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Expression Of Long Non-coding RNA TINCR In Lesions Of Psoriasis Vulgaris Patients

Posted on:2021-01-30Degree:MasterType:Thesis
Country:ChinaCandidate:M X XieFull Text:PDF
GTID:2404330629952229Subject:Dermatology and venereology
Abstract/Summary:PDF Full Text Request
OBJECTIVE:To compare the expression lncRNA TINCR and its target genes in lesions of psoriasis vulgaris patients and healthy human skin;to clarify the possible role of lncRNA TINCR in the pathogenesis of psoriasis vulgaris.Methods:Real-time fluorescent quantitative PCR was performed to determine the expression levels of lncRNA TINCR in 15 patients with psoriasis vulgaris and normal skin of 15 healthy human controls.Bioinformatics analysis was used to search for possible target genes of lncRNA TINCR,then the expression of Cyclin D1 and KLF4were detected by immunohistochemistry in 50 patients with psoriasis vulgaris and 23heslthy controls.Results:?1?The expression level of lncRNA TINCR in psoriasis vulgaris lesions was0.0627±0.0184,which was significantly lower than the expression level of normal skin tissue at 0.2089±0.1013,and the difference between the two groups was statistically significant?P<0.05?.?2?Bioinformatics analysis found that TINCR downstream may regulate the expression of Cyclin D1 and KLF4.?3?Cyclin D1 was expressed in the epidermis of psoriatic lesions at the lower spine layer,which was stronger than that of normal tissues,and the difference between the two groups was statistically significant?Z=-3.437,P<0.05?.?4?KLF4 was expressed in the epidermis of psoriatic lesions at 1/2 of the upper spine layer,and expressed in the basal layer of normal skin tissues,and the difference between the two groups was statistically significant(?2=27.205,P<0.05).CONCLUSION:The expression of lncRNA TINCR in skin lesions of psoriasis vulgaris is lower than that in normal skin tissues.The target proteins of TINCR,Cyclin D1 and KLF4,are differentially expressed in psoriasis vulgaris lesions and normal skin tissues.lncRNA TINCR may be involved in the pathogenesis of psoriasis vulgaris through the TINCR-KLF4/Cyclin D1 axis that control KC excessive abnormal proliferation and differentiation.
Keywords/Search Tags:psoriasis vulgaris, long non-coding RNA TINCR, target gene, Cyclin D1, KLF4
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