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  1. Article ; Online: Membrane progestin receptors

    Salhi Amel / Lemale Julie / Paris Nicolas / Bloch-Faure May / Crambert Gilles

    Biomolecular Concepts, Vol 1, Iss 1, Pp 41-

    beyond the controversy, can we move forward?

    2010  Volume 47

    Abstract: Steroids are well-known mediators of many different physiological functions. Their best characterized mechanism of action involves interaction with well-defined nuclear receptors and regulation of gene transcription. However, rapid effects of steroids ... ...

    Abstract Steroids are well-known mediators of many different physiological functions. Their best characterized mechanism of action involves interaction with well-defined nuclear receptors and regulation of gene transcription. However, rapid effects of steroids have been reported which are incompatible with their classical long-term/slow effects. Although the concept of membrane-bound receptors for steroids which can transduce their rapid effects has been proposed many years ago, it is only recently that such proteins have been identified and characterized. In this review, we will discuss recent data regarding the rapid action of progesterone mediated by newly characterized membrane-bound receptors belonging to the progestin and adiponectin receptor family.
    Keywords membrane-bound receptors ; non-genomic action ; progesterone ; steroid ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2010-05-01T00:00:00Z
    Publisher De Gruyter
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Mapping of sex hormone receptors and their modulators along the nephron of male and female mice.

    Grimont, Adrien / Bloch-Faure, May / El Abida, Boutaïna / Crambert, Gilles

    FEBS letters

    2009  Volume 583, Issue 10, Page(s) 1644–1648

    Abstract: Renal functions are regulated by steroid sex hormones, but the exhaustive identification of their receptors along the nephron is still lacking. Here, we have localized all known nuclear or membrane-bound sex hormone receptors and some of their activators ...

    Abstract Renal functions are regulated by steroid sex hormones, but the exhaustive identification of their receptors along the nephron is still lacking. Here, we have localized all known nuclear or membrane-bound sex hormone receptors and some of their activators along the nephron of male and female mice. Almost all receptors are present in male and female kidney, some of them having very restricted localization. Only one gene tested among 11 (ARA54) exhibits a gender difference in the level of its expression. This first "renal map" of sex steroid receptor expression may serve as a pre-requisite for investigating the role of these hormones on kidney functions.
    MeSH term(s) Animals ; Female ; Gonadal Steroid Hormones/metabolism ; Kidney/metabolism ; Male ; Mice ; Nephrons/metabolism ; RNA, Messenger/metabolism ; Receptors, Steroid/analysis ; Receptors, Steroid/metabolism
    Chemical Substances Gonadal Steroid Hormones ; RNA, Messenger ; Receptors, Steroid
    Language English
    Publishing date 2009-05-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2009.04.032
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  3. Article: Membrane progestin receptors: beyond the controversy, can we move forward?

    Salhi, Amel / Lemale, Julie / Paris, Nicolas / Bloch-Faure, May / Crambert, Gilles

    Biomolecular concepts

    2010  Volume 1, Issue 1, Page(s) 41–47

    Abstract: Steroids are well-known mediators of many different physiological functions. Their best characterized mechanism of action involves interaction with well-defined nuclear receptors and regulation of gene transcription. However, rapid effects of steroids ... ...

    Abstract Steroids are well-known mediators of many different physiological functions. Their best characterized mechanism of action involves interaction with well-defined nuclear receptors and regulation of gene transcription. However, rapid effects of steroids have been reported which are incompatible with their classical long-term/slow effects. Although the concept of membrane-bound receptors for steroids which can transduce their rapid effects has been proposed many years ago, it is only recently that such proteins have been identified and characterized. In this review, we will discuss recent data regarding the rapid action of progesterone mediated by newly characterized membrane-bound receptors belonging to the progestin and adiponectin receptor family.
    Language English
    Publishing date 2010-05-01
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2557908-3
    ISSN 1868-503X ; 1868-5021
    ISSN (online) 1868-503X
    ISSN 1868-5021
    DOI 10.1515/bmc.2010.001
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  4. Article ; Online: Chronic potassium depletion increases adrenal progesterone production that is necessary for efficient renal retention of potassium.

