scholarly journals The role of CFTR in bicarbonate secretion by pancreatic duct and airway epithelia

2009 ◽  
Vol 56 (Supplement) ◽  
pp. 336-342 ◽  
Author(s):  
Dusik Kim ◽  
Martin C Steward
Keyword(s):  
Pancreatic Duct ◽  
Bicarbonate Secretion ◽  
Airway Epithelia

Effect of Slc26a6 deletion on apical Cl−/HCO3− exchanger activity and cAMP-stimulated bicarbonate secretion in pancreatic duct

2007 ◽  
Vol 292 (1) ◽  
pp. G447-G455 ◽  
Author(s):  
Hiroshi Ishiguro ◽  
Wan Namkung ◽  
Akiko Yamamoto ◽  
Zhaohui Wang ◽  
Roger T. Worrell ◽  
...  
Keyword(s):  
Pancreatic Duct ◽  
Apical Membrane ◽  
Pancreatic Ducts ◽  
Bicarbonate Secretion ◽  
Wild Type ◽  
Rt Pcr ◽  
Secretory Rate ◽  
Transport Fluid ◽  
Exchange Activity

The role of Slc26a6 (PAT1) on apical Cl−/HCO3− exchange and bicarbonate secretion in pancreatic duct cells was investigated using Slc26a6 null and wild-type (WT) mice. Apical Cl−/HCO3− exchange activity was measured with the pH-sensitive dye BCECF in microperfused interlobular ducts. The HCO3−-influx mode of apical [Cl−]i/[HCO3−]o exchange (where brackets denote concentration and subscripts i and o denote intra- and extracellular, respectively) was dramatically upregulated in Slc26a6 null mice ( P < 0.01 vs. WT), whereas the HCO3−-efflux mode of apical [Cl−]o/[HCO3−]i exchange was decreased in Slc26a6 null mice ( P < 0.05 vs. WT), suggesting the unidirectionality of the Slc26a6-mediated HCO3− transport. Fluid secretory rate in interlobular ducts were comparable in WT and Slc26a6 null mice ( P > 0.05). In addition, when pancreatic juice was collected from whole animal in basal and secretin-stimulated conditions, neither juice volume nor its pH showed differences between WT and Slc26a6 null mice. Semiquantitative RT-PCR demonstrated more than fivefold upregulation in Slc26a3 (DRA) expression in Slc26a6 knockout pancreas. In conclusion, these results point to the role of Slc26a6 in HCO3− efflux at the apical membrane and also suggest the presence of a robust Slc26a3 compensatory upregulation, which can replace the function of Slc26a6 in pancreatic ducts.

scholarly journals Pulmonary fibrosis distal airway epithelia are dynamically and structurally dysfunctional

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ian T. Stancil ◽  
Jacob E. Michalski ◽  
Duncan Davis-Hall ◽  
Hong Wei Chu ◽  
Jin-Ah Park ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Airway Epithelium ◽  
Cell Types ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Airway Epithelia ◽  
Chronic Lung Diseases ◽  
Distal Airway ◽  
Signaling Axis

AbstractThe airway epithelium serves as the interface between the host and external environment. In many chronic lung diseases, the airway is the site of substantial remodeling after injury. While, idiopathic pulmonary fibrosis (IPF) has traditionally been considered a disease of the alveolus and lung matrix, the dominant environmental (cigarette smoking) and genetic (gain of function MUC5B promoter variant) risk factor primarily affect the distal airway epithelium. Moreover, airway-specific pathogenic features of IPF include bronchiolization of the distal airspace with abnormal airway cell-types and honeycomb cystic terminal airway-like structures with concurrent loss of terminal bronchioles in regions of minimal fibrosis. However, the pathogenic role of the airway epithelium in IPF is unknown. Combining biophysical, genetic, and signaling analyses of primary airway epithelial cells, we demonstrate that healthy and IPF airway epithelia are biophysically distinct, identifying pathologic activation of the ERBB-YAP axis as a specific and modifiable driver of prolongation of the unjammed-to-jammed transition in IPF epithelia. Furthermore, we demonstrate that this biophysical state and signaling axis correlates with epithelial-driven activation of the underlying mesenchyme. Our data illustrate the active mechanisms regulating airway epithelial-driven fibrosis and identify targets to modulate disease progression.

scholarly journals The role of cGMP-cGKI-signaling for duodenal bicarbonate secretion

2009 ◽  
Vol 9 (S1) ◽  
Author(s):  
Beate Spiessberger ◽  
Pascal Weinmeister ◽  
Franz Hofmann ◽  
Claudia Werner ◽  
Dieter Saur ◽  
...  
Keyword(s):  
Bicarbonate Secretion ◽  
Duodenal Bicarbonate Secretion

The role of endoscopic retrograde pancreatography in the treatment of traumatic pancreatic duct injury

2001 ◽  
Vol 54 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Hyun Soo Kim ◽  
Dong Ki Lee ◽  
Il Whoi Kim ◽  
Soon Koo Baik ◽  
Sang Ok Kwon ◽  
...  
Keyword(s):  
Pancreatic Duct ◽  
Endoscopic Retrograde Pancreatography ◽  
Endoscopic Retrograde

Protein kinase C potentiates cAMP-stimulated mouse duodenal mucosal bicarbonate secretion in vitro

