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Publication : Premature skin aging features rescued by inhibition of NADPH oxidase activity in XPC-deficient mice.

First Author  Hosseini M Year  2015
Journal  J Invest Dermatol Volume  135
Issue  4 Pages  1108-1118
PubMed ID  25437426 Mgi Jnum  J:220043
Mgi Id  MGI:5632062 Doi  10.1038/jid.2014.511
Citation  Hosseini M, et al. (2015) Premature Skin Aging Features Rescued by Inhibition of NADPH Oxidase Activity in XPC-Deficient Mice. J Invest Dermatol 135(4):1108-18
abstractText  Xeroderma pigmentosum type C (XP-C) is characterized mostly by a predisposition to skin cancers and accelerated photoaging, but little is known about premature skin aging in this disease. By comparing young and old mice, we found that the level of progerin and p16(INK4a) expression, beta-galactosidase activity, and reactive oxygen species, which increase with age, were higher in young Xpc(-/-) mice than in young Xpc(+/+) ones. The expression level of mitochondrial complexes and mitochondrial functions in the skin of young Xpc(-/-) was as low as in control aged Xpc(+/+)animals. Furthermore, the metabolic profile in young Xpc(-/-) mice resembled that found in aged Xpc(+/+) mice. Furthermore, premature skin aging features in young Xpc(-/-) mice were mostly rescued by inhibition of nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1) activity by using a NOX1 peptide inhibitor, suggesting that the continuous oxidative stress due to overactivation of NOX1 has a causative role in the underlying pathophysiology.
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