Human Polynucleotide Phosphorylase (
 hPNPase
 
 
 old-35
 )

Sarkar, Devanand; Lebedeva, Irina V.; Emdad, Luni; Kang, Dong Chul; Baldwin, Albert S.; Fisher, Paul B.

doi:10.1158/0008-5472.can-04-1772

Cited by 64 publications

(19 citation statements)

References 38 publications

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“…PNPase knockdown results in impaired mitochondrial membrane potential, which can readily affect fusion and fission (Chen et al, 2005). Interestingly, over expression of PNPase could also be harmful to cells, since it can cause increased production of ROS and inflammation (Sarkar et al, 2004). Thus, both up and down regulation of PNPase could impair cell function (Hayakawa and Sekiguchi, 2006).…”

Section: Discussionmentioning

confidence: 99%

The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle

Bori

Zhao

Koltai

et al. 2012

Experimental Gerontology

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Aging results in a significant decline in aerobic capacity and impaired mitochondrial function. We have tested the effects of moderate physical activity on aerobic capacity and a single bout of exercise on the expression profile of mitochondrial biogenesis, and fusion and fission related genes in skeletal muscle of human subjects. Physical activity attenuated the aging-associated decline in VO2 max (p<0.05). Aging increased and a single exercise bout decreased the expression of nuclear respiratory factor-1 (NRF1), while the transcription factor A (TFAM) expression showed a strong relationship with VO2max and increased significantly in the young physically active group. Mitochondrial fission representing FIS1 was induced by regular physical activity, while a bout of exercise decreased fusion-associated gene expression. The expression of polynucleotide phosphorylase (PNPase) changed inversely in young and old groups and decreased with aging. The A2 subunit of cyclic AMP-activated protein kinase (AMPK) was induced by a single bout of exercise in skeletal muscle samples of both young and old subjects (p<0.05). Our data suggest that moderate levels of regular physical activity increases a larger number of mitochondrial biogenesis-related gene expressions in young individuals than in aged subjects. Mitochondrial fission is impaired by aging and could be one of the most sensitive markers of the age-associated decline in the adaptive response to physical activity.

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Section: Discussionmentioning

confidence: 99%

The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle

Bori

Zhao

Koltai

et al. 2012

Experimental Gerontology

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“…IL-6 has been shown to be associated with DNA damage– and oncogenic stress–induced senescence of mouse and human keratinocytes, melanocytes, monocytes, fibroblasts, and epithelial cells (16, 18, 57, 58). Further, IL-6 secretion appears to be directly controlled by persistent DNA-damage signaling (ATM and CHK2), independent of the p53 pathway (59).…”

Section: The Secretory Phenotype Of Senescent Cellsmentioning

confidence: 99%

“…Most senescent cells overexpress IL-8 (CXCL-8) (see Figure 2 ), along with GROα and GROβ (CXCL-1 and -2; the murine CXCL-1 is named KC) (58, 66, 67). CCL family members that are generally upregulated in senescent cells include MCP-2, -4, and -1 (CCL-8, -13, and -2); HCC-4 (CCL-16); eotaxin-3 (CCL-26); and macrophage inflammatory protein (MIP)-3α and -1α (CCL-20, -3).…”

Section: The Secretory Phenotype Of Senescent Cellsmentioning

confidence: 99%

The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression

Coppé

Desprez

Krtolica

et al. 2010

Annu. Rev. Pathol. Mech. Dis.

4,006

3,705

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Cellular senescence is a tumor-suppressive mechanism that permanently arrests cells at risk for malignant transformation. However, accumulating evidence shows that senescent cells can have deleterious effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.

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“…Senescence, via adoption of a SASP, is therefore postulated to contribute to pathogenesis through the aberrant expression of genes and proteins associated with inflammation and tissue damage, including up-regulation of enzymes that induce ROS and activate NFκB [147]. Although the secretory phenotype of senescent hepatocytes remains unknown, studies in other cell types (such as fibroblasts) have demonstrated that senescent cells secrete a spectrum of proteins that have been previously implicated in the promotion of disease progression in NAFLD, including pro-inflammatory cytokines (e.g., IL-6, IL-8), matrix-degrading enzymes (e.g., MMPs), and other cell signalling molecules and growth factors important to liver disease (e.g., hepatocyte growth factor, platelet-derived growth factor and connective tissue growth factor).…”

Section: A Role For Hepatocyte Senescence In Disease Progressionmentioning

confidence: 99%

Evolving Concepts in the Pathogenesis of NASH: Beyond Steatosis and Inflammation

Peverill

Powell

Skoien

2014

IJMS

310

243

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Non-alcoholic steatohepatitis (NASH) is characterised by hepatic steatosis and inflammation and, in some patients, progressive fibrosis leading to cirrhosis. An understanding of the pathogenesis of NASH is still evolving but current evidence suggests multiple metabolic factors critically disrupt homeostasis and induce an inflammatory cascade and ensuing fibrosis. The mechanisms underlying these changes and the complex inter-cellular interactions that mediate fibrogenesis are yet to be fully elucidated. Lipotoxicity, in the setting of excess free fatty acids, obesity, and insulin resistance, appears to be the central driver of cellular injury via oxidative stress. Hepatocyte apoptosis and/or senescence contribute to activation of the inflammasome via a variety of intra- and inter-cellular signalling mechanisms leading to fibrosis. Current evidence suggests that periportal components, including the ductular reaction and expansion of the hepatic progenitor cell compartment, may be involved and that the Th17 response may mediate disease progression. This review aims to provide an overview of the pathogenesis of NASH and summarises the evidence pertaining to key mechanisms implicated in the transition from steatosis and inflammation to fibrosis. Currently there are limited treatments for NASH although an increasing understanding of its pathogenesis will likely improve the development and use of interventions in the future.

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Human Polynucleotide Phosphorylase ( hPNPase old-35 )

Abstract: ABSTRACT

Cited by 64 publications

References 38 publications

The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle

The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle

The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression

Evolving Concepts in the Pathogenesis of NASH: Beyond Steatosis and Inflammation

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