The Expression Of TNIP1and Its Coding Protein ABIN1’s Role In Advanced Vulgaris Psoriasis

Background：Psoriasis is a common chronic inflammatory skin disease mainly involving the skin,nails and joints, which affect the health and living quality of patients seriously. Thepathogenesis of psoriasis has not yet been fully elucidated, while it is currently acceptedthat the main pathological mechanism is inflammatory reaction mediated by immunedysfunction which is based on genetic and other factors. Psoriasis inflammatory response ismediated by the classic inflammatory signaling-nuclear factor-kappa B (NF-κB) signalingpathway. Genome-wide association study (GWAS) has identified a number of psoriasissusceptibility genes, in which TNFα-induced protein3interacting protein1(TNIP1) geneplays an important role in the regulation of NF-κB signaling pathway. TNIP1is a newlydiscovered endogenous inflammatory regulatory factors, which is not only involved in theregulation of inflammatory responses but also involved in immune function. Reseacheshave reported that the single nucleotide polymorphism (SNP) of TNIP1gene is associatedwith the pathogenesis of psoriasis in many countris. We investigated the expression of thethe observation TNIP1mRNA and its encoded A20binding inhibitor of NF-κB activation(ABIN1) protein in psoriasis, and analysised its correlation with the clinical types,preliminary to explore the role TNIP1in psoriasis and to lay the foundation for furtherresearch about the pathogenesis mechanisms of psoriasis.Methods：25psoriasis patients admitted to the Dermatology Department of The Third MilitaryMedical University Southwestern Hospital (Chongqing, China) from October2011to April2012were enrolled (13males and12females, mean age of33.0±8.3years).25healthycontrol subjects were enrolled from the physical examination department of the hospital (14males and11females, mean age of31.3±9.9years). There were no significant differences between these two groups in age or gender. We tested the mRNA of TNIP1and itstranslational protein ABIN1through QRT-PCR and Western Blot between patients andhealthy groups using their peripheral lymphocyte. Moreover，we also tested the expressionof ABIN1using immunohistochemistry in the skin between the healthy and patients.Results：1. TNIP1mRNA in peripheral blood lymphocytes of patients with psoriasis during theperiod of relative expression of was0.2921±0.1016and healthy control group was1.0859±0.2663, and the difference was statistically significant (P <0.05).2. Western blot detection results showed that ABIN1protein expression in theperipheral blood lymphocytes of patients with psoriasis (IOD=0.0932±0.0039) wassignificantly decreased compared with controls (IOD=0.2909±0.05779), and thedifference was statistically significant (P <0.05).3. Immunohistochemical staining showed the ABIN1distribution and expression isdifferent in the lesions skin compared with normal controls. The morphology and theexpression of very low expression in the ABIN1during the patients with psoriasis vulgarislesions even expression.4. We further tested the expression of ABIN1in lesions skin in different periods, andanalyze the relationship of the expression of psoriasis evolution of the disease. The resultsshowed that ABIN1expression in psoriasis is down-regulated, but in the resolution phaseand quiescent is up-regulated.Conclusion：1.The results revealed that the low expression of TNIP1and ABIN1maybe correlatedwith the pathogenesis of vulgaris psoriasis.2. The role of TNIP1in psoriasis may begin on the transcriptional level, whichsuggesting that genetic predisposition is the major determinant of the pathogenicity.3. The reduce expression of TNIP1is possibly an important reason to cause thepsoriatic inflammatory response can not be effectively suppressed.