| First Author | Poon MW | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Pages | 41224 | PubMed ID | 28106169 |
| Mgi Jnum | J:261884 | Mgi Id | MGI:6158106 |
| Doi | 10.1038/srep41224 | Citation | Poon MW, et al. (2017) Inhibition of NUCKS Facilitates Corneal Recovery Following Alkali Burn. Sci Rep 7:41224 |
| abstractText | Corneal wound healing involves a complex cascade of cytokine-controlled cellular events, including inflammatory and angiogenesis responses that are regulated by transcriptional chromatin remodeling. Nuclear Ubiquitous Casein and cyclin-dependent Kinase Substrate (NUCKS) is a key chromatin modifier and transcriptional regulator of metabolic signaling. In this study, we investigated the role of NUCKS in corneal wound healing by comparing its effects on corneal alkali burn in NUCKS knockout (NKO) and NUCKS wild-type (NWT) mice. Our data showed that following alkali-injury, inhibition of NUCKS (NKO) accelerated ocular resurfacing and suppressed neovascularization; the cytokine profile of alkali burned corneas in NKO mice showed suppressed expression of inflammation cytokines (IL1A &IL1B); upregulated expression of antiangiogenic factor (Pigment Epithelium-derived Factor; PEDF); and downregulated expression of angiogenic factor (Vascular Endothelial Growth Factor, VEGF); in vitro, following LPS-induced NFkappaB activation, NKO corneal cells showed reduced expression of IL6, IP10 and TNFalpha. In vitro, corneal epithelial cells showed reduced NF-kappab activation on silencing of NUCKS and corresponding NFkappaB-mediated cytokine expression was reduced. Here, we illustrate that inhibition of NUCKS played a role in cytokine modulation and facilitated corneal recovery. This reveals a potential new effective strategy for ocular burn treatment. |
