High HIF-1α expression genotypes in oral lichen planus
Autor: | Sabrina Ferreira de Jesus, Antonio Sergio Barcala Jorge, Luciano Marques-Silva, Daniel Nogueira Vilela, Adriana Alkmim de Sousa, Carlos Alberto de Carvalho Fraga, André Luiz Sena Guimarães, Ugo Borges Pinheiro, Lucas Rodrigues Alves, Alfredo Maurício Batista de Paula, Kimberly Marie Jones |
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Rok vydání: | 2013 |
Předmět: |
Pathology
medicine.medical_specialty Genotype business.industry Haplotype Inflammation Hypoxia-Inducible Factor 1 alpha Subunit medicine.disease Proinflammatory cytokine stomatognathic diseases medicine.anatomical_structure stomatognathic system Allelic Imbalance Immunology medicine Humans Oral lichen planus medicine.symptom Oral mucosa Restriction fragment length polymorphism business General Dentistry Lichen Planus Oral |
Zdroj: | Clinical Oral Investigations. 17:2011-2015 |
ISSN: | 1436-3771 1432-6981 |
Popis: | 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). Restriction fragment length polymorphism analysis was used to investigate HIF-1α C1779T and G1790A polymorphisms in 32 OLP and 88 individuals without OLP. 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. 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. 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. |
Databáze: | OpenAIRE |
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