Ca2+ Activates Cystic Fibrosis Transmembrane Conductance Regulator- and Cl−-dependent HCO<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" altimg="si10.gif"><mml:msubsup><mml:mrow /><mml:mrow><mml:mn>3</mml:mn></mml:mrow><mml:mrow><mml:mo>−</mml:mo></mml:mrow></mml:msubsup></mml:math> Transport in Pancreatic Duct Cells

Namkung, W.; Lee, Jin Ah; Ahn, Wooin; Han, Won Sun; Kwon, Sung Won; Ahn, Duk Sun; Kim, Kyung Hwan; Lee, Min Goo

doi:10.1074/jbc.m207199200

Cited by 68 publications

(60 citation statements)

References 33 publications

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“…3c) [122][123][124][125][126]. In addition, ATP/UTP also stimulated HCO À 3 efflux, associated with Cl À HCO À 3 exchange and monitored by intracellular pH measurements [125,126]. In some studies it was reported that nucleotides also stimulated K + currents [122,125].…”

Section: Pancreatic Acinimentioning

confidence: 99%

“…In most studies on cultured cells, cells were grown on coverslips and nucleotides were added to the apical side. However, in a few studies where nucleotides could be added to either the apical/luminal side as opposed to the basolateral/serosal side, they had a more pronounced effect from the apical side [102,124,126]. In two studies nucleotides had the following order of efficacy on stimulation of Cl − transport:…”

Section: Pancreatic Acinimentioning

confidence: 99%

“…Usually, the function of P2X 4 receptors has been difficult to separate from P2X 7 (Fig. 3c) [122][123][124][125][126]. In addition, ATP/UTP also stimulated HCO À 3 efflux, associated with Cl À HCO À 3 exchange and monitored by intracellular pH measurements [125,126].…”

Section: Pancreatic Acinimentioning

confidence: 99%

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Purinergic receptors in the endocrine and exocrine pancreas

Novak

2007

Purinergic Signalling

115

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The pancreas is a complex gland performing both endocrine and exocrine functions. In recent years there has been increasing evidence that both endocrine and exocrine cells possess purinergic receptors, which influence processes such as insulin secretion and epithelial ion transport. Most commonly, these processes have been viewed separately. In β cells, stimulation of P2Y 1 receptors amplifies secretion of insulin in the presence of glucose. Nucleotides released from secretory granules could also contribute to autocrine/paracrine regulation in pancreatic islets. In addition to P2Y 1 receptors, there is also evidence for other P2 and adenosine receptors in β cells (P2Y 2 , P2Y 4 , P2Y 6 , P2X subtypes and A 1 receptors) and in glucagon-secreting α cells (P2X 7 , A 2 receptors). In the exocrine pancreas, acini release ATP and ATP-hydrolysing and ATP-generating enzymes. P2 receptors are prominent in pancreatic ducts, and several studies indicate that P2Y 2 , P2Y 4 , P2Y 11 , P2X 4 and P2X 7 receptors could regulate secretion, primarily by affecting Cl − and K + channels and intracellular Ca 2+ signalling. In order to understand the physiology of the whole organ, it is necessary to consider the full complement of purinergic receptors on different cells as well as the structural and functional relation between various cells within the whole organ. In addition to the possible physiological function of purinergic receptors, this review analyses whether the receptors could be potential therapeutic targets for drug design aimed at treatment of pancreatic diseases.

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Section: Pancreatic Acinimentioning

confidence: 99%

Section: Pancreatic Acinimentioning

confidence: 99%

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Purinergic receptors in the endocrine and exocrine pancreas

Novak

2007

Purinergic Signalling

115

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“…It is expressed in a wide variety of epithelial cells including pancreatic ductal cells (Namkung et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

MUC4 expression is regulated by cystic fibrosis transmembrane conductance regulator in pancreatic adenocarcinoma cells via transcriptional and post-translational mechanisms

et al. 2006

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MUC4 mucin is a high molecular weight transmembrane glycoprotein that plays important roles in tumour biology. It is aberrantly expressed in pancreatic adenocarcinoma, while not being detectable in the normal pancreas. Previous studies have demonstrated that the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel that is defective in CF, is implicated in multiple cellular functions, including gene regulation. In the present study, using a CFTR-defective pancreatic cancer cell line and its derived subline expressing functional CFTR, we report that MUC4 expression is negatively regulated by CFTR. Short-interfering RNA (siRNA)-mediated silencing of CFTR also leads to an increased expression of MUC4. Additionally, our results suggest that CFTR-mediated regulation of MUC4 is cell densitydependent and is achieved by transcriptional and posttranslational mechanisms. Moreover, in a panel of pancreatic cancer cell lines and normal pancreas, we observed that CFTR was downregulated in pancreatic cancer cells and negatively correlated with MUC4 in most cases. An aberrant expression of MUC4 was also detected in the CF pancreas. Downregulation of CFTR in pancreatic adenocarcinoma and its inverse association with the tumour-linked mucin, MUC4, indicate novel function(s) of CFTR in pancreatic tumour biology and suggest the implication of new signalling pathway(s) in MUC4 regulation.

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“…Luminal ATP can then upregulate anion and fluid secretion, and this activity involves regulation of CaCC and IK (Hug et al 1994;Ishiguro et al 1999;Hede et al 2005;Jung et al 2006;Novak et al 2010;Hayashi et al 2012;Wang et al 2013). ATP also stimulates luminal anion exchange in duct epithelia expressing functional CFTR (Namkung et al 2003). In addition, ATP/uridine triphosphate (UTP) also potentiate cAMP-evoked mucin secretion (Jung et al 2010).…”

Section: Regulation Of Pancreatic Duct Secretionmentioning

confidence: 99%

The Cystic Fibrosis of Exocrine Pancreas

Wilschanski

Novak

2013

Cold Spring Harbor Perspectives in Medicine

125

113

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The cystic fibrosis transmembrane conductance regulator (CFTR) protein is highly expressed in the pancreatic duct epithelia and permits anions and water to enter the ductal lumen. This results in an increased volume of alkaline fluid allowing the highly concentrated proteins secreted by the acinar cells to remain in a soluble state. This work will expound on the pathophysiology and pathology caused by the malfunctioning CFTR protein with special reference to ion transport and acid-base abnormalities both in humans and animal models. We will also discuss the relationship between cystic fibrosis (CF) and pancreatitis, and outline present and potential therapeutic approaches in CF treatment relevant to the pancreas.

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Ca2+ Activates Cystic Fibrosis Transmembrane Conductance Regulator- and Cl−-dependent HCO3− Transport in Pancreatic Duct Cells

Cited by 68 publications

References 33 publications

Purinergic receptors in the endocrine and exocrine pancreas

Purinergic receptors in the endocrine and exocrine pancreas

MUC4 expression is regulated by cystic fibrosis transmembrane conductance regulator in pancreatic adenocarcinoma cells via transcriptional and post-translational mechanisms

The Cystic Fibrosis of Exocrine Pancreas

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