Nuclear Factor-κB: Central Regulator in Ocular Surface Inflammation and Diseases

Abstract The nuclear factor-κB (NF-κB) is a key transcription factor pathway that is responsible for many key biological processes, such as inflammation, apoptosis, stress response, corneal wound healing, angiogenesis, and lymphangiogenesis. Numerous recent studies have investigated NF-κB in the con...

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Bibliographic Details
Published in:The ocular surface 2012-07, Vol.10 (3), p.137-148
Main Authors: Lan, Wanwen, BSc, Petznick, Andrea, PhD, Heryati, Suzi, MD, Rifada, Maula, MD, Tong, Louis, FRCS, PhD
Format: Article
Language:English
Subjects:
angiogenesis
apoptosis
Conjunctivitis - metabolism
Epithelial Cells - metabolism
Humans
inflammation
Keratitis - metabolism
NF-kappa B - physiology
NF-κB
Ophthalmology
signal transduction
Signal Transduction - physiology
Toll-Like Receptors - metabolism
transcription factors
wound healing
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Summary:Abstract The nuclear factor-κB (NF-κB) is a key transcription factor pathway that is responsible for many key biological processes, such as inflammation, apoptosis, stress response, corneal wound healing, angiogenesis, and lymphangiogenesis. Numerous recent studies have investigated NF-κB in the context of ocular surface disorders, including chemical injury, ultraviolet radiation-induced injury, microbial infections, allergic eye diseases, dry eye, pterygium, and corneal graft rejection. The purpose this article is to summarize key findings with regard to the pathways regulating NF-κB and processes governed by the NF-κB pathway. In the innate defense system, NF-κB is involved in signaling from the toll-like receptors 2, 3, 4, 5 and 7, which are expressed in conjunctival, limbal, and corneal epithelial cells. These determine the ocular responses to infections, such as those caused by Pseudomonas aeruginosa, Staphylococcus aureus , adenovirus, and herpes simplex-1 virus. Natural angiogenic inhibitors enhance NF-κB, and this may occur through the mitogen-activated protein kinases and peroxisome proliferator-activated receptor γ. In alkali injury, inhibition of NF-κB can reduce corneal angiogenesis, suggesting a possible therapeutic strategy. The evaluation of NF-κB inhibitors in diseases is also discussed, including emodin, besifloxacin, BOL-303242-X (mapracorat), thymosin-β4, epigallocatechin gallate, Perilla frutescens leaf extract and IKKβ-targeting short interfering RNA.
ISSN:1542-0124
1937-5913
DOI:10.1016/j.jtos.2012.04.001