scholarly journals Neuronal Expression of GalNAc Transferase Is Sufficient to Prevent the Age-Related Neurodegenerative Phenotype of Complex Ganglioside-Deficient Mice

2014 ◽  
Vol 34 (3) ◽  
pp. 880-891 ◽  
Author(s):  
Denggao Yao ◽  
Rhona McGonigal ◽  
Jennifer A. Barrie ◽  
Joanna Cappell ◽  
Madeleine E. Cunningham ◽  
...  
Keyword(s):  
Age Related ◽  
Neuronal Expression ◽  
Complex Ganglioside ◽  
Deficient Mice

scholarly journals A low glycemic diet protects disease-prone Nrf2-deficient mice against age-related macular degeneration

2020 ◽  
Vol 150 ◽  
pp. 75-86 ◽  
Author(s):  
Sheldon Rowan ◽  
Shuhong Jiang ◽  
Min-Lee Chang ◽  
Jonathan Volkin ◽  
Christa Cassalman ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Age Related Macular Degeneration ◽  
Age Related ◽  
Deficient Mice

scholarly journals Immunological protein expression profile in Ccl2/Cx3cr1 deficient mice with lesions similar to age-related macular degeneration

2008 ◽  
Vol 86 (4) ◽  
pp. 675-683 ◽  
Author(s):  
Robert J. Ross ◽  
Min Zhou ◽  
Defen Shen ◽  
Robert N. Fariss ◽  
Xiaoyan Ding ◽  
...  
Keyword(s):  
Protein Expression ◽  
Macular Degeneration ◽  
Expression Profile ◽  
Age Related Macular Degeneration ◽  
Protein Expression Profile ◽  
Age Related ◽  
Deficient Mice

scholarly journals Accelerated Features of Age-Related Bone Loss in Zmpste24 Metalloproteinase-Deficient Mice

2009 ◽  
Vol 64A (10) ◽  
pp. 1015-1024 ◽  
Author(s):  
D. Rivas ◽  
W. Li ◽  
R. Akter ◽  
J. E. Henderson ◽  
G. Duque
Keyword(s):  
Bone Loss ◽  
Age Related ◽  
Deficient Mice

scholarly journals Collagen peptide and vitamin C additively attenuate age-related skin atrophy inSod1-deficient mice

2014 ◽  
Vol 78 (7) ◽  
pp. 1212-1220 ◽  
Author(s):  
Shuichi Shibuya ◽  
Yusuke Ozawa ◽  
Toshihiko Toda ◽  
Kenji Watanabe ◽  
Chisa Tometsuka ◽  
...  
Keyword(s):  
Vitamin C ◽  
Skin Atrophy ◽  
Collagen Peptide ◽  
Age Related ◽  
Deficient Mice

scholarly journals Immune-Deficient Pfp/Rag2-/- Mice Featured Higher Adipose Tissue Mass and Liver Lipid Accumulation with Growing Age than Wildtype C57BL/6N Mice

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 775 ◽  
Author(s):  
Winkler ◽  
Hempel ◽  
Hsu ◽  
Gericke ◽  
Kühne ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Lipid ◽  
Isolated Hepatocytes ◽  
Culture Conditions ◽  
Innate Immune ◽  
Lipid Storage ◽  
Tissue Mass ◽  
Age Related ◽  
Adipose Tissue Mass ◽  
Deficient Mice

Aging is a risk factor for adipose tissue dysfunction, which is associated with inflammatory innate immune mechanisms. Since the adipose tissue/liver axis contributes to hepatosteatosis, we sought to determine age-related adipose tissue dysfunction in the context of the activation of the innate immune system fostering fatty liver phenotypes. Using wildtype and immune-deficient mice, we compared visceral adipose tissue and liver mass as well as hepatic lipid storage in young (ca. 14 weeks) and adult (ca. 30 weeks) mice. Adipocyte size was determined as an indicator of adipocyte function and liver steatosis was quantified by hepatic lipid content. Further, lipid storage was investigated under normal and steatosis-inducing culture conditions in isolated hepatocytes. The physiological age-related increase in body weight was associated with a disproportionate increase in adipose tissue mass in immune-deficient mice, which coincided with higher triglyceride storage in the liver. Lipid storage was similar in isolated hepatocytes from wildtype and immune-deficient mice under normal culture conditions but was significantly higher in immune-deficient than in wildtype hepatocytes under steatosis-inducing culture conditions. Immune-deficient mice also displayed increased inflammatory, adipogenic, and lipogenic markers in serum and adipose tissue. Thus, the age-related increase in body weight coincided with an increase in adipose tissue mass and hepatic steatosis. In association with a (pro-)inflammatory milieu, aging thus promotes hepatosteatosis, especially in immune-deficient mice.

scholarly journals CCR 2 + monocytes infiltrate atrophic lesions in age‐related macular disease and mediate photoreceptor degeneration in experimental subretinal inflammation in Cx3cr1 deficient mice

2013 ◽  
Vol 5 (11) ◽  
pp. 1775-1793 ◽  
Author(s):  
Florian Sennlaub ◽  
Constance Auvynet ◽  
Bertrand Calippe ◽  
Sophie Lavalette ◽  
Lucie Poupel ◽  
...  
Keyword(s):  
Photoreceptor Degeneration ◽  
Macular Disease ◽  
Age Related ◽  
Deficient Mice

scholarly journals Impact of telomerase ablation on organismal viability, aging, and tumorigenesis in mice lacking the DNA repair proteins PARP-1, Ku86, or DNA-PKcs

2004 ◽  
Vol 167 (4) ◽  
pp. 627-638 ◽  
Author(s):  
Silvia Espejel ◽  
Peter Klatt ◽  
Josiane Ménissier-de Murcia ◽  
Juan Martín-Caballero ◽  
Juana M. Flores ◽  
...  
Keyword(s):  
Dna Repair ◽  
Aging Process ◽  
Telomere Shortening ◽  
Age Related ◽  
Dna Repair Proteins ◽  
Telomere Function ◽  
Telomere Capping ◽  
The Impact ◽  
Parp 1 ◽  
Deficient Mice

The DNA repair proteins poly(ADP-ribose) polymerase-1 (PARP-1), Ku86, and catalytic subunit of DNA-PK (DNA-PKcs) have been involved in telomere metabolism. To genetically dissect the impact of these activities on telomere function, as well as organismal cancer and aging, we have generated mice doubly deficient for both telomerase and any of the mentioned DNA repair proteins, PARP-1, Ku86, or DNA-PKcs. First, we show that abrogation of PARP-1 in the absence of telomerase does not affect the rate of telomere shortening, telomere capping, or organismal viability compared with single telomerase-deficient controls. Thus, PARP-1 does not have a major role in telomere metabolism, not even in the context of telomerase deficiency. In contrast, mice doubly deficient for telomerase and either Ku86 or DNA-PKcs manifest accelerated loss of organismal viability compared with single telomerase-deficient mice. Interestingly, this loss of organismal viability correlates with proliferative defects and age-related pathologies, but not with increased incidence of cancer. These results support the notion that absence of telomerase and short telomeres in combination with DNA repair deficiencies accelerate the aging process without impacting on tumorigenesis.

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