PubMed · 13758596
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M LAMY, J FREZAL, C NEZELOF, RAVERDY. 1961. [Acrogeria].. https://pubmed.ncbi.nlm.nih.gov/13758596/
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During the past decades, several cellular pathways have been discovered to be connected with the ageing process. These pathways, which either suppress or enhance the ageing process, include regulation of the insulin/growth hormone axis, pathways involved with caloric restriction, ROS metabolism and DNA repair. In this review, we will provide a comprehensive overview of cancer and/or accelerated ageing pathologies associated with defects in the multi-step nucleotide excision repair pathway. Moreover, we will discuss evidence suggesting that there is a causative link between transcription-coupled repair and ageing.
TRF2 is a telomere-binding protein that has a role in telomere protection. We generated mice that overexpress TRF2 in the skin. These mice had a severe phenotype in the skin in response to light, consisting of premature skin deterioration, hyperpigmentation and increased skin cancer, which resembles the human syndrome xeroderma pigmentosum. Keratinocytes from these mice were hypersensitive to ultraviolet irradiation and DNA crosslinking agents. The skin cells of these mice had marked telomere shortening, loss of the telomeric G-strand overhang and increased chromosomal instability. Telomere loss in these mice was mediated by XPF, a structure-specific nuclease involved in ultraviolet-induced damage repair and mutated in individuals with xeroderma pigmentosum. These findings suggest that TRF2 provides a crucial link between telomere function and ultraviolet-induced damage repair, whose alteration underlies genomic instability, cancer and aging. Finally, we show that a number of human skin tumors have increased expression of TRF2, further highlighting a role for TRF2 in skin cancer.
The species-typical behaviors have been extensively studied, especially in the rodents. But little is known about whether the aging impacts on these species-typical behaviors. In the present study, the species-typical behaviors, including burrowing, hoarding and nesting, were assessed in the accelerated senescence-prone mouse 8 (SAMP8, P8) and the control strain senescence-resistant mouse 1 (SAMR1, R1). Total 147 SAM mice including 74 P8 mice and 73 R1 mice were grouped according to the age, 3, 7 and 11 months, respectively. In the hoarding test, an age-related increase was observed in the both P8 and R1 mice, whereas in the burrowing task, the age-related increment only took place in the P8 mice. The nesting ability in the P8 mice at different ages was inferior to that in the age-matched R1 mice, and the 3-month P8 mice showed the poorest nesting ability. The principal component analysis revealed that the burrowing, hoarding and nesting tests detected the different aspects of species-typical behaviors respectively for all mice combined. Our findings indicated that all tasks of hoarding, burrowing and nesting could detect the aging effect in the P8 mice, whereas, only the hoarding test could detect the aging effect in the R1 mice. These different species-typical behaviors were dissociable.