    Elabida, Boutaïna / Edwards, Aurélie / Salhi, Amel / Azroyan, Anie / Fodstad, Heidi / Meneton, Pierre / Doucet, Alain / Bloch-Faure, May / Crambert, Gilles

    Kidney international

    2011  Volume 80, Issue 3, Page(s) 256–262

    Abstract: Modern dietary habits are characterized by high-sodium and low-potassium intakes, each of which was correlated with a higher risk for hypertension. In this study, we examined whether long-term variations in the intake of sodium and potassium induce ... ...

    Abstract Modern dietary habits are characterized by high-sodium and low-potassium intakes, each of which was correlated with a higher risk for hypertension. In this study, we examined whether long-term variations in the intake of sodium and potassium induce lasting changes in the plasma concentration of circulating steroids by developing a mathematical model of steroidogenesis in mice. One finding of this model was that mice increase their plasma progesterone levels specifically in response to potassium depletion. This prediction was confirmed by measurements in both male mice and men. Further investigation showed that progesterone regulates renal potassium handling both in males and females under potassium restriction, independent of its role in reproduction. The increase in progesterone production by male mice was time dependent and correlated with decreased urinary potassium content. The progesterone-dependent ability to efficiently retain potassium was because of an RU486 (a progesterone receptor antagonist)-sensitive stimulation of the colonic hydrogen, potassium-ATPase (known as the non-gastric or hydrogen, potassium-ATPase type 2) in the kidney. Thus, in males, a specific progesterone concentration profile induced by chronic potassium restriction regulates potassium balance.
    MeSH term(s) Adrenal Glands/drug effects ; Adrenal Glands/enzymology ; Adrenal Glands/metabolism ; Aldosterone/biosynthesis ; Analysis of Variance ; Animals ; Cell Line ; Chronic Disease ; Corticosterone/biosynthesis ; Disease Models, Animal ; Female ; Gene Expression Regulation, Enzymologic ; H(+)-K(+)-Exchanging ATPase/genetics ; H(+)-K(+)-Exchanging ATPase/metabolism ; Hormone Antagonists/pharmacology ; Humans ; Hypokalemia/enzymology ; Hypokalemia/genetics ; Hypokalemia/metabolism ; Kidney/drug effects ; Kidney/enzymology ; Kidney/metabolism ; Male ; Mice ; Mice, Knockout ; Mifepristone/pharmacology ; Models, Biological ; Potassium, Dietary/administration & dosage ; Potassium, Dietary/metabolism ; Potassium, Dietary/urine ; Progesterone/biosynthesis ; Progesterone/blood ; Receptors, Progesterone/antagonists & inhibitors ; Receptors, Progesterone/metabolism ; Sodium, Dietary/metabolism ; Time Factors ; Up-Regulation
    Chemical Substances Hormone Antagonists ; Potassium, Dietary ; Receptors, Progesterone ; Sodium, Dietary ; Mifepristone (320T6RNW1F) ; Aldosterone (4964P6T9RB) ; Progesterone (4G7DS2Q64Y) ; H(+)-K(+)-Exchanging ATPase (EC 3.6.3.10) ; Corticosterone (W980KJ009P)
    Language English
    Publishing date 2011-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1038/ki.2011.15
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  5. Article ; Online: NHE4 is critical for the renal handling of ammonia in rodents.

    Bourgeois, Soline / Meer, Leonie Van / Wootla, Bharath / Bloch-Faure, May / Chambrey, Régine / Shull, Gary E / Gawenis, Lara R / Houillier, Pascal

    The Journal of clinical investigation

    2010  Volume 120, Issue 6, Page(s) 1895–1904

    Abstract: Ammonia absorption by the medullary thick ascending limb of Henle's loop (MTALH) is thought to be a critical step in renal ammonia handling and excretion in urine, in which it is the main acid component. Basolateral Na+/H+ exchangers have been proposed ... ...

