Sphingomyelinase Activity Is Enhanced in Cerebral Cortex of Senescence-Accelerated Mouse-P/10 with Advancing Age

Kim, Sung Su; Kang, Mi Sun; Choi, Yoo Mi; Suh, Yoo‐Hun; Kim, Dae Kyong

doi:10.1006/bbrc.1997.7133

Cited by 19 publications

(9 citation statements)

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“…[17][18][19] LPS can induce intracellular ceramide generation, whereas ceramide and SMase mimic LPS action in murine Mφ. More important, age-related increase in brain and liver ceramide and neutral SMase levels has been reported, [20][21][22] suggesting that aging impacts ceramide synthesis. It is thus hypothesized that ceramide might mediate the age-associated increase in COX-2 expression and thus PGE 2 production.…”

Section: Cox-2 Expression With Agingmentioning

confidence: 98%

Nutrition and Age‐Associated Inflammation: Implications for Disease Prevention

Meydani

2008

J Parenter Enteral Nutr

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Accumulating evidence suggests that aging is associated with dysregulated immune and inflammatory responses. Investigation into the cellular and molecular mechanisms underlying this phenomenon suggests that an up-regulated cyclooxygenase (COX)-2 expression, and resulting increase in production of prostaglandin E(2) (PGE(2)), is a critical factor. Macrophages from old mice have significantly higher levels of PGE(2) production compared with those from young mice, a result of increased COX-2 expression and protein levels leading to increased COX enzyme activity. Furthermore, studies suggest that the age-associated increase in macrophage PGE(2) production is due to ceramide-induced up-regulation of nuclear factor-kappa B activation. Such processes may also occur in cell types other than macrophages, lending further insight into potential mechanisms of age-related diseases. Moreover, the excess PGE(2) induces harmful effects in other cell types such as T cells and adipocytes through the negative crosstalk between macrophages with other cells, resulting in further increased susceptibility to diseases. Nutrient/dietary medications, such as antioxidants and certain lipids have suggested a promising route to reduce the age-related increase in COX activity and PGE(2) production that is associated with several disease states.

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Section: Cox-2 Expression With Agingmentioning

confidence: 98%

Nutrition and Age‐Associated Inflammation: Implications for Disease Prevention

Meydani

2008

J Parenter Enteral Nutr

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“…Sphingomyelinase Kim et al [118] investigated agerelated changes in sphingomyelinase (SMase) in the cerebral cortex of SAMP10 and SAMR1 mice. The SMase activity increased uniquely in the membrane fraction, but not in the cytosolic fraction, of the cerebral cortex of SAMP10 mice with advancing age.…”

Section: Neuropathological Studiesmentioning

confidence: 99%

“…Studies on the changes in protein and gene expression in the brains of SAMP10 mice were reported as shown above [116][117][118][119]121]. Carter et al [104] also examined the gene expression in the hippocampus and retina of SAMP10 mice and found a mutation in a fibroblast growth factor, Fgf 1, resulting in a nonsense codon in the predicted amino acid sequence.…”

Section: Protein and Gene Expression Studiesmentioning

confidence: 99%

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice

Takeda¹

2009

Neurochem Res

217

188

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The SAM strains, a group of related inbred strains consisting of senescence-prone inbred strains (SAMP) and senescence-resistant inbred strains (SAMR), have been successfully developed by selective inbreeding of the AKR/J strain of mice donated by the Jackson laboratory in 1968. The characteristic feature of aging common to the SAMP and SAMR is accelerated senescence and normal aging, respectively. Furthermore, SAMP and SAMR strains of mice manifest various pathobiological phenotypes spontaneously. Among SAMP strains, SAMP8 and SAMP10 mice show age-related behavioral deterioration such as deficits in learning and memory, emotional disorders (reduced anxiety-like behavior and depressive behavior) and altered circadian rhythm associated with certain pathological, biochemical and pharmacological changes. Here, the previous and recent literature on SAM mice are reviewed with an emphasis on SAMP8 and SAMP10 mice. A spontaneous model like SAM with distinct advantages over the gene-modified model is hoped by investigators to be used more widely as a biogerontological resource to explore the etiopathogenesis of accelerated senescence and neurodegenerative disorders.

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“…The subcellular localization of the increases in the hippocampal APP in aged SAMP10 remains to be elucidated. Kim et al (1997) examined the activity of sphingomyelinase in SAMR1 and SAMP10 brains. This is a key enzyme producing a lipid second messenger, ceramide, which induces a variety of antiproliferative responses including apoptosis, cell cycle arrest, and aging.…”

Section: Introductionmentioning

confidence: 99%