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Pendrin inhibitor

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https://www.readbyqxmd.com/read/27161422/effect-of-known-inhibitors-of-ion-transport-on-pendrin-slc26a4-activity-in-a-human-kidney-cell-line
#1
Emanuele Bernardinelli, Roberta Costa, Charity Nofziger, Markus Paulmichl, Silvia Dossena
BACKGROUND/AIMS: Pendrin is a Cl-/I-/HCO3- exchanger playing a fundamental role in controlling blood pressure and airway function, therefore representing an attractive target for the treatment of hypertensive states and respiratory distresses. A review of the literature regarding the ability of some compounds (namely several known inhibitors of ion transport) to block pendrin activity revealed discordant findings. These incongruous findings may be due, in part, to the concentration of compound and/or the nature of the model system used in the study...
2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27153921/small-molecule-inhibitors-of-pendrin-potentiate-the-diuretic-action-of-furosemide
#2
Onur Cil, Peter M Haggie, Puay-Wah Phuan, Joseph-Anthony Tan, Alan S Verkman
Pendrin is a Cl(-)/HCO3(-) exchanger expressed in type B and non-A, non-B intercalated cells in the distal nephron, where it facilitates Cl(-) absorption and is involved in Na(+) absorption and acid-base balance. Pendrin-knockout mice show no fluid-electrolyte abnormalities under baseline conditions, although mice with double knockout of pendrin and the Na(+)/Cl(-) cotransporter (NCC) manifest profound salt wasting. Thus, pendrin may attenuate diuretic-induced salt loss, but this function remains unconfirmed...
December 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/26963391/the-role-of-epithelial-sodium-channel-enac-and-the-apical-cl-hco3-exchanger-pendrin-in-compensatory-salt-reabsorption-in-the-setting-of-na-cl-cotransporter-ncc-inactivation
#3
Mina Patel-Chamberlin, Mujan Varasteh Kia, Jie Xu, Sharon Barone, Kamyar Zahedi, Manoocher Soleimani
BACKGROUND: The absence of NCC does not cause significant salt wasting in NCC deficient mice under basal conditions. We hypothesized that ENaC and pendrin play important roles in compensatory salt absorption in the setting of NCC inactivation, and their inhibition and/or downregulation can cause significant salt wasting in NCC KO mice. METHODS: WT and NCC KO mice were treated with a daily injection of either amiloride, an inhibitor of ENaC, or acetazolamide (ACTZ), a blocker of salt and bicarbonate reabsorption in the proximal tubule and an inhibitor of carbonic anhydrases in proximal tubule and intercalated cells, or a combination of acetazolamide plus amiloride for defined durations...
2016: PloS One
https://www.readbyqxmd.com/read/26932931/inhibitors-of-pendrin-anion-exchange-identified-in-a-small-molecule-screen-increase-airway-surface-liquid-volume-in-cystic-fibrosis
#4
Peter M Haggie, Puay-Wah Phuan, Joseph-Anthony Tan, Lorna Zlock, Walter E Finkbeiner, A S Verkman
Pendrin (SLC26A4) is a Cl(-)/anion exchanger expressed in the epithelium of inflamed airways where it is thought to facilitate Cl(-) absorption and HCO3 (-) secretion. Studies using pendrin knockout mice and airway epithelial cells from hearing-impaired subjects with pendrin loss of function suggest involvement of pendrin in inflammatory lung diseases, including cystic fibrosis (CF), perhaps by regulation of airway surface liquid (ASL) volume. Here we identified small-molecule pendrin inhibitors and demonstrated their efficacy in increasing ASL volume...
June 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/25298423/anoctamin-1-tmem16a-is-the-major-apical-iodide-channel-of-the-thyrocyte
#5
L Twyffels, A Strickaert, M Virreira, C Massart, J Van Sande, C Wauquier, R Beauwens, J E Dumont, L J Galietta, A Boom, V Kruys
Iodide is captured by thyrocytes through the Na(+)/I(-) symporter (NIS) before being released into the follicular lumen, where it is oxidized and incorporated into thyroglobulin for the production of thyroid hormones. Several reports point to pendrin as a candidate protein for iodide export from thyroid cells into the follicular lumen. Here, we show that a recently discovered Ca(2+)-activated anion channel, TMEM16A or anoctamin-1 (ANO1), also exports iodide from rat thyroid cell lines and from HEK 293T cells expressing human NIS and ANO1...