    Abstract Ammonia absorption by the medullary thick ascending limb of Henle's loop (MTALH) is thought to be a critical step in renal ammonia handling and excretion in urine, in which it is the main acid component. Basolateral Na+/H+ exchangers have been proposed to play a role in ammonia efflux out of MTALH cells, which express 2 exchanger isoforms: Na+/H+ exchanger 1 (NHE1) and NHE4. Here, we investigated the role of NHE4 in urinary acid excretion and found that NHE4-/- mice exhibited compensated hyperchloremic metabolic acidosis, together with inappropriate urinary net acid excretion. When challenged with a 7-day HCl load, NHE4-/- mice were unable to increase their urinary ammonium and net acid excretion and displayed reduced ammonium medulla content compared with wild-type littermates. Both pharmacologic inhibition and genetic disruption of NHE4 caused a marked decrease in ammonia absorption by the MTALH. Finally, dietary induction of metabolic acidosis increased NHE4 mRNA expression in mouse MTALH cells and enhanced renal NHE4 activity in rats, as measured by in vitro microperfusion of MTALH. We therefore conclude that ammonia absorption by the MTALH requires the presence of NHE4 and that lack of NHE4 reduces the ability of MTALH epithelial cells to create the cortico-papillary gradient of NH3/NH4+ needed to excrete an acid load, contributing to systemic metabolic acidosis.
    MeSH term(s) Absorption ; Acidosis/genetics ; Acidosis/metabolism ; Ammonia/metabolism ; Ammonia/urine ; Animals ; Biological Transport/genetics ; Epithelial Cells/metabolism ; Female ; Kidney/metabolism ; Kidney/physiology ; Loop of Henle/metabolism ; Male ; Mice ; Mice, Knockout ; Quaternary Ammonium Compounds/metabolism ; Rats ; Rats, Sprague-Dawley ; Rodentia/genetics ; Rodentia/metabolism ; Specific Pathogen-Free Organisms
    Chemical Substances Quaternary Ammonium Compounds ; Ammonia (7664-41-7)
    Language English
    Publishing date 2010-05-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI36581
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  6. Article ; Online: Molecular identification of Sch28080-sensitive K-ATPase activities in the mouse kidney.

    Dherbecourt, Olivier / Cheval, Lydie / Bloch-Faure, May / Meneton, Pierre / Doucet, Alain

    Pflugers Archiv : European journal of physiology

    2006  Volume 451, Issue 6, Page(s) 769–775

    Abstract: Rat collecting ducts display either an ouabain-insensitive or an ouabain-sensitive K-ATPase activity inhibited by Sch28080 according as animals are fed a normal or a potassium-depleted diet (types I and III K-ATPase, respectively). Two isoforms of H,K- ... ...

    Abstract Rat collecting ducts display either an ouabain-insensitive or an ouabain-sensitive K-ATPase activity inhibited by Sch28080 according as animals are fed a normal or a potassium-depleted diet (types I and III K-ATPase, respectively). Two isoforms of H,K-ATPase have been cloned from rat gastric mucosa and colon, respectively. Gastric and colonic H,K-ATPase are expressed in the kidney, suggesting that they might account for types I and III K-ATPases. However, this hypothesis is not fully supported by segmental expression of gastric and colonic H,K-ATPase along the rat collecting duct, as well as by comparison of the pharmacological properties of gastric and colonic H,K-ATPase expressed in Xenopus ovocyte and types I and III K-ATPases in rat collecting ducts. The aim of the present work is to address directly the molecular origin of types I and III K-ATPases in the mouse collecting duct by measuring K-ATPase activities in collecting ducts of wild-type mice and mice genetically deficient in either gastric or colonic H,K-ATPase fed either a regular or a potassium-depleted diet. Like the rat, mouse collecting ducts display type I or III K-ATPase activity when fed a regular or a potassium-depleted diet, respectively. Type I K-ATPase activity is detected in colonic H,K-ATPase-deficient mice but not in gastric H,K-ATPase-deficient animals. Conversely, type III K-ATPase activity disappears in colonic H,K-ATPase-deficient but not in gastric H,K-ATPase-deficient mice. In conclusion, types I and III K-ATPases measured in collecting ducts of normal and potassium-depleted mice reflect the functional expression of gastric and colonic H,K-ATPase, respectively.
    MeSH term(s) Animals ; Colon/enzymology ; Diet ; H(+)-K(+)-Exchanging ATPase/genetics ; H(+)-K(+)-Exchanging ATPase/metabolism ; Imidazoles/pharmacology ; Kidney/enzymology ; Mice ; Mice, Knockout ; Potassium/metabolism ; Protein Subunits/genetics ; Protein Subunits/metabolism ; Stomach/enzymology
    Chemical Substances Imidazoles ; Protein Subunits ; Sch 28080 (00427X161I) ; H(+)-K(+)-Exchanging ATPase (EC 3.6.3.10) ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2006-03
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-005-1508-1
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  7. Article: Membrane progestin receptors alpha and gamma in renal epithelium.

