Aging but not dietary restriction alters the activation‐induced apoptosis in rat T cells

Pahlavani, Mohammad A.; Vargas, Daniel A.

doi:10.1016/s0014-5793(01)02184-6

Cited by 26 publications

(13 citation statements)

References 57 publications

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“…There have been some reports of increased apoptosis of peripheral blood T-cells with increasing age [21]. To investigate this possibility the control group was divided into two age categories, those aged ,50 yrs and those aged 55-70 yrs.…”

Section: Effect Of Age On Apoptosis Of Airway-derived T-cells and Epimentioning

confidence: 99%

Increased airway epithelial and T-cell apoptosis in COPD remains despite smoking cessation

Hodge

Hodge²,

Holmes³

et al. 2005

Eur Respir J

224

173

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There is heterogeneity in the propensity of smokers to develop chronic obstructive pulmonary disease (COPD), and improved treatment strategies are hindered by limited understanding of COPD pathogenesis, especially as distinct from the effects of smoking per se. Although apoptosis is essential for tissue homeostasis, increased apoptosis may cause tissue damage and inflammation.This study addressed whether airway T-lymphocytes and airway epithelial cells (AEC) show an increased likelihood of undergoing apoptosis in COPD and if this was related to smoking. Apoptosis (7-amino-actinomycin D, Annexin, single-stranded DNA and caspase), Bcl-2, Bax and p53 were assessed in cells obtained from bronchial bushing and bronchoalveolar lavage from exand continuing smokers with COPD, and nonsmoking controls, using flow cytometry.A mean 87% increase in apoptosis of AEC and a 103% increase in T-lymphocyte apoptosis were found in COPD. There were no significant differences in apoptosis of AEC between current and ex-smokers with COPD.Apoptosis may contribute to chronic obstructive pulmonary disease pathogenesis, and continued excess apoptosis after smoking cessation may offer a new target for therapeutic interventions. Whether the persistence of increased apoptosis after smoking cessation results from changes in the pulmonary milleau after years of noxious insult, or whether some individuals have a natural predisposition toward increased apoptosis and possible development of chronic obstructive pulmonary disease remains to be determined.

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Section: Effect Of Age On Apoptosis Of Airway-derived T-cells and Epimentioning

confidence: 99%

Increased airway epithelial and T-cell apoptosis in COPD remains despite smoking cessation

Hodge

Hodge²,

Holmes³

et al. 2005

Eur Respir J

224

173

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Section: Mip-1b Gm-csf Tnf-␣ Il-2 Il-4 and Egr2 Exhibited The Himentioning

confidence: 99%

“…Old T cells have been shown to be more susceptible to apoptosis (27,28). Several factors have been shown to be involved in higher susceptibility of old T cells to apoptosis including increased expression of Fas/ Fasl,TRADD (TNF receptor-associated death domain), FADD (Fas-associated death domain), and Bax, and decreased expression of Bcl2, TRAF-2, and TNF-RII (27). An increased expression of Fas, Fasl, and Bax and a decreased expression of Bcl2 expression were observed with aging in human peripheral blood lymphocytes (28), and an increased protein expression of p53, Bax, and caspase-3 with aging was reported in splenocytes from rats (29).…”

Section: Mip-1b Gm-csf Tnf-␣ Il-2 Il-4 and Egr2 Exhibited The Himentioning

confidence: 99%

Age and Vitamin E-Induced Changes in Gene Expression Profiles of T Cells

Han

Adolfsson

Lee

et al. 2006

The Journal of Immunology

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T cells are vulnerable to age-associated changes. Vitamin E has been shown to improve T cell functions in the old. We studied gene expression profiles of T cells to better understand the underlying mechanisms of age and vitamin E-induced changes in T cell function. Young and old C57BL mice were fed diets containing 30 (control) or 500 (supplemented) ppm of vitamin E for 4 wks. Gene expression profiles of T cells were assessed using microarray analysis with/without anti-CD3/anti-CD28 stimulation. Genes associated with cytokines/chemokines, transcriptional regulation, signal transduction, cell cycle, and apoptosis were significantly up-regulated upon stimulation. Higher SOCS3 and lower growth factor independent 1 (Gfi-1) expression in old T cells may contribute to age-associated decline in proliferation. Higher Gadd45 and lower Bcl2 expression may contribute to increased apoptosis in old T cells. Vitamin E supplementation resulted in higher expression of genes involved in cell cycle regulation (Ccnb2, Cdc2, Cdc6) in old T cells. Vitamin E supplementation resulted in higher up-regulation of IL-2 expression in young and old T cells and lower up-regulation of IL-4 expression in old T cells following stimulation. These findings suggest that aging has significant effects on the expression of genes associated with signal transduction, transcriptional regulation, and apoptosis pathways in T cells, and vitamin E has a significant impact on the expression of genes associated with cell cycle and Th1/Th2 balance in old T cells. Further studies are needed to determine whether these changes are due to the effects of aging at a single-cell level or to the shift in the ratio of naïve:memory T cells with age.

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“…When food resources are limited in group-housed animals, the hierarchy of the animals has a strong influence on the amount of food consumed by each individual. Even cannibalism has been reported in group-housed rats with DR. 25,26 Several attempts have been made to address these issues. Diet composition can be modified to provide health benefits even if the food is available AL.…”

mentioning

confidence: 99%

The diet board: welfare impacts of a novel method of dietary restriction in laboratory rats

Kasanen¹,

Inhilä²,

Vainio³

et al. 2009

Lab Anim

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Laboratory rats are commonly fed ad libitum (AL). Moderate dietary restriction (DR) decreases mortality and morbidity when compared with AL feeding, but there are several obstacles to the implementation of DR. Traditional methods of restricted feeding disrupt normal diurnal eating rhythms and are not compatible with group housing. We have designed a novel method, the diet board, to restrict the feeding of group-housed rats. Animals fed from the diet board had 15% lower body weight than the AL-fed animals at the age of 17 weeks. The welfare effects of diet board feeding were assessed by comparing the stress physiology of diet board fed animals with that of AL-fed animals. Diet board feeding was associated with higher serum corticosterone levels and lower faecal secretion of IgA, suggesting the diet board causes a stress reaction. However, the ALfed group had larger adrenal glands with higher adrenaline and noradrenaline content than the diet board animals. No gastric ulcers were found in any of the animals at necropsy. The diet board thus appears to cause a stress reaction when compared with AL-fed rats, but no apparent pathology was associated with this reaction. The diet board could help to solve the health problems associated with AL feeding, while allowing the rats to be group-housed and to maintain their normal diurnal eating rhythms. The diet board can also be seen as a functional cage furniture item, dividing the cage into compartments and thus increasing the structural complexity of the environment. In conclusion, the diet board appears to possess refinement potential compared with traditional methods of DR.

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Aging but not dietary restriction alters the activation‐induced apoptosis in rat T cells

Cited by 26 publications

References 57 publications

Increased airway epithelial and T-cell apoptosis in COPD remains despite smoking cessation

Increased airway epithelial and T-cell apoptosis in COPD remains despite smoking cessation

Age and Vitamin E-Induced Changes in Gene Expression Profiles of T Cells

The diet board: welfare impacts of a novel method of dietary restriction in laboratory rats

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