RELATIONSHIP BETWEEN POLYMORPHOSMS OF THE HIF-1α GENE WITH THE ANALYSIS OF IMMUNOISTOQUÍMUCA EXPRESSION OF VEGF165 AND VEGF165b IN ORAL FLAT LIQUID AND VULGAR PENFIGURE
Lichen Planus, Oral; Pemphigus; Neovascularization, Pathologic; Immunohistochemistry; Polymorphism, Genetic.
Oral Lichen Planus and Pemphigus Vulgaris are chronic mucocutaneous immunological diseases of unknown etiologies that can affect oral mucosa. Angiogenesis plays an important role in growth and progression tumor and, among all VEGF types, VEGF-A is the most potent angiogenic protein in both normal and pathological angiogenesis. Alternative splicing of exon 8 originates two known families of isoform proteins: one performing angiogenic role, VEGFxxxa, and another an antiangiogenic role, VEGFxxxb. HIF-1 plays a central role in a large number of biological processes (angiogenesis and carcinogenesis), some of which occur under hypoxia conditions. Polymorphisms of HIF-1α, C1772T / G1790A, consist nucleotide substitutions from C to T and from G to A, respectively, at positions 1772 and 1790 of exon 12 of HIF-1α. The mechanisms which these SNPs promote the activation of HIF-1α transcription, even under normoxia conditions, are still unknown but indicate that it has an important and independent effect on pathological angiogenesis. Analysis of proteins related to hypoxia and angiogenesis suggests that they may play an important role in the pathogenesis of oral lichen planus and another inflammatory autoimmune diseases, such as pemphigus vulgaris. In addition, the study of the angiogenic process in these lesions gives the possibility of improving the understanding of pathogenics mechanism in these lesions. The aim of this study is evaluate whether the polymorphism in HIF-1α gene (C1772T and G1790A) is associated with the risk of developing LPO and PV, as well as to evaluate its relationship with VEGF165 (angiogenic) and VEGF165b (antiangiogenic) immunohistochemical expression in serial cases of these lesions, in an attempt to better understand the pathogenesis, progression, and self-perpetuation of these chronic inflammatory autoimmune diseases.