    Lemale, Julie / Bloch-Faure, May / Grimont, Adrien / El Abida, Boutaïna / Imbert-Teboul, Martine / Crambert, Gilles

    Biochimica et biophysica acta

    2008  Volume 1783, Issue 12, Page(s) 2234–2240

    Abstract: Sex hormones have broader effects than regulating reproductive functions. Recent identification of membrane progestin receptors expressed in kidney prompted us to investigate their putative involvement in the renal effects of this hormone. We first ... ...

    Abstract Sex hormones have broader effects than regulating reproductive functions. Recent identification of membrane progestin receptors expressed in kidney prompted us to investigate their putative involvement in the renal effects of this hormone. We first focused our investigations on mPRalpha and gamma by analyzing three parameters 1/ their distribution along the mouse nephron and their subcellular location in native kidney, 2/ the ability of progesterone to stimulate ERK pathway and/or Ca(2+) release from internal stores in native kidney structures and 3/ the cellular localization of mPRalpha and its molecular determinants in heterologous expression system. We observed that 1/ mPRalpha expression is restricted to proximal tubules of both male and female mice whereas mPRgamma exhibits a much broader expression all along the nephron except the glomerulus, 2/ mPRalpha and gamma are not localized at the plasma membrane in native kidney, 3/ this expression does not permit either progesterone-induced ERK phosphorylation or Ca(2+) release and 4/ in HEK transfected cells, mPRalpha localizes in the endoplasmic reticulum (ER) due to a C-terminal ER retention motif (-KXX). Therefore, we have characterized mPRs in kidney but their role in renal physiology remains to be elucidated.
    MeSH term(s) Animals ; Blotting, Western ; Calcium/metabolism ; Cell Membrane/metabolism ; Cells, Cultured ; Endoplasmic Reticulum/metabolism ; Female ; Humans ; Immunoenzyme Techniques ; Kidney/metabolism ; Kidney Tubules, Proximal/cytology ; Kidney Tubules, Proximal/metabolism ; Male ; Mice ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Peptide Fragments ; Progesterone/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Progesterone/genetics ; Receptors, Progesterone/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Subcellular Fractions ; Triiodobenzoic Acids/pharmacology
    Chemical Substances Peptide Fragments ; RNA, Messenger ; Receptors, G-Protein-Coupled ; Receptors, Progesterone ; Triiodobenzoic Acids ; membrane progestin receptor alpha, human ; membrane progestin receptor gamma, human ; Progesterone (4G7DS2Q64Y) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; iodixanol (HW8W27HTXX) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2008-12
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamcr.2008.07.023
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  8. Article ; Online: GDF15 triggers homeostatic proliferation of acid-secreting collecting duct cells.

    Duong Van Huyen, Jean Paul / Cheval, Lydie / Bloch-Faure, May / Belair, Marie France / Heudes, Didier / Bruneval, Patrick / Doucet, Alain

    Journal of the American Society of Nephrology : JASN

    2008  Volume 19, Issue 10, Page(s) 1965–1974

    Abstract: Although adult kidney cells are quiescent, enlargement of specific populations of epithelial cells occurs during repair and adaptive processes. A prerequisite to the development of regenerative therapeutics is to identify the mechanisms and factors that ... ...

