Increase in cytosolic Ca2+ regulates exocytosis and Cl? conductance in HT29 cells

Greger, R.; Allert, Niels; Fröbe, U.; Normann, Claus

doi:10.1007/bf00384360

Cited by 37 publications

(26 citation statements)

References 16 publications

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“…More recently other functions of CFTR have emerged too. It has been claimed that CFTR functions as a regulator of Cl-channels [14,21], of exocytosis [2,10,13], and as a regulator of Na+ and K+ channels [17,18,22]. Moreover, previous studies fostering the Cl-channel function of CFTR by site-directed mutagenesis [1] could not be reproduced in our laboratory [12].…”

Section: Introductionmentioning

confidence: 74%

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cAMP Stimulation of CFTR-expressing Xenopus oocytes activates a chromanol-inhibitable K+ conductance

Mall

Kunzelmann

Hipper

et al. 1996

Pflugers Arch - Eur J Physiol

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Cystic fibrosis transmembrane conductance regulator (CFTR) functions as a Cl- channel in a large variety of cells expressing this protein. Recently evidence has accumulated that it also regulates other ion channels. A coordinated increase in Cl- and K+ conductances is necessary in many Cl--secreting epithelia. This has, for example, recently been demonstrated for the colonic crypt, for which a new type of K+ channel and a specific inhibitor of this channel, the chromanol 293B, have been described. In the present study we have examined whether the cAMP-evoked activation of CFTR, overexpressed in Xenopus oocytes, in addition to its known activation of a Cl- conductance, also upregulates endogenous K+ channels. It is shown that CFTR-cRNA-injected but not water-injected oocytes possess a cAMP-activated Cl- conductance. Of the cAMP-induced whole-cell current increase, 15-25% was due to a 293B-, Ba2+and TEA+-inhibitable K+ conductance. The cRNA of the mutated CFTR (DeltaF508 CFTR) had no such effect. We conclude that cAMP activated CFTR and an endogenous IsK-type and 293B-sensitive K+ conductance. Similar events, occurring, for example, in the colonic crypt possessing CFTR and 293B-sensitive K+ channels, might explain the coordinated cAMP-mediated increase in Cl- and K+ conductances.

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Section: Introductionmentioning

confidence: 74%

“…Comparison of the effects of Baz+ (5 mmol/1) + TEA+ (10 mmol/1) versus 293B (10 tmol/1) on the voltage and conductance for outward current (Go ) of wild-type CFTR-expressing oocytes (n =[10][11][12][13][14][15][16][17][18]. Mean values ±SEM.…”

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confidence: 99%

cAMP Stimulation of CFTR-expressing Xenopus oocytes activates a chromanol-inhibitable K+ conductance

Mall

Kunzelmann

Hipper

et al. 1996

Pflugers Arch - Eur J Physiol

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“…The activation of Cl -channels could, in principle, resemble the opening of closed channels already present in the luminal membrane, or the insertion of new channels via exocytosis. Recent evidence suggests that the latter mechanism contributes to the activation of Cl -channels: in preliminary studies in HT29 cells Cat -mobilizing agonists and cAMP led to an increase in membrane capacitance [31]. Furthermore, inhibitors of exocytosis, such as cytochalasin B or clostridial toxin (C2), interrupted the activation mechanisms [38].…”

Section: Coordinated Regulation Of Naci Secretionmentioning

confidence: 99%

The membrane transporters regulating epithelial NaCl secretion

Greger

1996

Pflügers Arch.

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Ten years ago, the basic principles operating in one specific, albeit non-mammalian, exocrine gland, the rectal gland of Squalus acanthias, were described in detail. The concept emerging from these studies appeared applicable to almost any other exocrine gland, because it involved membrane transporters which are also present in mammalian epithelial cells. Meanwhile, it has become clear that the mechanisms of NaCl secretion are diverse: the mechanisms of NaCl uptake; the ion channels involved; and also the mechanisms of hormonal control. Nevertheless, several steps in NaCl secretion still appear to be uniform: (1) several signalling pathways converge and act cooperatively, (2) one primary regulatory step is the upregulation of the luminal Cl- conductance, (3) secondarily active NaCl uptake mechanisms are upregulated, (4) increasing evidence links NaCl secretion to membrane trafficking and (5) the entire machinery seems to be primed to secure cellular homeostasis in terms of cytosolic ion concentrations. This brief review summarizes the mechanisms of control of NaCl secretion. The major issues addressed are the NaCl uptake mechanisms, the ion channels involved and the cellular mechanisms coordinating secretion. The major NaCl secreting cells discussed here will be the respiratory epithelial cells, the exocrine cells of pancreatic acini and the cells of colonic crypts.

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“…It is also unclear at this stage whether the cAMP-dependent upregulation in C1 conductance is due to a phosphorylation of preexisting C1-channels or to the incorporation of new channels by exocytosis. The comparison of the regulatory mechanisms present in other hormonally regulated C1-transporting epithelia suggest that exocytosis is one of the key steps in the regulation of C1-transport [12].…”

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confidence: 99%