Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8956010 | Biochemical and Biophysical Research Communications | 2018 | 8 Pages |
Abstract
CD80 has been known to be a co-stimulatory factor expressed in antigen presenting cells (APCs) involved in T-cell activation. It can be expressed in non-bone marrow-derived cells induced by lipopolysaccharide (LPS) or other stimulators, and directly involved in the pathogenesis following T cell activation. However, the intricate transcription mechanisms that underlying the upregulation of CD80 expression levels in LPS-activated non-bone marrow-derived cells is still unknown. LncRNAs are confirmed to be involved in transcriptional regulation by influencing transcription factors. Therefore, we wanted to determine whether the lncRNA MALAT1, which has been found to be related to LPS-induced inflammation, could regulate the transcription of CD80. Our results showed that CD80 was upregulated in low-dose LPS-activated A549â¯cells in a NF-κB-dependent manner. The lncRNA MALAT1 can interfere with NF-κB activation and disrupt its binding efficiency with the CD80 promoter. Thus, the lncRNA MALAT1 can regulate CD80 transcription via the NF-κB signaling pathway in the LPS-activated A549â¯cell line.
Keywords
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Biochemistry
Authors
Chenxia Juan, Yan Mao, Qian Wang, Qian Cao, Yan Chen, Guoping Zhou,