December 15, 2014: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/25148130/contractile-force-is-enhanced-in-aortas-from-pendrin-null-mice-due-to-stimulation-of-angiotensin-ii-dependent-signaling
#6
Roy L Sutliff, Erik R Walp, Young Hee Kim, Lori A Walker, Alexander M El-Ali, Jing Ma, Robert Bonsall, Semra Ramosevac, Douglas C Eaton, Jill W Verlander, Laura Hansen, Rudolph L Gleason, Truyen D Pham, Seongun Hong, Vladimir Pech, Susan M Wall
Pendrin is a Cl-/HCO3- exchanger expressed in the apical regions of renal intercalated cells. Following pendrin gene ablation, blood pressure falls, in part, from reduced renal NaCl absorption. We asked if pendrin is expressed in vascular tissue and if the lower blood pressure observed in pendrin null mice is accompanied by reduced vascular reactivity. Thus, the contractile responses to KCl and phenylephrine (PE) were examined in isometrically mounted thoracic aortas from wild-type and pendrin null mice. Although pendrin expression was not detected in the aorta, pendrin gene ablation changed contractile protein abundance and increased the maximal contractile response to PE when normalized to cross sectional area (CSA)...
2014: PloS One
https://www.readbyqxmd.com/read/25069981/epithelial-anion-transporter-pendrin-contributes-to-inflammatory-lung-pathology-in-mouse-models-of-bordetella-pertussis-infection
#7
Karen M Scanlon, Yael Gau, Jingsong Zhu, Ciaran Skerry, Susan M Wall, Manoocher Soleimani, Nicholas H Carbonetti
Pertussis disease, characterized by severe and prolonged coughing episodes, can progress to a critical stage with pulmonary inflammation and death in young infants. However, there are currently no effective treatments for pertussis. We previously studied the role of pertussis toxin (PT), an important Bordetella pertussis virulence factor, in lung transcriptional responses to B. pertussis infection in mouse models. One of the genes most highly upregulated in a PT-dependent manner encodes an epithelial transporter of bicarbonate, chloride, and thiocyanate, named pendrin, that contributes to asthma pathology...
October 2014: Infection and Immunity
https://www.readbyqxmd.com/read/24900070/the-effect-of-tanespimycin-17-aag-on-radioiodine-accumulation-in-sodium-iodide-symporter-expressing-cells
#8
Kyoung Hyun Yu, Hyewon Youn, Myung Geun Song, Dong Soo Lee, June-Key Chung
PURPOSE: The heat shock protein 90 inhibitor, tanespimycin, is an anticancer agent known to increase iodine accumulation in normal and cancerous thyroid cells. Iodine accumulation is regulated by membrane proteins such as sodium iodide symporter (NIS) and pendrin (PDS), and thus we attempted to characterize the effects of tanespimycin on those genes. METHODS: Cells were incubated with tanespimycin in order to evaluate (125)I accumulation and efflux ability. Radioiodine uptake and efflux were measured by a gamma counter and normalized by protein amount...
December 2012: Nuclear Medicine and Molecular Imaging
https://www.readbyqxmd.com/read/24260196/potentiation-of-the-effect-of-thiazide-derivatives-by-carbonic-anhydrase-inhibitors-molecular-mechanisms-and-potential-clinical-implications
#9
Kamyar Zahedi, Sharon Barone, Jie Xu, Manoocher Soleimani
BACKGROUND: Carbonic anhydrase inhibitors (CAI) are mild diuretics, hence not widely used in fluid overloaded states. They are however the treatment of choice for certain non-kidney conditions. Thiazides, specific inhibitors of Na-Cl cotransport (NCC), are mild agents and the most widely used diuretics in the world for control of mild hypertension. HYPOTHESIS: In addition to inhibiting the salt reabsorption in the proximal tubule, CAIs down-regulate pendrin, therefore leaving NCC as the major salt absorbing transporter in the distal nephron, and hence allowing for massive diuresis by the inhibitors of NCC in the setting of increased delivery of salt from the proximal tubule...
2013: PloS One
https://www.readbyqxmd.com/read/24231659/protein-phosphatase-1-inhibitor-1-deficiency-reduces-phosphorylation-of-renal-nacl-cotransporter-and-causes-arterial-hypotension
#10
Nicolas Picard, Katja Trompf, Chao-Ling Yang, R Lance Miller, Monique Carrel, Dominique Loffing-Cueni, Robert A Fenton, David H Ellison, Johannes Loffing
The thiazide-sensitive NaCl cotransporter (NCC) of the renal distal convoluted tubule (DCT) controls ion homeostasis and arterial BP. Loss-of-function mutations of NCC cause renal salt wasting with arterial hypotension (Gitelman syndrome). Conversely, mutations in the NCC-regulating WNK kinases or kelch-like 3 protein cause familial hyperkalemic hypertension. Here, we performed automated sorting of mouse DCTs and microarray analysis for comprehensive identification of novel DCT-enriched gene products, which may potentially regulate DCT and NCC function...
