Localization of connexin 30 in the luminal membrane of cells in the distal nephron

McCulloch, Fiona; Chambrey, Régine; Eladari, Dominique; Peti‐Peterdi, Janos

doi:10.1152/ajprenal.00203.2005

Cited by 65 publications

(85 citation statements)

References 34 publications

(47 reference statements)

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“…The anti-rabbit polyclonal Ab to the thiazide-sensitive NaCl cotransporter (Ncc), a gift from D.H. Ellison (Oregon Health and Science University, Portland, Oregon, USA), has been previously characterized (37,38), as well as the Ab to pendrin (gift from P. Aronson, Yale University School of Medicine, New Haven, Connecticut, USA) (39,40). Anti-Na + ,K + -ATPase α1 subunit Ab was a gift from F. Jaisser (Cordeliers Research Centre, Paris, France) (41).…”

Section: Antibodiesmentioning

confidence: 99%

See 1 more Smart Citation

PTH-independent regulation of blood calcium concentration by the calcium-sensing receptor

Loupy¹,

Ramakrishnan²,

Wootla³

et al. 2012

J. Clin. Invest.

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177

171

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Tight regulation of calcium levels is required for many critical biological functions. The Ca 2+ -sensing receptor (CaSR) expressed by parathyroid cells controls blood calcium concentration by regulating parathyroid hormone (PTH) secretion. However, CaSR is also expressed in other organs, such as the kidney, but the importance of extraparathyroid CaSR in calcium metabolism remains unknown. Here, we investigated the role of extraparathyroid CaSR using thyroparathyroidectomized, PTH-supplemented rats. Chronic inhibition of CaSR selectively increased renal tubular calcium absorption and blood calcium concentration independent of PTH secretion change and without altering intestinal calcium absorption. CaSR inhibition increased blood calcium concentration in animals pretreated with a bisphosphonate, indicating that the increase did not result from release of bone calcium. Kidney CaSR was expressed primarily in the thick ascending limb of the loop of Henle (TAL). As measured by in vitro microperfusion of cortical TAL, CaSR inhibitors increased calcium reabsorption and paracellular pathway permeability but did not change NaCl reabsorption. We conclude that CaSR is a direct determinant of blood calcium concentration, independent of PTH, and modulates renal tubular calcium transport in the TAL via the permeability of the paracellular pathway. These findings suggest that CaSR inhibitors may provide a new specific treatment for disorders related to impaired PTH secretion, such as primary hypoparathyroidism.

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Section: Antibodiesmentioning

confidence: 99%

“…All immunohistochemistry experiments were performed exactly as previously detailed (38,(45)(46)(47). The affinity-purified anti-CaSR Abs were diluted (1:500 and 1:700 for Ab10-12 and MA1-934, respectively) in background reducing buffer and applied for 1 hour at room temperature.…”

Section: Western Blotting and Immunolabelingmentioning

confidence: 99%

PTH-independent regulation of blood calcium concentration by the calcium-sensing receptor

Loupy¹,

Ramakrishnan²,

Wootla³

et al. 2012

J. Clin. Invest.

Self Cite

177

171

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show abstract

“…In the mouse kidney, ATP-permeable hemichannel connexin 30 (Cx30), which has been localized solely to the apical membrane of β-ICs of the distal nephron (45), is involved in ATP release from the collecting duct cells (15,28). More recently, pannexin 1 channels (Panx1), expressed at the apical membrane of ICs, has also been proposed to regulate ATP release as Panx1-deficient mice excrete less ATP than their wild-type littermates (15,46).…”

Section: Figurementioning

confidence: 99%

Renal β-intercalated cells maintain body fluid and electrolyte balance

Gueutin¹,

Vallet²,

Jayat³

et al. 2013

J. Clin. Invest.

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111

116

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Inactivation of the B1 proton pump subunit (ATP6V1B1) in intercalated cells (ICs) leads to type I distal renal tubular acidosis (dRTA), a disease associated with salt-and potassium-losing nephropathy. Here we show that mice deficient in ATP6V1B1 (Atp6v1b1 -/-mice) displayed renal loss of NaCl, K + , and water, causing hypovolemia, hypokalemia, and polyuria. We demonstrated that NaCl loss originated from the cortical collecting duct, where activity of both the epithelial sodium channel (ENaC) and the pendrin/Na + -driven chloride/ bicarbonate exchanger (pendrin/NDCBE) transport system was impaired. ENaC was appropriately increased in the medullary collecting duct, suggesting a localized inhibition in the cortex. We detected high urinary prostaglandin E 2 (PGE 2 ) and ATP levels in Atp6v1b1 -/-mice. Inhibition of PGE 2 synthesis in vivo restored ENaC protein levels specifically in the cortex. It also normalized protein levels of the large conductance calciumactivated potassium channel and the water channel aquaporin 2, and improved polyuria and hypokalemia in mutant mice. Furthermore, pharmacological inactivation of the proton pump in β-ICs induced release of PGE 2 through activation of calcium-coupled purinergic receptors. In the present study, we identified ATP-triggered PGE 2 paracrine signaling originating from β-ICs as a mechanism in the development of the hydroelectrolytic imbalance associated with dRTA. Our data indicate that in addition to principal cells, ICs are also critical in maintaining sodium balance and, hence, normal vascular volume and blood pressure.

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“…Connexin hemichannels have been shown to be localised in the luminal membrane of the distal nephron and may be the mechanism underlying ATP release from these cells and play a role in the regulation of salt reabsorption [239]. Multiple P2X r e c e p t o r s ( P 2 X 4 , P 2 X 5 a n d P 2 X 6 ) h a v e b e e n immunolocalised in the distal tubule cells [411].…”

Section: Distal Tubulesmentioning

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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Localization of connexin 30 in the luminal membrane of cells in the distal nephron

Abstract: McCulloch, Fiona, Régine Chambrey, Dominique Eladari, and János Peti-Peterdi. Localization of connexin 30 in the luminal membrane of cells in the distal nephron.

Cited by 65 publications

References 34 publications

PTH-independent regulation of blood calcium concentration by the calcium-sensing receptor

PTH-independent regulation of blood calcium concentration by the calcium-sensing receptor

Renal β-intercalated cells maintain body fluid and electrolyte balance

Purinergic signalling in the kidney in health and disease

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