Transient Activation and Delayed Inhibition of Na+,K+,Cl–Cotransport in ATP-treated C11-MDCK Cells Involve Distinct P2Y Receptor Subtypes and Signaling Mechanisms

Akimova, Olga A.; Grygorczyk, Alexandra; Bundey, Richard A.; Bourcier, Nathalie; Gekle, Michael; Insel, Paul A.; Orlov, Sergei N.

doi:10.1074/jbc.m602117200

Cited by 23 publications

(26 citation statements)

References 49 publications

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“…This occurred despite a fall in GFR and suggested that proximal tubular reabsorption was markedly reduced [353]. Ap 4 A can stimulate a number of P2 receptor subtypes, including P2Y 1 and P2Y 4 receptors [331,410], which are both expressed in the rat proximal tubule (P2Y 1 apically, P2Y 4 basolaterally); intravenous delivery of the agonist does not allow differentiation between these possibilities.…”

Section: Renal Tubulesmentioning

confidence: 98%

“…Diadenosine polyphosphates, which influence renal perfusion pressure, activate Cl − and non-selective cation conductance in rat mesangial cells as do ATP and angiotensin II (Ang II); Ap 4 A was the most effective of the dinucleotides [194,318,325]. Diadenosine pentaphosphate (Ap 5 A) and diadenosine hexaphosphate appear to play a regulatory role in mesangial cell proliferation [129].…”

Section: Mesangial Cellsmentioning

confidence: 99%

“…Diadenosine pentaphosphate (Ap 5 A) and diadenosine hexaphosphate appear to play a regulatory role in mesangial cell proliferation [129]. Ap 4 A and Ap 5 A decrease, while diadenosine triphosphate appears to increase glomerular filtration rate [359].…”

Section: Mesangial Cellsmentioning

confidence: 99%

“…P2Y 1 and P2X5 receptors have been immunolocalised to the apical membrane in the S3 segment of the rat pars recta and P2Y 4 and P2X6 receptor protein is found basolaterally in the proximal convoluted tubule (PCT). Low level expression of P2X4 protein is also seen in the PCT but not ascribed to a specific membrane domain [375].…”

Section: Renal Tubulesmentioning

confidence: 99%

“…Mitochondria play an important role in adenosine-induced ATP release from MDCK cells [245]. Activation of the Na + -K + -Cl − co-transporter in MDCK cells is via Ca 2+ -independent signalling triggered by apical P2Y 2 and basolateral P2Y 1 receptors [4]. Rapid pressure changes induce both apical and basolateral ATP release [299].…”

Section: Distal Tubulesmentioning

confidence: 99%

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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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Section: Renal Tubulesmentioning

confidence: 98%

Section: Mesangial Cellsmentioning

confidence: 99%

Section: Mesangial Cellsmentioning

confidence: 99%

Section: Renal Tubulesmentioning

confidence: 99%

Section: Distal Tubulesmentioning

confidence: 99%

See 3 more Smart Citations

Purinergic signalling in the kidney in health and disease

Burnstock

Evans

Bailey

2013

Purinergic Signalling

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Slow spontaneous [Ca2+]i oscillations reflect nucleotide release from renal epithelia

Geyti

Odgaard

Overgaard

et al. 2007

Pflugers Arch - Eur J Physiol

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Renal epithelia can be provoked mechanically to release nucleotides, which subsequently increases the intracellular Ca(2+) concentration [Ca(2+)](i) through activation of purinergic (P2) receptors. Cultured cells often show spontaneous [Ca(2+)](i) oscillations, a feature suggested to involve nucleotide signalling. In this study, fluo-4 loaded Madin-Darby canine kidney (MDCK) cells are used as a model for quantification and characterisation of spontaneous [Ca(2+)](i) increases in renal epithelia. Spontaneous [Ca(2+)](i) increases occurred randomly as single cell events. During an observation period of 1 min, 10.9 +/- 6.7% (n = 23) of the cells showed spontaneous [Ca(2+)](i) increases. Spontaneous adenosine triphosphate (ATP) release from MDCK cells was detected directly by luciferin/luciferase. Scavenging of ATP by apyrase or hexokinase markedly reduced the [Ca(2+)](i) oscillatory activity, whereas inhibition of ecto-ATPases (ARL67156) enhanced the [Ca(2+)](i) oscillatory activity. The association between spontaneous [Ca(2+)](i) increases and nucleotide signalling was further tested in 132-1N1 cells lacking P2 receptors. These cells hardly showed any spontaneous [Ca(2+)](i) increases. Transfection with either hP2Y(6) or hP2Y(2) receptors revealed a striking degree of oscillations. Similar spontaneous [Ca(2+)](i) increases were observed in freshly isolated, perfused mouse medullary thick ascending limb (mTAL). The oscillatory activity was reduced by basolateral apyrase and substantially lower in mTAL from P2Y(2) knock out mice (0.050 +/- 0.020 events per second, n = 8) compared to the wild type (0.147 +/- 0.018 events per second, n = 9). These findings indicate that renal epithelia spontaneously release nucleotides leading to P2-receptor-dependent [Ca(2+)](i) oscillations. Thus, tonic nucleotide release is likely to modify steady state renal function.

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The Na–K–Cl Co-transporter in astrocyte swelling

2010

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Ion channels, exchangers and transporters are known to be involved in cell volume regulation. A disturbance in one or more of these systems may result in loss of ion homeostasis and cell swelling. In particular, activation of the Na(+)-K(+)-Cl(-) cotransporters has been shown to regulate cell volume in many conditions. The Na(+)-K(+)-Cl- cotransporters (NKCC) are a class of membrane proteins that transport Na, K, and Cl ions into and out of a wide variety of epithelial and nonepithelial cells. Studies have established the role of NKCC1 in astrocyte swelling/brain edema in ischemia and trauma. Our recent studies suggest that NKCC1 activation is also involved in astrocyte swelling induced by ammonia and in the brain edema in the thioacetamide model of acute liver failure. This review will focus on mechanisms of NKCC1 activation and its contribution to astrocyte swelling/brain edema in neurological disorders, with particular emphasis on ammonia neurotoxicity and acute liver failure.

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Transient Activation and Delayed Inhibition of Na⁺,K⁺,Cl^–Cotransport in ATP-treated C11-MDCK Cells Involve Distinct P2Y Receptor Subtypes and Signaling Mechanisms

Cited by 23 publications

References 49 publications

Purinergic signalling in the kidney in health and disease

Purinergic signalling in the kidney in health and disease

Slow spontaneous [Ca2+]i oscillations reflect nucleotide release from renal epithelia

The Na–K–Cl Co-transporter in astrocyte swelling

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