Simultaneous determination of cell aging and ATP release from erythrocytes and its implications in type 2 diabetes

Subasinghe, Wasanthi; Spence, Dana M.

doi:10.1016/j.aca.2008.04.061

Cited by 47 publications

(53 citation statements)

References 32 publications

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“…Notably, ATP concentration in trophocytes and fat cells have also been shown to decrease with advancing age in worker bees reared in a thermostatic chamber at 34°C (Hsu and Chan 2011a), providing further support for the idea that young and old workers reared in a field hive can be used for studying aging. This decrease in ATP concentration in trophocytes and fat cells of older workers is also consistent with previous studies showing that ATP levels decrease with advancing age in the gastric mucosa and muscle of humans (Kawano et al 1991;Conley et al 2000;Petersen et al 2003;Gurd et al 2008), the blood and brains of mice (Jayachandran et al 2005;Joo et al 1999), the erythrocytes of rabbits (Subasinghe and Spence 2008) and cows (Bartosz et al 1982), and the hearts of rats (Guerrieri et al 1996). This finding is also consistent with the results of ΔΨm measurements reported in this study; as was the case for NAD + , a decrease in ΔΨm can result in a decrease in ATP concentration.…”

Section: δψMsupporting

confidence: 92%

Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera)

Chuang

Hsu

2012

AGE

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Trophocytes and fat cells in honeybees (Apis mellifera) have served as targets for cellular senescence studies, but mitochondrial energy utilization with advancing age in workers is unknown. In this study, mitochondrial energy utilization was evaluated in the trophocytes and fat cells of young and old workers reared in a field hive. The results showed that (1) mitochondrial density increased with advancing age; (2) mitochondrial membrane potential (ΔΨm), nicotinamide adenine dinucleotide oxidized form (NAD + ) concentration, adenosine triphosphate (ATP) concentration, and NAD + /nicotinamide adenine dinucleotide reduced form (NADH) ratio decreased with advancing age; and (3) the expression of NADH dehydrogenase 1 (ND1), ATP synthase, and voltage-dependent anion channel 1 (VDAC1) increased with advancing age, whereas ND1 and ATP synthase did not differ with advancing age after normalization to mitochondrial density and VDAC1. These results show that the trophocytes and fat cells of young workers have higher mitochondrial energy utilization efficiency than those of old workers and that aging results in a decline in mitochondrial energy utilization in the trophocytes and fat cells of worker honeybees.

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Section: δψMsupporting

confidence: 92%

Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera)

Chuang

Hsu

2012

AGE

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“…ATP concentration decreases with age in the gastric mucosa and muscle of humans (Kawano et al 1991;Gurd et al 2008), the blood and brain of mice (Jayachandran et al 2005;Joo et al 1999), the erythrocytes of rabbits (Subasinghe and Spence 2008) and cows (Bartosz et al 1982), and the heart of rats (Guerrieri et al 1996). Similarly, we have found that ATP concentration decreases with age in the trophocytes and oenocytes of worker bees (Hsu and Chan 2013;Chuang and Hsu 2013).…”

Section: Nad + Nadh and Atp Concentrationsmentioning

confidence: 52%

Mitochondrial energy utilization maintains young status in the trophocytes and oenocytes of old queen honeybees

Hsu

2015

Apidologie

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-The lifespans of queen honeybees (Apis mellifera ) are much longer than those of worker bees. Mitochondrial energy utilization in the trophocytes and oenocytes of worker bees during aging has been determined, but it remains unknown in queen bees. In this study, mitochondrial energy utilization was assayed in the trophocytes and oenocytes of young and old queen bees. The mitochondrial density and mitochondrial membrane potential (Δψm); nicotinamide adenine dinucleotide (NAD + ), nicotinamide adenine dinucleotide reduced form (NADH), and adenosine triphosphate (ATP) levels; NAD + /NADH ratio; and relative expression of NADH dehydrogenase 1 (ND1) and ATP synthase normalized against mitochondrial density were not significantly different between young and old queen bees. These results indicate that mitochondrial energy utilization maintains a young status in the trophocytes and oenocytes of old queen bees and that trophocytes and oenocytes have longevity-promoting mechanisms that can be investigated to clarify the secret of longevity in queen bees.