    Abstract Although adult kidney cells are quiescent, enlargement of specific populations of epithelial cells occurs during repair and adaptive processes. A prerequisite to the development of regenerative therapeutics is to identify the mechanisms and factors that control the size of specific populations of renal cells. Unfortunately, in most cases, it is unknown whether the growth of cell populations results from transdifferentiation or proliferation and whether proliferating cells derive from epithelial cells or from circulating or resident progenitors. In this study, the mechanisms underlying the enlargement of the acid-secreting cell population in the mouse kidney collecting duct in response to metabolic acidosis was investigated. Acidosis led to two phases of proliferation that preferentially affected the acid-secreting cells of the outer medullary collecting duct. All proliferating cells displayed polarized expression of functional markers. The first phase of proliferation, which started within 24 h and peaked at day 3, was dependent on the overexpression of growth differentiation factor 15 (GDF15) and cyclin D1 and was abolished when phosphatidylinositol-3 kinase and mammalian target of rapamycin were inhibited. During this phase, cells mostly divided along the tubular axis, contributing to tubule lengthening. The second phase of proliferation was independent of GDF15 but was associated with induction of cyclin D3. During this phase, cells divided transversely. In summary, acid-secreting cells proliferate as the collecting duct adapts to metabolic acidosis, and GDF15 seems to be an important determinant of collecting duct lengthening.
    MeSH term(s) Acid-Base Equilibrium/physiology ; Acidosis, Renal Tubular/etiology ; Acidosis, Renal Tubular/metabolism ; Acidosis, Renal Tubular/pathology ; Animals ; Cell Proliferation ; Cell Transdifferentiation/physiology ; Cyclin D3 ; Cyclins/metabolism ; Cytokines/genetics ; Cytokines/metabolism ; Female ; Growth Differentiation Factor 15 ; Kidney Tubules, Collecting/metabolism ; Kidney Tubules, Collecting/pathology ; Male ; Mice ; Mice, Inbred C57BL ; RNA, Messenger/metabolism
    Chemical Substances Ccnd3 protein, mouse ; Cyclin D3 ; Cyclins ; Cytokines ; Gdf15 protein, mouse ; Growth Differentiation Factor 15 ; RNA, Messenger
    Language English
    Publishing date 2008-07-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2007070781
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  9. Article ; Online: Renal phenotype in mice lacking the Kir5.1 (Kcnj16) K+ channel subunit contrasts with that observed in SeSAME/EAST syndrome.

    Paulais, Marc / Bloch-Faure, May / Picard, Nicolas / Jacques, Thibaut / Ramakrishnan, Suresh Krishna / Keck, Mathilde / Sohet, Fabien / Eladari, Dominique / Houillier, Pascal / Lourdel, Stéphane / Teulon, Jacques / Tucker, Stephen J

    Proceedings of the National Academy of Sciences of the United States of America

    2011  Volume 108, Issue 25, Page(s) 10361–10366

    Abstract: The heteromeric inwardly rectifying Kir4.1/Kir5.1 K(+) channel underlies the basolateral K(+) conductance in the distal nephron and is extremely sensitive to inhibition by intracellular pH. The functional importance of Kir4.1/Kir5.1 in renal ion ... ...

    Abstract The heteromeric inwardly rectifying Kir4.1/Kir5.1 K(+) channel underlies the basolateral K(+) conductance in the distal nephron and is extremely sensitive to inhibition by intracellular pH. The functional importance of Kir4.1/Kir5.1 in renal ion transport has recently been highlighted by mutations in the human Kir4.1 gene (KCNJ10) that result in seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME)/epilepsy, ataxia, sensorineural deafness, and renal tubulopathy (EAST) syndrome, a complex disorder that includes salt wasting and hypokalemic alkalosis. Here, we investigated the role of the Kir5.1 subunit in mice with a targeted disruption of the Kir5.1 gene (Kcnj16). The Kir5.1(-/-) mice displayed hypokalemic, hyperchloremic metabolic acidosis with hypercalciuria. The short-term responses to hydrochlorothiazide, an inhibitor of ion transport in the distal convoluted tubule (DCT), were also exaggerated, indicating excessive renal Na(+) absorption in this segment. Furthermore, chronic treatment with hydrochlorothiazide normalized urinary excretion of Na(+) and Ca(2+), and abolished acidosis in Kir5.1(-/-) mice. Finally, in contrast to WT mice, electrophysiological recording of K(+) channels in the DCT basolateral membrane of Kir5.1(-/-) mice revealed that, even though Kir5.1 is absent, there is an increased K(+) conductance caused by the decreased pH sensitivity of the remaining homomeric Kir4.1 channels. In conclusion, disruption of Kcnj16 induces a severe renal phenotype that, apart from hypokalemia, is the opposite of the phenotype seen in SeSAME/EAST syndrome. These results highlight the important role that Kir5.1 plays as a pH-sensitive regulator of salt transport in the DCT, and the implication of these results for the correct genetic diagnosis of renal tubulopathies is discussed.
    MeSH term(s) Acidosis/genetics ; Acidosis/physiopathology ; Amiloride/pharmacology ; Animals ; Diuretics/pharmacology ; Furosemide/pharmacology ; Humans ; Hydrochlorothiazide/pharmacology ; Hypokalemia/genetics ; Hypokalemia/physiopathology ; Kidney Tubules/cytology ; Kidney Tubules/drug effects ; Kidney Tubules/physiology ; Kidney Tubules/physiopathology ; Mice ; Mice, Knockout ; Patch-Clamp Techniques ; Phenotype ; Potassium Channels, Inwardly Rectifying/genetics ; Potassium Channels, Inwardly Rectifying/metabolism ; Sodium Channel Blockers/pharmacology ; Sodium Potassium Chloride Symporter Inhibitors/pharmacology ; Syndrome ; Kir5.1 Channel
    Chemical Substances Diuretics ; Potassium Channels, Inwardly Rectifying ; Sodium Channel Blockers ; Sodium Potassium Chloride Symporter Inhibitors ; Hydrochlorothiazide (0J48LPH2TH) ; Amiloride (7DZO8EB0Z3) ; Furosemide (7LXU5N7ZO5)
    Language English
    Publishing date 2011-06-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1101400108
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  10. Article: Renal phenotype in mice lacking the Kir5.1 (Kcnj16) K⁺ channel subunit contrasts with that observed in SeSAME/EAST syndrome

