Adenosine-induced apoptosis in glomerular mesangial cells

Zhao, Zhihui; Kapoian, Toros; Shepard, Michelle; Lianos, Elias A.

doi:10.1046/j.1523-1755.2002.00256.x

Cited by 40 publications

(29 citation statements)

References 18 publications

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“…More recent studies using various cell types that implicate increased adenosine toxicity via increased SAH levels have employed comparable adenosine concentrations as used by us [24,[26][27][28][29]42]. The mechanism of action of adenosine appears to be via its ability to act as a substrate for as well as an inhibitor of SAH hydrolase thereby elevating intracellular SAH.…”

Section: Discussionmentioning

confidence: 99%

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Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: Protection by betaine

Kharbanda

Rogers²,

Mailliard

et al. 2005

Biochemical Pharmacology

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Previous studies from our laboratory have shown that ethanol consumption results in an increase in hepatocellular S-adenosylhomocysteine levels. Because S-adenosylhomocysteine is a potent inhibitor of methylation reactions, we propose that increased intracellular S-adenosylhomocysteine levels could be a major contributor to ethanol-induced pathologies. To test this hypothesis, hepatocytes isolated from rat livers were grown on collagen-coated plates in Williams' medium E containing 5% FCS and exposed to varying concentrations of adenosine in order to increase intracellular S-adenosylhomocysteine levels. We observed increases in caspase-3 activity following exposure to adenosine. This increase in caspase activity correlated with increases in intracellular S-adenosylhomocysteine levels and DNA hypoploidy. The adenosine-induced changes could be significantly attenuated by betaine administration. The mechanism of betaine action appeared to be via the methylation reaction catalyzed by betaine-homocysteine-methyltransferase. To conclude, our results indicate that the elevation of S-adenosylhomocysteine levels in the liver by ethanol is a major factor in altering methylation reactions and in increasing apoptosis in the liver. We conclude that ethanol-induced alteration in methionine metabolic pathways may play a crucial role in the pathologies associated with alcoholic liver injury and that betaine administration may have beneficial therapeutic effects. Published by Elsevier Inc.

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Section: Discussionmentioning

confidence: 99%

“…In recent years there have been reports of increased intracellular SAH levels inducing apoptosis in many different cell types [23][24][25][26][27][28][29]. Therefore, we put forth the hypothesis that increased intracellular SAH generation may be responsible for hepatocyte apoptosis seen after ethanol administration.…”

Section: Introductionmentioning

confidence: 95%

Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: Protection by betaine

Kharbanda

Rogers²,

Mailliard

et al. 2005

Biochemical Pharmacology

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“…A 2 receptors have been identified on human glomerular mesangial cells [350]. Adenosine activates mesangial cell proliferation [235], but can also induce apoptosis of mesangial cells [437]. High concentrations of glucose increase extracellular levels of ATP in mesangial cells, which in turn activates ERK1/2.…”

Section: Mesangial Cellsmentioning

confidence: 99%

Purinergic signalling in the kidney in health and disease

Burnstock

Evans

Bailey

2013

Purinergic Signalling

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The involvement of purinergic signalling in kidney physiology and pathophysiology is rapidly gaining recognition and this is a comprehensive review of early and recent publications in the field. Purinergic signalling involvement is described in several important intrarenal regulatory mechanisms, including tuboglomerular feedback, the autoregulatory response of the glomerular and extraglomerular microcirculation and the control of renin release. Furthermore, purinergic signalling influences water and electrolyte transport in all segments of the renal tubule. Reports about purine-and pyrimidine-mediated actions in diseases of the kidney, including polycystic kidney disease, nephritis, diabetes, hypertension and nephrotoxicant injury are covered and possible purinergic therapeutic strategies discussed.

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“…In these experiments, cells were treated with 10 μM of different adenine nucleotides, and the number of cells that migrated into the leasioned area of 1 mm 2 in size was counted 24 h later [57]. Increases in migration were induced by cAMP, adenosine, AMP, and ATP suggesting purinergic receptors activation; however, P1 receptors may promote contrary functions in this context, as adenosine can induce apoptosis in glomerular mesangial cells causing glomerular injury [58]. Babelova et al showed that the secretion of the pro-inflammatory master cytokine interleukin (IL)-1β during inflammatory renal injury interacts with purinergic P2X4/P2X7 receptors [59].…”

Section: Bladder Dysfunction and Glomerular Injurymentioning

confidence: 99%

Perspectives of purinergic signaling in stem cell differentiation and tissue regeneration

Glaser

Cappellari

Pillat

et al. 2011

Purinergic Signalling

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Replacement of lost or dysfunctional tissues by stem cells has recently raised many investigations on therapeutic applications. Purinergic signaling has been shown to regulate proliferation, differentiation, cell death, and successful engraftment of stem cells originated from diverse origins. Adenosine triphosphate release occurs in a controlled way by exocytosis, transporters, and lysosomes or in large amounts from damaged cells, which is then subsequently degraded into adenosine. Paracrine and autocrine mechanisms induced by immune responses present critical factors for the success of stem cell therapy. While P1 receptors generally exert beneficial effects including anti-inflammatory activity, P2 receptor-mediated actions depend on the subtype of stimulated receptors and localization of tissue repair. Pro-inflammatory actions and excitatory tissue damages mainly result from P2X7 receptor activation, while other purinergic receptor subtypes participate in proliferation and differentiation, thereby providing adequate niches for stem cell engraftment and novel mechanisms for cell therapy and endogenous tissue repair. Therapeutic applications based on regulation of purinergic signaling are foreseen for kidney and heart muscle regeneration, Clara-like cell replacement for pulmonary and bronchial epithelial cells as well as for induction of neurogenesis in case of neurodegenerative diseases.

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Adenosine-induced apoptosis in glomerular mesangial cells

Abstract: The observations indicate that ADO induces mesangial cell apoptosis via stimulation of the A3 receptor.

Cited by 40 publications

References 18 publications

Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: Protection by betaine

Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: Protection by betaine

Purinergic signalling in the kidney in health and disease

Perspectives of purinergic signaling in stem cell differentiation and tissue regeneration

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