Parathyroid hormone stimulates ATP-dependent calcium pump activity by a different mode in proximal and distal tubules of the rat

Tsukamoto, Yusuke; Saka, Satoshi; Saitoh, Michiyo

doi:10.1016/0005-2736(92)90070-3

Cited by 26 publications

(7 citation statements)

References 19 publications

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“…35 TFP treatment induced marked suppression of Ca 2ϩ efflux in LLC-PK1 cells (Fig. [36][37][38][39] Also the Na ϩ /Ca 2ϩ exchanger is exclusively localized in the DCT. This result indicates that Ca 2ϩ pumps in the plasma membrane of LLC-PK1 cells are dependent on calmodulin.…”

Section: Discussionmentioning

confidence: 93%

Senescence marker protein-30 (SMP30) enhances the calcium efflux from renal tubular epithelial cells

Inoue

Fujita

Kitamura

et al. 1999

Clinical and Experimental Nephrology

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Background. Senescence marker protein-30 (SMP30), a calcium binding protein, is preferentially expressed in the renal proximal tubules and hepatocytes and is presumed to play a role in Ca 2ϩ homeostasis. Methods. To explore its physiological functions in the tubular cells, we investigated the effect of SMP30 on Ca 2ϩ efflux via the ATP-dependent plasma membrane calcium pump. LLC-PK1 cells were stably transfected with a cDNA encoding SMP30, and the established transfectants were subjected to ATP responses. Results. Overexpression of SMP30 significantly increased Ca 2ϩ efflux under both basal and ATP-stimulated conditions. Inhibition of calmodulin by trifluoperazine abrogated the enhanced Ca 2ϩ efflux, suggesting that SMP30 activated the calmodulin-dependent Ca 2ϩ pump. It is known that Ca 2ϩ superfluous influx induces cellular injury. Compared with mock-transfected cells, LLC-PK1 cells expressing SMP30 showed resistance to cellular death triggered by Ca 2ϩ superfluous influx. Conclusion. These results suggest the possibility that, in renal tubular cells, endogenous SMP30 participates in Ca 2ϩ efflux via activating the calmodulin-dependent Ca 2ϩ pump and thereby confers resistance of the cells against injury caused by high intracellular Ca 2ϩ concentrations.

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Section: Discussionmentioning

confidence: 93%

Senescence marker protein-30 (SMP30) enhances the calcium efflux from renal tubular epithelial cells

Inoue

Fujita

Kitamura

et al. 1999

Clinical and Experimental Nephrology

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“…PMCA is positively and negatively regulated by a number of intracellular substances including calmodulin, proteases, protein kinases, and acidic phospholipids (29). In the distal tubule, PMCA activity is stimulated by PTH (40), which provides an indirect feedback loop to regulate calcium absorption. The present study demonstrates that one mechanism by which the CaR inhibits calcium absorption is by inhibiting PMCA activity.…”

Section: Discussionmentioning

confidence: 99%

The calcium-sensing receptor regulates calcium absorption in MDCK cells by inhibition of PMCA

Blankenship

Williams

Lawrence

et al. 2001

American Journal of Physiology-Renal Physiology

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Calcium transport across a monolayer of Madin-Darby canine kidney (MDCK) cells was measured in response to stimulation of the basal surface with calcium-sensing receptor (CaR) agonists. Stimulation of the CaR resulted in a time- and concentration-dependent inhibition of calcium transport but did not change transepithelial voltage or resistance. Inhibition of transport was not altered by pretreatment of cells with pertussis toxin but was blocked by the phospholipase C (PLC) inhibitor U-73122. To determine a potential mechanism by which the CaR could inhibit calcium transport, we measured activity of the plasma membrane calcium ATPase (PMCA). Stimulation of the CaR on the basal surface resulted in an inhibition of the PMCA in a concentration- and PLC-dependent manner. Thus stimulation of the CaR inhibits both calcium transport and PMCA activity through a PLC-dependent pathway. These studies provide the first direct evidence that calcium can inhibit its own transcellular absorption in a model of the distal tubule. In addition, they provide a potential mechanism for the CaR to inhibit calcium transport, inhibition of PMCA.

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“…These studies demonstrated equivocally that PTH increases transepithelial Ca 2ϩ transport via a dual signaling mechanism involving PKA-and PKC-dependent processes (124,170). Various mechanisms of PTH action have been postulated including membrane insertion of apical Ca 2ϩ channels (12), opening of basolateral chloride channels resulting in cellular hyperpolarization (127), and modulation of PMCA activity (383). Friedman and colleagues (12) examined Ca 2ϩ influx in single cultured cells from distal renal tubules sensitive to PTH by measuring intracellular Ca 2ϩ .…”

Section: B Regulation By Pthmentioning

confidence: 99%

Calcium Absorption Across Epithelia

Hoenderop

Nilius²,

Bindels³

2005

Physiological Reviews

755

694

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Ca(2+) is an essential ion in all organisms, where it plays a crucial role in processes ranging from the formation and maintenance of the skeleton to the temporal and spatial regulation of neuronal function. The Ca(2+) balance is maintained by the concerted action of three organ systems, including the gastrointestinal tract, bone, and kidney. An adult ingests on average 1 g Ca(2+) daily from which 0.35 g is absorbed in the small intestine by a mechanism that is controlled primarily by the calciotropic hormones. To maintain the Ca(2+) balance, the kidney must excrete the same amount of Ca(2+) that the small intestine absorbs. This is accomplished by a combination of filtration of Ca(2+) across the glomeruli and subsequent reabsorption of the filtered Ca(2+) along the renal tubules. Bone turnover is a continuous process involving both resorption of existing bone and deposition of new bone. The above-mentioned Ca(2+) fluxes are stimulated by the synergistic actions of active vitamin D (1,25-dihydroxyvitamin D(3)) and parathyroid hormone. Until recently, the mechanism by which Ca(2+) enter the absorptive epithelia was unknown. A major breakthrough in completing the molecular details of these pathways was the identification of the epithelial Ca(2+) channel family consisting of two members: TRPV5 and TRPV6. Functional analysis indicated that these Ca(2+) channels constitute the rate-limiting step in Ca(2+)-transporting epithelia. They form the prime target for hormonal control of the active Ca(2+) flux from the intestinal lumen or urine space to the blood compartment. This review describes the characteristics of epithelial Ca(2+) transport in general and highlights in particular the distinctive features and the physiological relevance of the new epithelial Ca(2+) channels accumulating in a comprehensive model for epithelial Ca(2+) absorption.

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Parathyroid hormone stimulates ATP-dependent calcium pump activity by a different mode in proximal and distal tubules of the rat

Cited by 26 publications

References 19 publications

Senescence marker protein-30 (SMP30) enhances the calcium efflux from renal tubular epithelial cells

Senescence marker protein-30 (SMP30) enhances the calcium efflux from renal tubular epithelial cells

The calcium-sensing receptor regulates calcium absorption in MDCK cells by inhibition of PMCA

Calcium Absorption Across Epithelia

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