| First Author | Tan S | Year | 2019 |
| Journal | Cell Death Dis | Volume | 10 |
| Issue | 10 | Pages | 748 |
| PubMed ID | 31582729 | Mgi Jnum | J:293321 |
| Mgi Id | MGI:6452526 | Doi | 10.1038/s41419-019-1954-x |
| Citation | Tan S, et al. (2019) IL-6-driven FasL promotes NF-kappaBp65/PUMA-mediated apoptosis in portal hypertensive gastropathy. Cell Death Dis 10(10):748 |
| abstractText | Mucosal epithelial apoptosis with non-specific inflammation is an essential pathological characteristic in portal hypertensive gastropathy (PHG). However, whether a coordinated crosstalk between myeloid cells and epithelial cells involved in PHG remains unclear. IL-6, which is induced in the mucosa of PHG patients and mice, promotes FasL production via enhancing NF-kappaBp65 activation in myeloid cells, while blockage of IL-6 signaling by Tocilizumab or deletion of NF-kappaBp65 in myeloid cells attenuates the inflammatory response and Fas/FasL-mediated epithelial apoptosis in PHG. IL-6-driven FasL from myeloid cells combines with epithelial Fas receptor to encourage NF-kappaBp65/PUMA-mediated epithelial apoptosis in PHG, and inhibition of NF-kappaBp65 or knockout of PUMA alleviates Fas/FasL-mediated epithelial apoptosis in PHG. These results indicate that IL-6 drives FasL generation via NF-kappaBp65 in myeloid cells to promote Fas/NF-kappaBp65/PUMA-mediated epithelial apoptosis in PHG, and this coordinated crosstalk between myeloid cells and epithelial cells may provide a potential therapeutic target for PHG. |
