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Title: Nrf2 null enhances UVB-induced skin inflammation and extracellular matrix damages
Authors: Saw, C.L.L 
Yang, A.Y
Huang, M.-T
Liu, Y
Lee, J.H
Khor, T.O
Su, Z.-Y
Shu, L
Lu, Y
Conney, A.H
Kong, A.N.T
Issue Date: 2014
Citation: Saw, C.L.L, Yang, A.Y, Huang, M.-T, Liu, Y, Lee, J.H, Khor, T.O, Su, Z.-Y, Shu, L, Lu, Y, Conney, A.H, Kong, A.N.T (2014). Nrf2 null enhances UVB-induced skin inflammation and extracellular matrix damages. Cell and Bioscience 4 (1) : 39. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Nrf2 plays a critical role in defending against oxidative stress and inflammation. We previously reported that Nrf2 confers protection against ultraviolet-B (UVB)-induced inflammation, sunburn reaction, and is involved in sulforaphane-mediated photo-protective effects in the skin. In this study, we aimed to demonstrate the protective role of Nrf2 against inflammation-mediated extracellular matrix (ECM) damage induced by UVB irradiation. Ear biopsy weights were significantly increased in both Nrf2 wild-type (Nrf2 WT) and knockout (Nrf2 KO) mice one week after UVB irradiation. However, these weights increased more significantly in KO mice compared to WT mice, suggesting a greater inflammatory response in KO mice. In addition, we analyzed the protein expression of numerous markers, including macrophage inflammatory protein-2 (MIP-2), pro-matrix metalloproteinase-9 (MMP-9), and p53. p53, a regulator of DNA repair, was overexpressed in Nrf2 KO mice, indicating that the absence of Nrf2 led to more sustained DNA damage. There was also more substantial ECM degradation and increased inflammation in UVB-irradiated Nrf2 KO mice compared to UVB-irradiated WT mice. Furthermore, the protective effects of Nrf2 in response to UVB irradiation were mediated by increased HO-1 protein expression. Collectively, our results show that Nrf2 plays a key role in protecting against UVB irradiation and that the photo-protective effect of Nrf2 is closely related to the inhibition of ECM degradation and inflammation. © 2014 Saw et al.; licensee BioMed Central Ltd.
Source Title: Cell and Bioscience
ISSN: 20453701
DOI: 10.1186/2045-3701-4-39
Rights: Attribution 4.0 International
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