| First Author | Han X | Year | 2019 |
| Journal | Sci Adv | Volume | 5 |
| Issue | 12 | Pages | eaax9230 |
| PubMed ID | 31844669 | Mgi Jnum | J:285275 |
| Mgi Id | MGI:6393226 | Doi | 10.1126/sciadv.aax9230 |
| Citation | Han X, et al. (2019) LncRNA PTPRE-AS1 modulates M2 macrophage activation and inflammatory diseases by epigenetic promotion of PTPRE. Sci Adv 5(12):eaax9230 |
| abstractText | Long noncoding RNAs (lncRNAs) are important regulators of diverse biological processes; however, their function in macrophage activation is undefined. We describe a new regulatory mechanism, where an unreported lncRNA, PTPRE-AS1, targets receptor-type tyrosine protein phosphatase epsilon (PTPRE) to regulate macrophage activation. PTPRE-AS1 was selectively expressed in IL-4-stimulated macrophages, and its knockdown promoted M2 macrophage activation via MAPK/ERK 1/2 pathway. In vivo, PTPRE-AS1 deficiency enhanced IL-4-mediated M2 macrophage activation and accelerated pulmonary allergic inflammation while reducing chemical-induced colitis. Mechanistically, PTPRE-AS1 bound WDR5 directly, modulating H3K4me3 of the PTPRE promoter to regulate PTPRE-dependent signaling during M2 macrophage activation. Further, the expression of PTPRE-AS1 and PTPRE was significantly lower in peripheral blood mononuclear cells from patients with allergic asthma. These results provide evidence supporting the importance of PTPRE-AS1 in controlling macrophage function and the potential utility of PTPRE-AS1 as a target for controlling inflammatory diseases. |
