LINC00176 facilitates CD4+T cell adhesion in systemic lupus erythematosus via the WNT5a signaling pathway by regulating WIF1
| Autor: | Xue Shao, Shengzhu Zhou, Chang Lu, Chenyu Pan |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Cd4 t cell Immunology Translation (biology) Context (language use) Adhesion Biology WIF1 WNT5A 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Expression pattern immune system diseases Cancer research Signal transduction skin and connective tissue diseases Molecular Biology 030215 immunology |
| Zdroj: | Molecular Immunology. 134:202-209 |
| ISSN: | 0161-5890 |
| Popis: | Accruing research shows the implications of long non-coding RNAs (lncRNAs) in the progression of various autoimmune diseases including systemic lupus erythematosus (SLE). The present study aimed to identify the expression pattern of LINC00176 in SLE and to explore its effects on CD4+T cell adhesion in this context. The biological functions of LINC00176, WIF1 and WNT5a on CD4+T cells in SLE were evaluated via gain- and loss-of-function experiments, following delivery of pcDNA3-LINC00176, siRNA-LINC00176, pcDNA3-WIF1 and WNT-sFRP5 (an inhibitor for the WNT5a signaling pathway). High LINC00176 expression was evident in the CD4+T cells of SLE patients. Additionally, WIF1 was identified as a potential target gene of LINC00176, and was negatively regulated by LINC00176. The overexpression of LINC00176 could promote proliferation and adhesion of CD4+T cells in SLE. Such alternations were reversed following up-regulation of WIF1 or inhibition of the WNT5a signaling pathway. Taken together, the key findings of our study highlight the ability of LINC00176 to potentially promote the proliferation and adhesion of CD4+T cells in SLE by down-regulating WIF1 and activating the WNT5a signaling pathway, providing new insight and a theoretical basis for translation in SLE therapy. |
| Databáze: | OpenAIRE |
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