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  • 1
    Online Resource
    Online Resource
    Bile acids stimulate chloride secretion through CFTR and calcium-activated Cl − channels in Calu-3 airway epithelial cells
    American Physiological Society ; 2014
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 307, No. 5 ( 2014-09-01), p. L407-L418
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 307, No. 5 ( 2014-09-01), p. L407-L418
    Abstract: Bile acids resulting from the aspiration of gastroesophageal refluxate are often present in the lower airways of people with cystic fibrosis and other respiratory distress diseases. Surprisingly, there is little or no information on the modulation of airway epithelial ion transport by bile acids. The secretory effect of a variety of conjugated and unconjugated secondary bile acids was investigated in Calu-3 airway epithelial cells grown under an air-liquid interface and mounted in Ussing chambers. Electrogenic transepithelial ion transport was measured as short-circuit current ( I sc ). The taurine-conjugated secondary bile acid, taurodeoxycholic acid (TDCA), was found to be the most potent modulator of basal ion transport. Acute treatment (5 min) of Calu-3 cells with TDCA (25 μM) on the basolateral side caused a stimulation of I sc , and removal of extracellular Cl − abolished this response. TDCA produced an increase in the cystic fibrosis transmembrane conductance regulator (CFTR)-dependent current that was abolished by pretreatment with the CFTR inhibitor CFTR inh172 . TDCA treatment also increased Cl − secretion through calcium-activated chloride (CaCC) channels and increased the Na + /K + pump current. Acute treatment with TDCA resulted in a rapid cellular influx of Ca 2+ and increased cAMP levels in Calu-3 cells. Bile acid receptor-selective activation with INT-777 revealed TGR5 localized at the basolateral membrane as the receptor involved in TDCA-induced Cl − secretion. In summary, we demonstrate for the first time that low concentrations of bile acids can modulate Cl − secretion in airway epithelial cells, and this effect is dependent on both the duration and sidedness of exposure to the bile acid.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00352.2013
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 1477300-4
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  • 2
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    Online Resource
    Lipoxin A 4 -mediated K ATP potassium channel activation results in cystic fibrosis airway epithelial repair
    American Physiological Society ; 2013
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 305, No. 2 ( 2013-07-15), p. L193-L201
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 305, No. 2 ( 2013-07-15), p. L193-L201
    Abstract: The main cause of morbidity and mortality in cystic fibrosis (CF) is progressive lung destruction as a result of persistent bacterial infection and inflammation, coupled with reduced capacity for epithelial repair. Levels of the anti-inflammatory mediator lipoxin A 4 (LXA 4 ) have been reported to be reduced in bronchoalveolar lavages of patients with CF. We investigated the ability of LXA 4 to trigger epithelial repair through the initiation of proliferation and migration in non-CF (NuLi-1) and CF (CuFi-1) airway epithelia. Spontaneous repair and cell migration were significantly slower in CF epithelial cultures (CuFi-1) compared with controls (NuLi-1). LXA 4 triggered an increase in migration, proliferation, and wound repair of non-CF and CF airway epithelia. These responses to LXA 4 were completely abolished by the ALX/FPR2 receptor antagonist, Boc2 and ALX/FPR2 siRNA. The K ATP channel opener pinacidil mimicked the LXA 4 effect on migration, proliferation, and epithelial repair, whereas the K ATP channel inhibitor, glibenclamide, blocked the responses to LXA 4 . LXA 4 did not affect potassium channel expression but significantly upregulated glibenclamide-sensitive (K ATP ) currents through the basolateral membrane of NuLi-1 and CuFi-1 cells. MAP kinase (ERK1/2) inhibitor, PD98059 , also inhibited the LXA 4 -induced proliferation of NuLi-1 and CuFi-1 cells. Finally, both LXA 4 and pinacidil stimulated ERK-MAP kinase phosphorylation, whereas the effect of LXA 4 on ERK phosphorylation was inhibited by glibenclamide. Taken together, our results provided evidence for a role of LXA 4 in triggering epithelial repair through stimulation of the ALX/FPR2 receptor, K ATP potassium channel activation, and ERK phosphorylation. This work suggests exogenous delivery of LXA 4 , restoring levels in patients with CF, perhaps as a potential therapeutic strategy.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00058.2013
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1477300-4
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  • 3
    Online Resource
    Online Resource
