironment and supporting sequential release of inflammatory mediators or cellular events in OLP. It appears unlikely that inhibition of a single proinflammatory mediator will prove useful in clinical practice, but several ways to reprogram mediators engaged in a wide array of roles simultaneously are encouraging. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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