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“…The released ATP from RBCs, for example, binds and activates the purinergic G protein-coupled receptors (P2Y receptors) on vascular endothelial cells and induces the synthesis and release of nitric oxide (12,13), a well-known vasodilator. Moreover, impaired release of ATP from RBCs has been linked to diseases, such as type II diabetes and cystic fibrosis (14,15). Given that RBCs experience shear stresses continuously during the circulation cycle and that the released ATP plays a central role in vascular pathophysiology, understanding of the mechanotransductive release of ATP from RBCs will provide not only fundamental insights to the roles of RBCs in vascular homeostasis but also, potential therapeutic strategies for red cell dysfunction and vascular disease.…”

mentioning

confidence: 99%

Piezo1 regulates mechanotransductive release of ATP from human RBCs

Çinar

Zhou

DeCourcey

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

163

157

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Piezo proteins (Piezo1 and Piezo2) are recently identified mechanically activated cation channels in eukaryotic cells and associated with physiological responses to touch, pressure, and stretch. In particular, human RBCs express Piezo1 on their membranes, and mutations of Piezo1 have been linked to hereditary xerocytosis. To date, however, physiological functions of Piezo1 on normal RBCs remain poorly understood. Here, we show that Piezo1 regulates mechanotransductive release of ATP from human RBCs by controlling the shear-induced calcium (Ca 2+ ) influx. We find that, in human RBCs treated with Piezo1 inhibitors or having mutant Piezo1 channels, the amounts of shear-induced ATP release and Ca 2+ influx decrease significantly. Remarkably, a critical extracellular Ca 2+ concentration is required to trigger significant ATP release, but membrane-associated ATP pools in RBCs also contribute to the release of ATP. Our results show how Piezo1 channels are likely to function in normal RBCs and suggest a previously unidentified mechanotransductive pathway in ATP release. Thus, we anticipate that the study will impact broadly on the research of red cells, cellular mechanosensing, and clinical studies related to red cell disorders and vascular disease. Previous studies have shown that the addition of chemicals that stiffen RBC membranes decreases the amount of ATP released (9, 16), indicating that deformation of the cell membrane is a necessary trigger. In addition, biological mediators, such as cystic fibrosis transmembrane conductance regulator (CFTR) and pannexin-1 hemichannels, are involved in the release pathways of mechanotransductive ATP release from RBCs (9,14,17,18). Inhibition of CFTR leads to an impaired ATP release from deformed RBCs (14). Recent studies, including our previous findings, suggest that interactions between membrane-associated actin and CFTR play important roles in the mechanotransductive ATP release from RBCs (9, 17). Pannexin-1, however, is a channel-forming protein and has been suggested as a mechanosensing ATP release channel (18). Under osmotic stress, for example, ATP released from RBCs was attenuated by carbenoxolone, a highly effective pannexin channel blocker, suggesting that pannexin-1 might be one of the conductance channels responsible for the mechanotransductive release of ATP (18). Although progress has been made in understanding mechanotransductive ATP release from RBCs, many questions remain about the signal transduction pathways. For example, how does mechanical force transduce signals to ATP release channels? Are there any stretch-activated ion channels on RBCs that may sense mechanical forces and activate ATP release? If so, are there any secondary messengers that could be generated by mechanical stimuli and regulate ATP release?Piezo proteins (Piezo1 and Pizeo2) are recently identified mechanically activated cation channels in mammals (19,20) and can be fully activated without involvement of additional proteins (20, 21). Piezo-induced cationic currents were first observe...

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Simultaneous determination of cell aging and ATP release from erythrocytes and its implications in type 2 diabetes

Cited by 47 publications

References 32 publications

Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera)

Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera)

Mitochondrial energy utilization maintains young status in the trophocytes and oenocytes of old queen honeybees

Piezo1 regulates mechanotransductive release of ATP from human RBCs

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