In:
Immunology, Wiley, Vol. 155, No. 1 ( 2018-09), p. 137-149
Abstract:
Circular RNA s (circRNAs) represent a class of non‐coding RNA s that form covalently closed RNA circles with extensive expression and conservation in mammals. Circular RNA s regulate gene expression through acting as competitive endogenous RNA s (ceRNAs) and modulating gene transcription. Accumulating evidence supports the implication of circRNAs in a variety of human diseases, but studies of circRNA role in systemic lupus erythematosus ( SLE ) are lacking. The present study measured the circRNA expression profiles in T cells from patients with SLE and healthy controls with human circRNA microarray and identified 127 differentially expressed circRNAs in SLE patients. Down‐regulation of hsa_circ_0045272 in SLE T cells was verified with quantitative PCR . Jurkat cells with stable hsa_circ_0045272 knockdown were generated using specific lentiviral short hairpin RNA for functional studies. Flow cytometric analysis indicated that hsa_circ_0045272 knockdown significantly up‐regulated the early apoptosis of Jurkat cells. Meanwhile, ELISA showed that hsa_circ_0045272 knockdown significantly enhanced interleukin‐2 production of activated Jurkat cells. Then, ceRNAs were predicted for hsa_circ_0045272 and the significant down‐regulation of two mRNA s predicted as ceRNAs, NM _003466 ( PAX 8) and NM _015177 ( DTX 4), but not their corresponding proteins, was validated. Furthermore, dual luciferase reporter assay indicated binding of hsa_circ_0045272 with hsa‐miR‐6127. Circular RNA – mRNA co‐expression networks showed the correlation of circRNAs with mRNA s and provided additional clues to circRNA functions. Our study demonstrated dysregulated circRNAs in SLE and revealed the function of hsa_circ_0045272 in negatively regulating apoptosis and interleukin‐2 secretion and its potential mechanism. The implication of hsa_circ_0045272 and other abnormal circRNAs in SLE merits further investigation.
Type of Medium:
Online Resource
ISSN:
0019-2805
,
1365-2567
DOI:
10.1111/imm.2018.155.issue-1
Language:
English
Publisher:
Wiley
Publication Date:
2018
detail.hit.zdb_id:
2006481-0
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