Hao Wang1, Li-Wei Ran, Ke Hui, Xin-Yang Wang, Yan Zheng. 1. Department of Dermatology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China. E-mail: wanghaonxyc@163.com.
Abstract
OBJECTIVE: To explore the role of survivin and PI3K/AKT pathway in the pathogenesis of psoriasis vulgaris (PV). METHODS: Plaque-like lesions collected from 22 patients with PV in progressive stage and 18 normal control skin specimens were examined using immunohistochemical staining, Western blotting and real-time quantitative PCR for expressions of survivin, PI3K and AKT in the keratinocytes, and their correlation was analyzed. A small interfering RNA (siRNA) was used to knock down AKT in cultured HaCaT cells, and Western blotting was used to detect the changes in the expression of survivin. RESULTS Compared with normal skin, PV lesions showed obviously up-regulated expressions of survivin, PI3K and AKT in the keratinocytes. Survivin expression was positively correlated with PI3K (r=0.4510, P=0.0351) and AKT (r=0.4423, P=0.0393) in the keratinocytes in PV lesions. In cultured HaCaT cells, siRNA-mediated knockdown of AKT caused down-regulation of survivin expression. CONCLUSION: Survivin and PI3K/AKT signaling pathway may participate in the occurrence and progression of PV.
OBJECTIVE: To explore the role of survivin and PI3K/AKT pathway in the pathogenesis of psoriasis vulgaris (PV). METHODS: Plaque-like lesions collected from 22 patients with PV in progressive stage and 18 normal control skin specimens were examined using immunohistochemical staining, Western blotting and real-time quantitative PCR for expressions of survivin, PI3K and AKT in the keratinocytes, and their correlation was analyzed. A small interfering RNA (siRNA) was used to knock down AKT in cultured HaCaT cells, and Western blotting was used to detect the changes in the expression of survivin. RESULTS Compared with normal skin, PV lesions showed obviously up-regulated expressions of survivin, PI3K and AKT in the keratinocytes. Survivin expression was positively correlated with PI3K (r=0.4510, P=0.0351) and AKT (r=0.4423, P=0.0393) in the keratinocytes in PV lesions. In cultured HaCaT cells, siRNA-mediated knockdown of AKT caused down-regulation of survivin expression. CONCLUSION: Survivin and PI3K/AKT signaling pathway may participate in the occurrence and progression of PV.
Authors: Kim M Keppler-Noreuil; Victoria E R Parker; Thomas N Darling; Julian A Martinez-Agosto Journal: Am J Med Genet C Semin Med Genet Date: 2016-11-18 Impact factor: 3.908
Authors: Jean Christopher Chamcheu; Maria-Ines Chaves-Rodriquez; Vaqar M Adhami; Imtiaz A Siddiqui; Gary S Wood; B Jack Longley; Hasan Mukhtar Journal: Acta Derm Venereol Date: 2016-08-23 Impact factor: 4.437