    Hormonally controlled chloride movement across Drosophila tubules is via ion channels in stellate cells
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 274, No. 4 ( 1998-04-01), p. R1039-R1049
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 274, No. 4 ( 1998-04-01), p. R1039-R1049
    Abstract: Anion conductance across the Drosophila melanogaster Malpighian (renal) tubule was investigated by a combination of physiological and transgenic techniques. Patch-clamp recordings identified clusters of 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS)-sensitive “maxi-chloride” channels in a small domain of the apical membrane. Fluid secretion assays demonstrated sensitivity to the chloride channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid, diphenylamine-2-carboxylate, anthracene-9-carboxylic acid, and niflumic acid. Electrophysiological analysis showed that the calcium-mediated increase in anion conductance was blocked by the same agents. Vibrating probe analysis revealed a small number of current density hot spots, coincident with “stellate” cells, that were abolished by low-chloride saline or the same chloride channel blockers. GAL-4-targeted expression of an aequorin transgene revealed that the neurohormone leucokinin elicits a rapid increase in intracellular calcium levels in stellate cells that precedes the fastest demonstrable physiological effect. Taken together, these data show that leucokinins act on stellate cells through intracellular calcium to increase transcellular chloride conductance through channels. As electrogenic cation conductance is confined to principal cells, the two pathways are spatially segregated in this tissue.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.1998.274.4.R1039
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477297-8
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  • 4
    Online Resource
    Online Resource
    JNK mitogen-activated protein kinase limits calcium-dependent chloride secretion across colonic epithelial cells
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 298, No. 1 ( 2010-01), p. G37-G44
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 298, No. 1 ( 2010-01), p. G37-G44
    Abstract: Neuroimmune agonists induce epithelial Cl − secretion through elevations in intracellular Ca 2+ or cAMP. Previously, we demonstrated that epidermal growth factor receptor (EGFR) transactivation and subsequent ERK MAPK activation limits secretory responses to Ca 2+ -dependent, but not cAMP-dependent, agonists. Although JNK MAPKs are also expressed in epithelial cells, their role in regulating transport function is unknown. Here, we investigated the potential role for JNK in regulating Cl − secretion in T 84 colonic epithelial cells. Western blot analysis revealed that a prototypical Ca 2+ -dependent secretagogue, carbachol (CCh; 100 μM), induced phosphorylation of both the 46-kDa and 54-kDa isoforms of JNK. This effect was mimicked by thapsigargin (TG), which specifically elevates intracellular Ca 2+ , but not by forskolin (FSK; 10 μM), which elevates cAMP. CCh-induced JNK phosphorylation was attenuated by the EGFR inhibitor, tyrphostin-AG1478 (1 μM). Pretreatment of voltage-clamped T 84 cells with SP600125 (2 μM), a specific JNK inhibitor, potentiated secretory responses to both CCh and TG but not to FSK. The effects of SP600125 on CCh-induced secretion were not additive with those of the ERK inhibitor, PD98059. Finally, in apically permeabilized T 84 cell monolayers, SP600125 potentiated CCh-induced K + conductances but not Na + /K + ATPase activity. These data demonstrate a novel role for JNK MAPK in regulating Ca 2+ but not cAMP-dependent epithelial Cl − secretion. JNK activation is mediated by EGFR transactivation and exerts its antisecretory effects through inhibition of basolateral K + channels. These data further our understanding of mechanisms regulating epithelial secretion and underscore the potential for exploitation of MAPK-dependent signaling in treatment of intestinal transport disorders.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00202.2009
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477329-6
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  • 5
    Online Resource
    Online Resource
    Sex and Salt Hormones: Rapid Effects in Epithelia
    American Physiological Society ; 2001
    In:  Physiology Vol. 16, No. 4 ( 2001-08), p. 174-177
    Details
    In: Physiology, American Physiological Society, Vol. 16, No. 4 ( 2001-08), p. 174-177
    Abstract: Recent evidence points to protein kinase C isoforms as highly specific receptors for aldosterone and estradiol in epithelia. The end targets of the kinase activation are Na + /H + exchange and K + and Ca 2+ channels. The physiological role of the nongenomic response is to increase electrolyte absorption and inhibit secretion in pluripotential epithelia.
