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Impaired genome maintenance suppresses the growth hormone--insulin-like growth factor 1 axis in mice with Cockayne syndrome

van der Pluijm, Ingrid ; Garinis, George A ; Brandt, Renata M C ; Gorgels, Theo G M F ; Wijnhoven, Susan W ; Diderich, Karin E M ; de Wit, Jan ; Mitchell, James R ; van Oostrom, Conny ; Beems, Rudolf ; Niedernhofer, Laura J ; Velasco, Susana ; Friedberg, Errol C ; Tanaka, Kiyoji ; van Steeg, Harry ; Hoeijmakers, Jan H J ; van der Horst, Gijsbertus T J Cooper, Priscilla

PLoS biology, 2007-01, Vol.5 (1), p.e2-e2 [Periódico revisado por pares]

United States: Public Library of Science

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Título:
Impaired genome maintenance suppresses the growth hormone--insulin-like growth factor 1 axis in mice with Cockayne syndrome
Autor: van der Pluijm, Ingrid ; Garinis, George A ; Brandt, Renata M C ; Gorgels, Theo G M F ; Wijnhoven, Susan W ; Diderich, Karin E M ; de Wit, Jan ; Mitchell, James R ; van Oostrom, Conny ; Beems, Rudolf ; Niedernhofer, Laura J ; Velasco, Susana ; Friedberg, Errol C ; Tanaka, Kiyoji ; van Steeg, Harry ; Hoeijmakers, Jan H J ; van der Horst, Gijsbertus T J
Cooper, Priscilla
Assuntos: Age ; Aging ; Animals ; Antioxidants - pharmacology ; Cockayne Syndrome - etiology ; Cockayne Syndrome - genetics ; Computational Biology ; Defects ; Deoxyribonucleic acid ; Diabetes and Endocrinology ; Diethylhexyl Phthalate - pharmacology ; DNA ; DNA damage ; DNA Repair ; DNA Repair Enzymes - genetics ; DNA-Binding Proteins - genetics ; Experiments ; Fatty Acids - biosynthesis ; Genetics and Genomics ; Genome - genetics ; Genomes ; Geriatrics ; Glucose - metabolism ; Growth Hormone - genetics ; Hypotheses ; Insulin-Like Growth Factor I - genetics ; Insulin-Like Growth Factor I - metabolism ; Insulin-like growth factors ; Liver - metabolism ; Male ; Mammals ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mus (Mouse) ; Oxidative stress ; Poly-ADP-Ribose Binding Proteins ; Proteins ; Radiation, Ionizing ; Rodents ; Somatotrophs - metabolism ; Xeroderma Pigmentosum Group A Protein - genetics
É parte de: PLoS biology, 2007-01, Vol.5 (1), p.e2-e2
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Descrição: Cockayne syndrome (CS) is a photosensitive, DNA repair disorder associated with progeria that is caused by a defect in the transcription-coupled repair subpathway of nucleotide excision repair (NER). Here, complete inactivation of NER in Csb(m/m)/Xpa(-/-) mutants causes a phenotype that reliably mimics the human progeroid CS syndrome. Newborn Csb(m/m)/Xpa(-/-) mice display attenuated growth, progressive neurological dysfunction, retinal degeneration, cachexia, kyphosis, and die before weaning. Mouse liver transcriptome analysis and several physiological endpoints revealed systemic suppression of the growth hormone/insulin-like growth factor 1 (GH/IGF1) somatotroph axis and oxidative metabolism, increased antioxidant responses, and hypoglycemia together with hepatic glycogen and fat accumulation. Broad genome-wide parallels between Csb(m/m)/Xpa(-/-) and naturally aged mouse liver transcriptomes suggested that these changes are intrinsic to natural ageing and the DNA repair-deficient mice. Importantly, wild-type mice exposed to a low dose of chronic genotoxic stress recapitulated this response, thereby pointing to a novel link between genome instability and the age-related decline of the somatotroph axis.
Editor: United States: Public Library of Science
Idioma: Inglês

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Impaired genome maintenance suppresses the growth hormone--insulin-like growth factor 1 axis in mice with Cockayne syndrome

United States: Public Library of Science

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