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  1. Article ; Online: Inhibition of pannexin-1 does not restore electrolyte balance in precystic Pkd1 knockout mice.

    van Megen, Wouter H / van Houtert, Teun J / Bos, Caro / Peters, Dorien J M / de Baaij, Jeroen H F / Hoenderop, Joost G J

    Physiological reports

    2024  Volume 12, Issue 7, Page(s) e15956

    Abstract: Mutations in PKD1 and PKD2 cause autosomal dominant polycystic kidney disease (ADPKD), which is characterized by the formation of fluid-filled cysts in the kidney. In a subset of ADPKD patients, reduced blood calcium ( ... ...

    Abstract Mutations in PKD1 and PKD2 cause autosomal dominant polycystic kidney disease (ADPKD), which is characterized by the formation of fluid-filled cysts in the kidney. In a subset of ADPKD patients, reduced blood calcium (Ca
    MeSH term(s) Animals ; Humans ; Mice ; Adenosine Triphosphate/metabolism ; Kidney/metabolism ; Mice, Knockout ; Mutation ; Polycystic Kidney, Autosomal Dominant/metabolism ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism ; TRPP Cation Channels/pharmacology ; Water-Electrolyte Balance
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE) ; TRPP Cation Channels ; polycystic kidney disease 1 protein ; Panx1 protein, mouse
    Language English
    Publishing date 2024-04-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15956
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Differential parathyroid and kidney Ca

    van Megen, Wouter H / Tan, Rebecca Siu Ga / Alexander, R Todd / Dimke, Henrik

    EBioMedicine

    2022  Volume 78, Page(s) 103947

    Abstract: Background: Parathyroid Ca: Methods: Activation of the CaSR was studied in mouse models and a ADH1 patient. In vitro CaSR activation was studied in HEK293 cells.: Findings: Cldn14 showed blood Ca: Interpretation: Our findings suggest that ... ...

    Abstract Background: Parathyroid Ca
    Methods: Activation of the CaSR was studied in mouse models and a ADH1 patient. In vitro CaSR activation was studied in HEK293 cells.
    Findings: Cldn14 showed blood Ca
    Interpretation: Our findings suggest that parathyroid CaSR overactivity can reduce plasma Ca
    Funding: Erasmus+ 2018/E+/4458087, the Canadian Institutes for Health research, the Novo Nordisk Foundation, the Beckett Foundation, the Carlsberg Foundation and Independent Research Fund Denmark.
    MeSH term(s) Animals ; Calcium/metabolism ; Canada ; HEK293 Cells ; Humans ; Hypercalciuria/genetics ; Hypocalcemia/genetics ; Hypoparathyroidism/congenital ; Kidney/metabolism ; Mice ; Parathyroid Hormone ; Receptors, Calcium-Sensing/genetics ; Receptors, Calcium-Sensing/metabolism
    Chemical Substances Parathyroid Hormone ; Receptors, Calcium-Sensing ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-03-18
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2022.103947
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7090: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Extracellular vesicles contribute to early cyst development in autosomal dominant polycystic kidney disease by cell-to-cell communication.

    Carotti, Valentina / van Megen, Wouter H / Rigalli, Juan P / Barros, Eric R / Sommers, Vera / Rutten, Luco / Sommerdijk, Nico / Peters, Dorien J M / van Asbeck-van der Wijst, Jenny / Hoenderop, Joost G J

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2023  Volume 37, Issue 7, Page(s) e23006

    Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of fluid-filled cysts within the kidney due to mutations in PKD1 or PKD2. Although the disease remains incompletely understood, one of the factors associated with ... ...

    Abstract Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of fluid-filled cysts within the kidney due to mutations in PKD1 or PKD2. Although the disease remains incompletely understood, one of the factors associated with ADPKD progression is the release of nucleotides (including ATP), which can initiate autocrine or paracrine purinergic signaling by binding to their receptors. Recently, we and others have shown that increased extracellular vesicle (EVs) release from PKD1 knockout cells can stimulate cyst growth through effects on recipient cells. Given that EVs are an important communicator between different nephron segments, we hypothesize that EVs released from PKD1 knockout distal convoluted tubule (DCT) cells can stimulate cyst growth in the downstream collecting duct (CD). Here, we show that administration of EVs derived from Pkd1
    MeSH term(s) Mice ; Animals ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/metabolism ; Kidney/metabolism ; Cell Communication ; Extracellular Vesicles/metabolism ; Adenosine Triphosphate/metabolism ; Cysts/metabolism ; TRPP Cation Channels/metabolism
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE) ; TRPP Cation Channels
    Language English
    Publishing date 2023-07-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202300490R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 296: Show issues

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  4. Article ; Online: Fluid shear stress stimulates ATP release without regulating purinergic gene expression in the renal inner medullary collecting duct.

    van Megen, Wouter H / Canki, Esra / Wagenaar, Vera H A / van Waes, Charlotte R M M / Peters, Dorien J M / Van Asbeck-Van der Wijst, Jenny / Hoenderop, Joost G J

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2023  Volume 37, Issue 11, Page(s) e23232

    Abstract: In the kidney, the flow rate of the pro-urine through the renal tubules is highly variable. The tubular epithelial cells sense these variations in pro-urinary flow rate in order to regulate various physiological processes, including electrolyte ... ...

