Shike Feng1, Lin Wang2, Wang Liu1, Yan Zhong1, Shijun Xu3. 1. Department of Dermatology, The First People's Hospital of Zigong, Zigong, China. 2. Department of Dermatology, The People's Hospital of Pengzhou, Chengdu, China. 3. Department of Dermatology, Fuling Centre Hospital of Chongqing, Chongqing, China.
Abstract
BACKGROUND: This study aimed to investigate the miR-126 expression in lesional skin and its correlation with clinical features in psoriasis patients and to explore the effect of upregulated miR-126 on cells' proliferation, apoptosis, and inflammation in human keratinocytes. METHODS: A total of 102 psoriasis patients were consecutively enrolled in this study. MiR-126 expressions in lesional skin and paired nonlesional skin were detected by quantitative polymerase chain reaction (qPCR). Human keratinocytes (HaCaT cells) were transfected with miR-126 mimic plasmids and blank mimic plasmid. Cell Counting Kit-8 and annexin V/propidium iodide assays were performed to assess the cells' proliferation and apoptosis, and protein levels of apoptotic markers (cleaved caspase-3 [C-caspase-3] and B-cell lymphoma-2 [Bcl-2]) were detected by Western blot assay. Inflammatory cytokines mRNA and protein levels were detected by qPCR and Western blot assays, respectively. RESULTS: MiR-126 expression was upregulated in lesional skin tissue compared with paired nonlesional skin tissue, and its expression positively associated with Psoriasis Area and Severity Index score in psoriasis patients. MiR-126 expression was increased in miR-126 mimic group compared with negative control (NC) mimic group after plasmids transfection into HaCaT cells, and cells' proliferation was enhanced while cells' apoptosis rate was reduced in miR-126 mimic group than NC mimic group. Protein expressions of C-caspase and Bcl-2 also indicated miR-126 mimic decreased the cells' apoptosis. In addition, miR-126 mimic increased TNF-α, IFN-γ, IL-17A, and IL-22 expressions while decreased IL-10 expression. CONCLUSION: In conclusion, miR-126 correlates with elevated risk and increased disease severity in psoriasis patients, and upregulation of miR-126 promotes cells' proliferation and inflammation while inhibits cells' apoptosis in keratinocytes.
BACKGROUND: This study aimed to investigate the miR-126 expression in lesional skin and its correlation with clinical features in psoriasispatients and to explore the effect of upregulated miR-126 on cells' proliferation, apoptosis, and inflammation in human keratinocytes. METHODS: A total of 102 psoriasispatients were consecutively enrolled in this study. MiR-126 expressions in lesional skin and paired nonlesional skin were detected by quantitative polymerase chain reaction (qPCR). Human keratinocytes (HaCaT cells) were transfected with miR-126 mimic plasmids and blank mimic plasmid. Cell Counting Kit-8 and annexin V/propidium iodide assays were performed to assess the cells' proliferation and apoptosis, and protein levels of apoptotic markers (cleaved caspase-3 [C-caspase-3] and B-cell lymphoma-2 [Bcl-2]) were detected by Western blot assay. Inflammatory cytokines mRNA and protein levels were detected by qPCR and Western blot assays, respectively. RESULTS:MiR-126 expression was upregulated in lesional skin tissue compared with paired nonlesional skin tissue, and its expression positively associated with Psoriasis Area and Severity Index score in psoriasispatients. MiR-126 expression was increased in miR-126 mimic group compared with negative control (NC) mimic group after plasmids transfection into HaCaT cells, and cells' proliferation was enhanced while cells' apoptosis rate was reduced in miR-126 mimic group than NC mimic group. Protein expressions of C-caspase and Bcl-2 also indicated miR-126 mimic decreased the cells' apoptosis. In addition, miR-126 mimic increased TNF-α, IFN-γ, IL-17A, and IL-22 expressions while decreased IL-10 expression. CONCLUSION: In conclusion, miR-126 correlates with elevated risk and increased disease severity in psoriasispatients, and upregulation of miR-126 promotes cells' proliferation and inflammation while inhibits cells' apoptosis in keratinocytes.
Authors: Michelle A Lowes; Chris B Russell; David A Martin; Jennifer E Towne; James G Krueger Journal: Trends Immunol Date: 2013-01-03 Impact factor: 16.687