March 2014: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/23515718/nitric-oxide-reduces-cl%C3%A2-absorption-in-the-mouse-cortical-collecting-duct-through-an-enac-dependent-mechanism
#11
Vladimir Pech, Monika Thumova, Sergey I Dikalov, Edith Hummler, Bernard C Rossier, David G Harrison, Susan M Wall
Since nitric oxide (NO) participates in the renal regulation of blood pressure, in part, by modulating transport of Na⁺ and Cl⁻ in the kidney, we asked whether NO regulates net Cl⁻ flux (JCl) in the cortical collecting duct (CCD) and determined the transporter(s) that mediate NO-sensitive Cl⁻ absorption. Cl⁻ absorption was measured in CCDs perfused in vitro that were taken from aldosterone-treated mice. Administration of an NO donor (10 μM MAHMA NONOate) reduced JCl and transepithelial voltage (VT) both in the presence or absence of angiotensin II...
June 1, 2013: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/23215877/protein-phosphatase-1-coordinates-cftr-dependent-airway-epithelial-hco3-secretion-by-reciprocal-regulation-of-apical-and-basolateral-membrane-cl-hco3-exchangers
#12
James P Garnett, Emma Hickman, Orathai Tunkamnerdthai, Alan W Cuthbert, Michael A Gray
BACKGROUND AND PURPOSE: Our recent studies on human airway serous-like Calu-3 cells showed that cAMP agonists stimulated a HCO3(-) rich secretion containing up to 80 mM HCO3(-). This alkaline secretion relied on a coordinated switch in the activity of distinct Cl(-)-HCO3(-) anion exchangers (AE) located at different regions of the cell. At the apical membrane, cAMP agonists activated the electroneutral AE pendrin (SLC26A4), together with cystic fibrosis transmembrane conductance regulator (CFTR), while at the basolateral membrane the agonists inhibited AE2 (SLC4A2)...
April 2013: British Journal of Pharmacology
https://www.readbyqxmd.com/read/23007642/expression-of-anion-exchangers-in-cultured-human-endolymphatic-sac-epithelia
#13
Hyun Jae Lee, Won Sun Yang, Hyun Woo Park, Hyun Seung Choi, Sung Huhn Kim, Jin Young Kim, Jae Young Choi
HYPOTHESIS: Pendrin acts as a Cl-/HCO3- exchanger and is responsible for endolymphatic fluid volume and pH homeostasis in human endolymphatic sac epithelial cells. BACKGROUND: The endolymphatic sac (ES) is part of the membranous labyrinth in the inner ear that plays an important role in maintaining homeostasis of the endolymphatic fluid system. However, the exact mechanism of fluid volume and pH regulation is not fully understood yet. We aimed to demonstrate the expression of various anion exchangers (AEs), including pendrin, in cultured human endolymphatic sac epithelial (HESE) cells...
December 2012: Otology & Neurotology
https://www.readbyqxmd.com/read/22811483/pendrin-protein-abundance-in-the-kidney-is-regulated-by-nitric-oxide-and-camp
#14
Monika Thumova, Vladimir Pech, Otto Froehlich, Diana Agazatian, Xiaonan Wang, Jill W Verlander, Young Hee Kim, Susan M Wall
Pendrin is a Cl(-)/HCO(3)(-) exchanger, expressed in the apical regions of some intercalated cell subtypes, and is critical in the pressor response to angiotensin II. Since angiotensin type 1 receptor inhibitors reduce renal pendrin protein abundance in mice in vivo through a mechanism that is dependent on nitric oxide (NO), we asked if NO modulates renal pendrin expression in vitro and explored the mechanism by which it occurs. Thus we quantified pendrin protein abundance by confocal fluorescent microscopy in cultured mouse cortical collecting ducts (CCDs) and connecting tubules (CNTs)...
September 15, 2012: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/22750442/roles-of-17-aag-induced-molecular-chaperones-and-rma1-e3-ubiquitin-ligase-in-folding-and-degradation-of-pendrin
#15
Kanghyun Lee, Tae-Joon Hong, Ji-Sook Hahn
Pendrin is a transmembrane chloride/anion exchanger highly expressed in thyroid, kidney, and inner ear. Endoplasmic reticulum (ER)-retention of improperly folded Pendrin mutants is considered as the major cause for Pendred syndrome. However, the folding and degradation mechanisms of Pendrin are poorly understood. Here, we report that treatment of 17-AAG, an Hsp90 inhibitor, facilitates the folding of Pendrin through heat shock transcription factor 1 (Hsf1)-dependent induction of molecular chaperones. Furthermore, we demonstrate that Rma1, an E3 ubiquitin ligase localized in the ER membrane, is involved in Pendrin degradation...
