| First Author | Wang L | Year | 2013 |
| Journal | J Biol Chem | Volume | 288 |
| Issue | 34 | Pages | 24363-71 |
| PubMed ID | 23843455 | Mgi Jnum | J:317578 |
| Mgi Id | MGI:6843434 | Doi | 10.1074/jbc.M113.458141 |
| Citation | Wang L, et al. (2013) Epidermal growth factor (EGF)-induced corneal epithelial wound healing through nuclear factor kappaB subtype-regulated CCCTC binding factor (CTCF) activation. J Biol Chem 288(34):24363-71 |
| abstractText | Epidermal growth factor (EGF) plays an important role in corneal epithelial migration and proliferation to improve the wound healing process. This study aimed to understand the role of NFkappaB in EGF-induced corneal epithelial wound healing through regulation of CTCF activity, which plays important roles in cell motility and migration to promote wound healing. The effect of NFkappaB p50 on corneal epithelial wound healing was investigated by comparing the eyes of wild-type and p50 knockout mice. We found that there was a significant retardation in corneal epithelial wound healing in the corneas of p50 knockout mice. Wound closure rates were measured in human corneal epithelial cells transfected with an NFkappaB activation-sensitive CTCF expression construct to demonstrate the effect of human CTCF expression under the control of EGF-induced NFkappaB activation on wound healing. EGF stimulation activated NFkappaB, which directly triggered the expression of the exogenous human CTCF in transfected cells and, subsequently, promoted human corneal epithelial cell motility, migration, and wound healing. Overexpression of CTCF in corneal epithelial cells and mouse corneas significantly enhanced the wound healing process. Furthermore, the effect of overexpressing NFkappaB p50 in corneal epithelial cells on the promotion of wound healing was abolished by knockdown of CTCF with CTCF-specific shRNA. Thus, a direct regulatory relationship between EGF-induced NFkappaB p50 and CTCF activation affecting corneal epithelial wound healing has been established, indicating that CTCF is, indeed, a NFkappaB p50-targeted and effective gene product in the core transcriptional network downstream from the growth factor-induced NFkappaB signaling pathway. |