    Paulais, Marc / Bloch-Faure, May / Picard, Nicolas / Jacques, Thibaut / Ramakrishnan, Suresh Krishna / Keck, Mathilde / Sohet, Fabien / Eladari, Dominique / Houillier, Pascal / Lourdel, Stéphane / Teulon, Jacques / Tucker, Stephen J

    Proceedings of the National Academy of Sciences of the United States of America. 2011 June 21, v. 108, no. 25

    2011  

    Abstract: The heteromeric inwardly rectifying Kir4.1/Kir5.1 K⁺ channel underlies the basolateral K⁺ conductance in the distal nephron and is extremely sensitive to inhibition by intracellular pH. The functional importance of Kir4.1/Kir5.1 in renal ion ... ...

    Abstract The heteromeric inwardly rectifying Kir4.1/Kir5.1 K⁺ channel underlies the basolateral K⁺ conductance in the distal nephron and is extremely sensitive to inhibition by intracellular pH. The functional importance of Kir4.1/Kir5.1 in renal ion transport has recently been highlighted by mutations in the human Kir4.1 gene (KCNJ10) that result in seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME)/epilepsy, ataxia, sensorineural deafness, and renal tubulopathy (EAST) syndrome, a complex disorder that includes salt wasting and hypokalemic alkalosis. Here, we investigated the role of the Kir5.1 subunit in mice with a targeted disruption of the Kir5.1 gene (Kcnj16). The Kir5.1⁻/⁻ mice displayed hypokalemic, hyperchloremic metabolic acidosis with hypercalciuria. The short-term responses to hydrochlorothiazide, an inhibitor of ion transport in the distal convoluted tubule (DCT), were also exaggerated, indicating excessive renal Na⁺ absorption in this segment. Furthermore, chronic treatment with hydrochlorothiazide normalized urinary excretion of Na⁺ and Ca²⁺, and abolished acidosis in Kir5.1⁻/⁻ mice. Finally, in contrast to WT mice, electrophysiological recording of K⁺ channels in the DCT basolateral membrane of Kir5.1⁻/⁻ mice revealed that, even though Kir5.1 is absent, there is an increased K⁺ conductance caused by the decreased pH sensitivity of the remaining homomeric Kir4.1 channels. In conclusion, disruption of Kcnj16 induces a severe renal phenotype that, apart from hypokalemia, is the opposite of the phenotype seen in SeSAME/EAST syndrome. These results highlight the important role that Kir5.1 plays as a pH-sensitive regulator of salt transport in the DCT, and the implication of these results for the correct genetic diagnosis of renal tubulopathies is discussed.
    Keywords absorption ; acidosis ; alkalosis ; ataxia (disorder) ; calcium ; deafness ; electrolytes ; electrophysiology ; excretion ; genes ; humans ; hydrochlorothiazide ; hypokalemia ; mice ; mutation ; pH ; phenotype ; potassium ; potassium channels ; seizures ; sodium
    Language English
    Dates of publication 2011-0621
    Size p. 10361-10366.
    Publishing place National Academy of Sciences
    Document type Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1101400108
    Database NAL-Catalogue (AGRICOLA)

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