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Start Over Author "Rossignol R" Journal journal of investigative dermatology
4 results on '"Rossignol R"'

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

Author

Hosseini M, Mahfouf W, Serrano-Sanchez M, Raad H, Harfouche G, Bonneu M, Claverol S, Mazurier F, Rossignol R, Taieb A, and Rezvani HR

Subjects
Adaptor Proteins, Signal Transducing, Animals, Cyclin-Dependent Kinase Inhibitor p16 metabolism, Humans, Keratinocytes cytology, Lamin Type A, Light, Mice, Mice, Knockout, Mitochondria metabolism, NADPH Oxidase 1, Oxidative Stress, Proteins genetics, Reactive Oxygen Species metabolism, Xeroderma Pigmentosum metabolism, beta-Galactosidase metabolism, DNA-Binding Proteins genetics, NADH, NADPH Oxidoreductases antagonists & inhibitors, NADH, NADPH Oxidoreductases metabolism, Nuclear Proteins metabolism, Protein Precursors metabolism, Skin Aging
Abstract

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, β-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.

Published
2015
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