Abstract
Long non-coding RNAs are essential regulators of the inflammatory response, especially for transcriptional regulation of inflammatory genes. It has been reported that the expression of transmembrane channel-like 3 (TMC3)–AS1 is increased following lipopolysaccharide stimulation. However, the potential function of TMC3-AS1 in immunity is largely unknown. Herein, we report a specific role for TMC3-AS1 in the regulation of inflammatory gene expression. TMC3-AS1 negatively regulates the expression of interleukin 10 (IL-10) in macrophage and intestinal epithelial cell lines. Mechanistically, TMC3-AS1 may interact with p65 in the nucleus, preventing p65 from binding to the κB consensus site within IL-10 promoter. These findings suggest that TMC3-AS1 may function as an important regulator in the innate immune response.
Highlights
The innate immune system is the primary barrier to microbial pathogens [1]
We found that there was a higher level of TLR4 than TLR1, TLR2, and TLR3 in SW480 cells (Figure 1D); the level of transmembrane channel-like 3 (TMC3)-AS1 reached a peak level at 4 h and increased at 8 h and 12 h following Pam3CSK4 stimulation (Figure 1E); when exposed to poly(I:C), the level of TMC3-AS1 reached a peak level at 12 h and increased at 24 h
TLR4 signaling pathways and Toll-like receptors (TLRs) 1/2 and TLR3 signaling pathways were involved in transcriptional regulation of TMC3AS1, which suggested that TMC3-AS1 may play essential roles in the innate immune system
Summary
The innate immune system is the primary barrier to microbial pathogens [1]. Macrophages and epithelial cells, with importance in the innate immune defense, are equipped with specific pathogen pattern recognition receptors (PRRs), functionally to recognize pathogen-associated molecular patterns, against pathogens causing infection [2, 3]. The Toll-like receptors (TLRs) are classic PRRs. Response to specific pathogen recognition, TLRs recruit adaptor proteins and activate specific signaling cascades, such as nuclear factor kappa-B (NF-κB) signaling, to regulate the transcription of inflammatory genes, involved in antimicrobial host response [3,4,5,6,7]. Inflammatory factors produced by immune cells mediate the inflammatory response, which is under the tight regulation to orchestrate the development of complex gene expression programs [1, 3, 4, 8]. The TMC3-AS1 Modulates Inflammatory Responses potential molecular mechanisms of lncRNAs in the regulation of inflammatory genes expression are still largely unknown
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