    Type of Medium: Online Resource
    ISSN: 1548-9213 , 1548-9221
    URL: Article
    DOI: 10.1152/physiologyonline.2001.16.4.174
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 3115360-4
    detail.hit.zdb_id: 2005759-3
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  • 6
    Online Resource
    Online Resource
    Basolateral outward rectifier chloride channel in isolated crypts of mouse colon
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 279, No. 2 ( 2000-08-01), p. G277-G287
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 279, No. 2 ( 2000-08-01), p. G277-G287
    Abstract: Single channel patch-clamp techniques were used to demonstrate the presence of outwardly rectifying chloride channels in the basolateral membrane of crypt cells from mouse distal colon. These channels were rarely observed in the cell-attached mode and, in the inside-out configuration, only became active after a delay and depolarizing voltage steps. Single channel conductance was 23.4 pS between −100 and −40 mV and increased to 90.2 pS between 40 and 100 mV. The channel permeability sequence for anions was: I − 〉 SCN − 〉 Br − 〉 Cl − 〉 NO 3 − 〉 F − ≫ SO 4 2− ≈ gluconate. In inside-out patches, the channel open probability was voltage dependent but insensitive to intracellular Ca 2+ concentration. In cell-attached mode, forskolin, histamine, carbachol, A-23187, and activators of protein kinase C all failed to activate the channel, and activity could not be evoked in inside-out patches by exposure to the purified catalytic subunit of cAMP-dependent protein kinase A. The channel was inhibited by 5-nitro-2-(3-phenylpropylamino)benzoate, 9-anthracenecarboxylic acid, and DIDS. Stimulation of G proteins with guanosine 5′- O-(3-thiotriphosphate) decreased the channel open probability and conductance, whereas subsequent addition of guanosine 5′- O-(2-thiodiphosphate) reactivated the channel.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.2000.279.2.G277
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477329-6
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  • 7
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    Online Resource
    Lipoxin A 4 prevents tight junction disruption and delays the colonization of cystic fibrosis bronchial epithelial cells by Pseudomonas aeruginosa
    American Physiological Society ; 2016
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 310, No. 11 ( 2016-06-01), p. L1053-L1061
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 310, No. 11 ( 2016-06-01), p. L1053-L1061
    Abstract: The specialized proresolution lipid mediator lipoxin A 4 (LXA 4 ) is abnormally produced in cystic fibrosis (CF) airways. LXA 4 increases the CF airway surface liquid height and stimulates airway epithelial repair and tight junction formation. We report here a protective effect of LXA 4 (1 nM) against tight junction disruption caused by Pseudomonas aeruginosa bacterial challenge together with a delaying action against bacterial invasion in CF airway epithelial cells from patients with CF and immortalized cell lines. Bacterial invasion and tight junction integrity were measured by gentamicin exclusion assays and confocal fluorescence microscopy in non-CF (NuLi-1) and CF (CuFi-1) bronchial epithelial cell lines and in primary CF cultures, grown under an air/liquid interface, exposed to either a clinical or laboratory strains of P. aeruginosa. LXA 4 delayed P. aeruginosa invasion and transepithelial migration in CF and normal bronchial epithelial cell cultures. These protective effects of LXA 4 were inhibited by the ALX/FPR2 lipoxin receptor antagonist BOC-2. LXA 4 prevented the reduction in mRNA biosynthesis and protein abundance of the tight junction protein ZO-1 and reduced tight junction disruption induced by P. aeruginsosa inoculation. In conclusion, LXA 4 plays a protective role in bronchial epithelium by stimulating tight junction repair and by delaying and reducing the invasion of CF bronchial epithelial cells by P. aeruginsosa.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00368.2015
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 1477300-4
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  • 8
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    Online Resource
    Sympathetic responsiveness is not increased in women with a history of hypertensive pregnancy
    American Physiological Society ; 2017
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 312, No. 1 ( 2017-01-01), p. R49-R54
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 312, No. 1 ( 2017-01-01), p. R49-R54
    Abstract: Hypertensive pregnancy (HTNP) is a risk factor for future cardiovascular disease. Exaggerated cardiovascular responses to physical stress are also considered an independent marker of cardiovascular disease risk. However, there are limited data regarding the blood pressure (BP) responses to acute stress in women, who have a history of HTNP. Hence, the aim of the study is to compare BP responses to a physical stress in postmenopausal women with a history of HTNP to age- and parity-matched women with a history of normotensive pregnancy (NP). Beat-to-beat BP and heart rate was recorded in 64 postmenopausal women with [age = 58.5 (55.2, 62.2) yr, where values are the median, 25th percentile, and 75th percentile] and without [age = 59.4 (55.9, 62.4) yr] a history of HTNP before and during isometric handgrip (IHG) exercise (30% of maximal voluntary contraction) to fatigue. Muscle metaboreflex was measured during postexercise ischemia following IHG exercise. BP variables increased similarly in response to IHG exercise [systolic: NP = 11.5 (8.9, 17.6) %, HTNP = 11.3 (9.5, 15.9) %; diastolic NP = 11.2 (7.9, 13.3) %, HTNP = 9.5 (7.1, 14.3) %; mean blood pressure: NP = 9.8 (5.0, 13.6) %, and HTNP = 7.2 (4.4, 10.4) %] and postexercise ischemia [systolic: NP = 14.1 (10.3, 23.0) %, HTNP = 15.8 (10.6, 21.4) %; diastolic NP = 12.2 (4.8, 17.0) %, HTNP = 10.4 (5.3, 17.1) %; and mean blood pressure: NP = 11.1 (6.1, 17.9) %, HTNP = 9.4 (2.9, 14.8) %] in both groups. Although having a history of HTNP is associated with future cardiovascular disease risk, results from this study suggest that the risk may not be manifested through altered cardiovascular metaboreflex response to physical stressors.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00379.2016
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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