2004 ◽  
Vol 286 (5) ◽  
pp. G814-G821 ◽  
Author(s):  
Bi-Guang Tuo ◽  
Jimmy Y. C. Chow ◽  
Kim E. Barrett ◽  
Jon I. Isenberg
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Duodenal Mucosa ◽  
Bicarbonate Secretion ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Ussing Chambers ◽  
Duodenal Bicarbonate Secretion

PKC has been shown to regulate epithelial Cl- secretion in a variety of models. However, the role of PKC in duodenal mucosal bicarbonate secretion is less clear. We aimed to investigate the role of PKC in regulation of duodenal mucosal bicarbonate secretion. Bicarbonate secretion by murine duodenal mucosa was examined in vitro in Ussing chambers using a pH-stat technique. PKC isoform expression and activity were assessed by Western blotting and in vitro kinase assays, respectively. PMA (an activator of PKC) alone had no effect on duodenal bicarbonate secretion or short-circuit current ( Isc). When PMA and dibutyryl-cAMP (db-cAMP) were added simultaneously, PMA failed to alter db-cAMP-stimulated duodenal bicarbonate secretion or Isc ( P > 0.05). However, a 1-h preincubation with PMA potentiated db-cAMP-stimulated duodenal bicarbonate secretion and Isc in a concentration-dependent manner (from 10-8 to 10-5M) ( P < 0.05). PMA preincubation had no effects on carbachol- or heat-stable toxin-stimulated bicarbonate secretion. Western blot analysis revealed that PKCα, -γ, -ϵ, -θ, -μ, and -ι/λ were expressed in murine duodenal mucosa. Ro 31–8220 (an inhibitor active against PKCϵ, -α, -β, and -γ), but not Gö 6983 (an inhibitor active against PKCα, -γ, -β, and -δ), reversed the potentiating effect of PMA on db-cAMP-stimulated bicarbonate secretion. PMA also time- and concentration-dependently increased the activity of PKCϵ, an effect that was prevented by Ro 31–8220 but not Gö 6983. These results demonstrate that activation of PKC potentiates cAMP-stimulated duodenal bicarbonate secretion, whereas it does not modify basal secretion. The effect of PKC on cAMP-stimulated bicarbonate secretion is mediated by the PKCϵ isoform.

Role of Protein Kinases on Acid-Induced Duodenal Bicarbonate Secretion in Rats

2002 ◽  
pp. 139-142
Author(s):  
Osamu Furukawa ◽  
Masahiko Hirokawa ◽  
Paul H. Guth ◽  
Eli Engel ◽  
Jonathan D. Kaunitz
Keyword(s):  
Protein Kinases ◽  
Bicarbonate Secretion ◽  
Duodenal Bicarbonate Secretion

Duodenum-Preserving Pancreatic Resection with Pancreatic Duct Drainage: What Is the Role of Supraduodenal Biliary Drainage?

2009 ◽  
pp. 67-70
Author(s):  
Emre F. Yekebas ◽  
Christos Dervenis ◽  
Richard M. Charnley ◽  
Bettina M. Rau ◽  
Jens Werner ◽  
...  
Keyword(s):  
Pancreatic Duct ◽  
Pancreatic Resection ◽  
Biliary Drainage ◽  
Pancreatic Duct Drainage

Aquaporin water channels and lung physiology

2000 ◽  
Vol 278 (5) ◽  
pp. L867-L879 ◽  
Author(s):  
A. S. Verkman ◽  
Michael A. Matthay ◽  
Yuanlin Song
Keyword(s):  
Water Permeability ◽  
Water Movement ◽  
Alveolar Epithelial Cells ◽  
Minor Effect ◽  
Type I ◽  
Lung Water ◽  
Airway Epithelia ◽  
Lung Physiology ◽  
Osmotic Water

Fluid transport across epithelial and endothelial barriers occurs in the neonatal and adult lungs. Biophysical measurements in the intact lung and cell isolates have indicated that osmotic water permeability is exceptionally high across alveolar epithelia and endothelia and moderately high across airway epithelia. This review is focused on the role of membrane water-transporting proteins, the aquaporins (AQPs), in high lung water permeability and lung physiology. The lung expresses several AQPs: AQP1 in microvascular endothelia, AQP3 in large airways, AQP4 in large- and small-airway epithelia, and AQP5 in type I alveolar epithelial cells. Lung phenotype analysis of transgenic mice lacking each of these AQPs has been informative. Osmotically driven water permeability between the air space and capillary compartments is reduced ∼10-fold by deletion of AQP1 or AQP5 and reduced even more by deletion of AQP1 and AQP4 or AQP1 and AQP5 together. AQP1 deletion greatly reduces osmotically driven water transport across alveolar capillaries but has only a minor effect on hydrostatic lung filtration, which primarily involves paracellular water movement. However, despite the major role of AQPs in lung osmotic water permeabilities, AQP deletion has little or no effect on physiologically important lung functions, such as alveolar fluid clearance in adult and neonatal lung, and edema accumulation after lung injury. Although AQPs play a major role in renal and central nervous system physiology, the data to date on AQP knockout mice do not support an important role of high lung water permeabilities or AQPs in lung physiology. However, there remain unresolved questions about possible non-water-transporting roles of AQPs and about the role of AQPs in airway physiology, pleural fluid dynamics, and edema after lung infection.

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