July 30, 2012: FEBS Letters
https://www.readbyqxmd.com/read/22649419/epigenetics-modifications-and-therapeutic-prospects-in-human-thyroid-cancer
#16
Maria Graziella Catalano, Nicoletta Fortunati, Giuseppe Boccuzzi
At present no successful treatment is available for advanced thyroid cancer, which comprises poorly differentiated, anaplastic, and metastatic or recurrent differentiated thyroid cancer not responding to radioiodine. In the last few years, biologically targeted therapies for advanced thyroid carcinomas have been proposed on the basis of the recognition of key oncogenic mutations. Although the results of several phase II trials look promising, none of the patients treated had a complete response, and only a minority of them had a partial response, suggesting that the treatment is, at best, effective in stabilizing patients with progressive disease...
2012: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/22178794/iodide-treatment-acutely-increases-pendrin-slc26a4-mrna-expression-in-the-rat-thyroid-and-the-pccl3-thyroid-cell-line-by-transcriptional-mechanisms
#17
Jamile Calil-Silveira, Caroline Serrano-Nascimento, Maria Tereza Nunes
Iodine is a critical element involved in thyroid hormone synthesis. Its efflux into the follicular lumen is thought to occur, in part, through pendrin at the apical membrane of thyrocytes. This study attempted to investigate whether iodide administration affects SLC26A4 mRNA expression in rat thyroid and in PCCl3 cells. Rats and cells were treated or not with NaI from 30 min up to 48 h. One group was concomitantly treated with sodium perchlorate. SLC26A4 mRNA expression was also investigated in PCCl3 cells treated with actinomycin D prior to NaI treatment...
March 5, 2012: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/22116365/angiotensin-ii-stimulates-h%C3%A2-%C2%BA-atpase-activity-in-intercalated-cells-from-isolated-mouse-connecting-tubules-and-cortical-collecting-ducts
#18
Carsten A Wagner, Nilufar Mohebbi, Ulrike Uhlig, Gerhard H Giebisch, Sylvie Breton, Dennis Brown, John P Geibel
Intercalated cells in the collecting duct system express V-type H(+)-ATPases which participate in acid extrusion, bicarbonate secretion, and chloride absorption depending on the specific subtype. The activity of H(+)-ATPases is regulated by acid-base status and several hormones, including angiotensin II and aldosterone. Angiotensin II stimulates chloride absorption mediated by pendrin in type B intercalated cells and this process is energized by the activity of H(+)-ATPases. Moreover, angiotensin II stimulates bicarbonate secretion by the connecting tubule (CNT) and early cortical collecting duct (CCD)...
2011: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/21921024/angiotensin-ii-acts-through-the-angiotensin-1a-receptor-to-upregulate-pendrin
#19
Jill W Verlander, Seongun Hong, Vladimir Pech, James L Bailey, Diana Agazatian, Sharon W Matthews, Thomas M Coffman, Thu Le, Tadashi Inagami, Florence M Whitehill, I David Weiner, Donna B Farley, Young Hee Kim, Susan M Wall
Pendrin is an anion exchanger expressed in the apical regions of B and non-A, non-B intercalated cells. Since angiotensin II increases pendrin-mediated Cl(-) absorption in vitro, we asked whether angiotensin II increases pendrin expression in vivo and whether angiotensin-induced hypertension is pendrin dependent. While blood pressure was similar in pendrin null and wild-type mice under basal conditions, following 2 wk of angiotensin II administration blood pressure was 31 mmHg lower in pendrin null than in wild-type mice...
December 2011: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/20389022/the-na-dependent-chloride-bicarbonate-exchanger-slc4a8-mediates-an-electroneutral-na-reabsorption-process-in-the-renal-cortical-collecting-ducts-of-mice
#20
Françoise Leviel, Christian A Hübner, Pascal Houillier, Luciana Morla, Soumaya El Moghrabi, Gaëlle Brideau, Hatim Hassan, Hassan Hatim, Mark D Parker, Ingo Kurth, Alexandra Kougioumtzes, Anne Sinning, Vladimir Pech, Kent A Riemondy, R Lance Miller, Edith Hummler, Gary E Shull, Peter S Aronson, Alain Doucet, Susan M Wall, Régine Chambrey, Dominique Eladari
Regulation of sodium balance is a critical factor in the maintenance of euvolemia, and dysregulation of renal sodium excretion results in disorders of altered intravascular volume, such as hypertension. The amiloride-sensitive epithelial sodium channel (ENaC) is thought to be the only mechanism for sodium transport in the cortical collecting duct (CCD) of the kidney. However, it has been found that much of the sodium absorption in the CCD is actually amiloride insensitive and sensitive to thiazide diuretics, which also block the Na-Cl cotransporter (NCC) located in the distal convoluted tubule...
May 2010: Journal of Clinical Investigation
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