| First Author | Shin MW | Year | 2016 |
| Journal | Int J Oncol | Volume | 48 |
| Issue | 2 | Pages | 821-8 |
| PubMed ID | 26677008 | Mgi Jnum | J:304581 |
| Mgi Id | MGI:6695680 | Doi | 10.3892/ijo.2015.3296 |
| Citation | Shin MW, et al. (2016) Ninjurin1 regulates lipopolysaccharide-induced inflammation through direct binding. Int J Oncol 48(2):821-8 |
| abstractText | Ninjurin1 is a transmembrane protein involved in macrophage migration and adhesion during inflammation. It was recently reported that repression of Ninjurin1 attenuated the lipopolysaccharide (LPS)-induced inflammatory response in macrophages; however, the precise mechanism by which Ninjurin1 modulates LPS-induced inflammation remains poorly understood. In the present study, we found that the interaction between Ninjurin1 and LPS contributed to the LPS-induced inflammatory response. Notably, pull-down assays using lysates from HEK293T cells transfected with human or mouse Ninjurin1 and biotinylated LPS (LPS-biotin) showed that LPS directly bound Ninjurin1. Subsequently, LPS binding assays with various truncated forms of Ninjurin1 protein revealed that amino acids (aa) 81-100 of Ninjurin1 were required for LPS binding. In addition, knockdown experiments using Ninj1 siRNA resulted in decreased nitric oxide (NO) and tumor necrosis factor-alpha (TNFalpha) secretion upon LPS treatment in Raw264.7 cells. Collectively, our results suggest that Ninjurin1 regulates the LPS-induced inflammatory response through its direct binding to LPS, thus, identifying Ninjurin1 as a putative target for the treatment of inflammatory diseases, such as sepsis and inflammation-associated carcinogenesis. |
