Proinflammatory cytokine interferon-γ increases the expression of BANCR, a long non-coding RNA, in retinal pigment epithelial cells
| Autor: | William Samuel, Todd Duncan, Olga Postnikova, Cynthia Jaworski, R. Krishnan Kutty, Chandrasekharam N. Nagineni, T. Michael Redmond |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Adult medicine.medical_treatment Immunology Retinal Pigment Epithelium Biology Biochemistry Article Proinflammatory cytokine Cell Line 03 medical and health sciences Interferon-gamma Downregulation and upregulation medicine Immunology and Allergy Humans STAT1 Molecular Biology Retinal pigment epithelium Epithelial Cells Hematology Long non-coding RNA 030104 developmental biology medicine.anatomical_structure Cytokine Gene Expression Regulation Cancer research biology.protein Phosphorylation RNA Long Noncoding sense organs Signal transduction Inflammation Mediators |
| Popis: | The inflammatory response may contribute to retinal pigment epithelial (RPE) dysfunction associated with the pathogenesis of age-related macular degeneration (AMD). We investigated whether the inflammatory response affects the expression of long coding RNAs (lncRNAs) in human RPE-derived ARPE-19 cells. This class of regulatory RNA molecules recently came to prominence due to their involvement in many pathophysiological processes. A proinflammatory cytokine mixture consisting of IFN-γ, IL-1β and TNF-α altered the expression several lncRNAs including BANCR in these cells. The cytokine responsible for increasing BANCR expression in ARPE-19 cells was found to be IFN-γ. BANCR expression induced by IFN-γ was suppressed when STAT1 phosphorylation was blocked by JAK inhibitor 1. Thus, proinflammatory cytokines could modulate the expression of lncRNAs in RPE cells and IFN-γ could upregulate the expression of BANCR by activating JAK-STAT1 signaling pathway. |
| Databáze: | OpenAIRE |
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