Inhibition of NUCKS Facilitates Corneal Recovery Following Alkali Burn View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Ming-Wai Poon, Dan Jiang, Peng Qin, Yuelin Zhang, Beiying Qiu, Sumit Chanda, Vinay Tergaonkar, Qing Li, Ian Y Wong, Zhendong Yu, Hung-Fat Tse, David S H Wong, Qizhou Lian

ABSTRACT

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 NFκB activation, NKO corneal cells showed reduced expression of IL6, IP10 and TNFα. In vitro, corneal epithelial cells showed reduced NF-κb activation on silencing of NUCKS and corresponding NFκB-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. More... »

PAGES

41224

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep41224

DOI

http://dx.doi.org/10.1038/srep41224

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053767119

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28106169


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