    Abstract In the kidney, the flow rate of the pro-urine through the renal tubules is highly variable. The tubular epithelial cells sense these variations in pro-urinary flow rate in order to regulate various physiological processes, including electrolyte reabsorption. One of the mechanosensitive pathways activated by flow is the release of ATP, which can then act as a autocrine or paracrine factor. Increased ATP release is observed in various kidney diseases, among others autosomal dominant polycystic kidney disease (ADPKD). However, the mechanisms underlying flow-induced ATP release in the collecting duct, especially in the inner medullary collecting duct, remain understudied. Using inner medullary collecting duct 3 (IMCD3) cells in a microfluidic setup, we show here that administration of a high flow rate for 1 min results in an increased ATP release compared to a lower flow rate. Although the ATP release channel pannexin-1 contributed to flow-induced ATP release in Pkd1
    MeSH term(s) Humans ; Polycystic Kidney, Autosomal Dominant/metabolism ; Kidney/metabolism ; Gene Expression ; Adenosine Triphosphate/metabolism ; Kidney Tubules, Collecting/metabolism
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2023-10-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202301434R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 296: Show issues

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  5. Article ; Online: Renal claudin-14 expression is not required for regulating Mg

    Ferreira, Patrícia G / van Megen, Wouter H / Tan, Rebecca / Lee, Christy H L / Svenningsen, Per / Alexander, R Todd / Dimke, Henrik

    American journal of physiology. Renal physiology

    2021  Volume 320, Issue 5, Page(s) F897–F907

    Abstract: The kidneys play a crucial role in maintaining ... ...

    Abstract The kidneys play a crucial role in maintaining Ca
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium/urine ; Claudins/genetics ; Claudins/metabolism ; Diet ; Female ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Kidney/metabolism ; Magnesium/administration & dosage ; Magnesium/blood ; Magnesium/metabolism ; Magnesium/urine ; Mice ; Mice, Knockout ; Mice, Transgenic
    Chemical Substances Claudins ; Magnesium (I38ZP9992A) ; Calcium (SY7Q814VUP) ; claudin 14 (W7WL5ZNY9I)
    Language English
    Publishing date 2021-04-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00590.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.89: Show issues Location:
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  6. Article ; Online: Gentamicin Inhibits Ca

    van Megen, Wouter H / Beggs, Megan R / An, Sung-Wan / Ferreira, Patrícia G / Lee, Justin J / Wolf, Matthias T / Alexander, R Todd / Dimke, Henrik

    Journal of the American Society of Nephrology : JASN

    2022  Volume 33, Issue 3, Page(s) 547–564

    Abstract: Background: Treatment with the aminoglycoside antibiotic gentamicin can be associated with severe adverse effects, including renal Ca: Methods: We studied the effect of gentamicin : Results: Gentamicin increased urinary Ca: Conclusions: ... ...

    Abstract Background: Treatment with the aminoglycoside antibiotic gentamicin can be associated with severe adverse effects, including renal Ca
    Methods: We studied the effect of gentamicin
    Results: Gentamicin increased urinary Ca
    Conclusions: Gentamicin does not cause hypercalciuria
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium Channels/metabolism ; Carrier Proteins ; Claudins ; Gentamicins/pharmacology ; HEK293 Cells ; Humans ; Mice ; Rabbits ; Receptors, Calcium-Sensing/genetics ; TRPV Cation Channels/genetics
    Chemical Substances Calcium Channels ; Carrier Proteins ; Claudins ; Gentamicins ; Receptors, Calcium-Sensing ; TRPV Cation Channels ; TRPV5 protein, human ; Trpv5 protein, mouse ; Calcium (SY7Q814VUP) ; claudin 14 (W7WL5ZNY9I)
    Language English
    Publishing date 2022-01-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2021030392
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3344: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Renal sodium and magnesium reabsorption are not coupled in a mouse model of Gordon syndrome.

    van Megen, Wouter H / Grimm, Paul R / Welling, Paul A / van der Wijst, Jenny

    Physiological reports

    2018  Volume 6, Issue 14, Page(s) e13728

    Abstract: Active reabsorption of magnesium ( ... ...

    Abstract Active reabsorption of magnesium (Mg
    MeSH term(s) Animals ; Arthrogryposis/metabolism ; Cation Transport Proteins/genetics ; Cation Transport Proteins/metabolism ; Cleft Palate/metabolism ; Clubfoot/metabolism ; Female ; Hand Deformities, Congenital/metabolism ; Hydrochlorothiazide/pharmacology ; Kidney/drug effects ; Kidney/metabolism ; Magnesium/metabolism ; Male ; Mice ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Renal Reabsorption ; Sodium/metabolism ; Sodium Chloride Symporter Inhibitors/pharmacology ; Solute Carrier Family 12, Member 3/genetics ; Solute Carrier Family 12, Member 3/metabolism ; TRPM Cation Channels/genetics ; TRPM Cation Channels/metabolism
    Chemical Substances Cation Transport Proteins ; Slc12a3 protein, mouse ; Sodium Chloride Symporter Inhibitors ; Solute Carrier Family 12, Member 3 ; TRPM Cation Channels ; Trpm6 protein, mouse ; solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2 ; Hydrochlorothiazide (0J48LPH2TH) ; Sodium (9NEZ333N27) ; Stk39 protein, mouse (EC 2.7.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Magnesium (I38ZP9992A)
    Language English
    Publishing date 2018-07-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.13728
    Database MEDical Literature Analysis and Retrieval System OnLINE

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