| First Author | Do KK | Year | 2024 |
| Journal | iScience | Volume | 27 |
| Issue | 5 | Pages | 109694 |
| PubMed ID | 38660397 | Mgi Jnum | J:352343 |
| Mgi Id | MGI:7625070 | Doi | 10.1016/j.isci.2024.109694 |
| Citation | Do KK, et al. (2024) Conditional deletion of Zeb1 in Csf1r(+) cells reduces inflammatory response of the cornea to alkali burn. iScience 27(5):109694 |
| abstractText | ZEB1 is an essential factor in embryonic development. In adults, it is often highly expressed in malignant tumors with low expression in normal tissues. The major biological function of ZEB1 in developing embryos and progressing cancers is to transdifferentiate cells from an epithelial to mesenchymal phenotype; but what roles ZEB1 plays in normal adult tissues are largely unknown. We previously reported that the reduction of Zeb1 in monoallelic global knockout (Zeb1(+/-)) mice reduced corneal inflammation-associated neovascularization following alkali burn. To uncover the cellular mechanism underlying the Zeb1 regulation of corneal inflammation, we functionally deleted Zeb1 alleles in Csf1r(+) myeloid cells using a conditional knockout (cKO) strategy and found that Zeb1 cKO reduced leukocytes in the cornea after alkali burn. The reduction of immune cells was due to their increased apoptotic rate and linked to a Zeb1-downregulated apoptotic pathway. We conclude that Zeb1 facilitates corneal inflammatory response by maintaining Csf1r(+) cell viability. |
