Literature DB >> 32455507

Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome.

Mengyun Xiao1, Bernhard N Bohnert1,2,3, Hande Aypek4, Oliver Kretz4, Florian Grahammer4, Ute Aukschun5, Matthias Wörn1, Andrea Janessa1, Daniel Essigke1, Christoph Daniel6, Kerstin Amann6, Tobias B Huber4, Edward F Plow7, Andreas L Birkenfeld1,2,3, Ferruh Artunc1,2,3.   

Abstract

AIM: Sodium retention is the hallmark of nephrotic syndrome (NS) and mediated by the proteolytic activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases. Plasmin is highly abundant in nephrotic urine and has been proposed to be the principal serine protease responsible for ENaC activation in NS. However, a proof of the essential role of plasmin in experimental NS is lacking.
METHODS: We used a genetic mouse model of NS based on an inducible podocin knockout (Bl6-Nphs2tm3.1Antc *Tg(Nphs1-rtTA*3G)8Jhm *Tg(tetO-cre)1Jaw or nphs2Δipod ). These mice were crossed with plasminogen deficient mice (Bl6-Plgtm1Jld or plg-/- ) to generate double knockout mice (nphs2Δipod *plg-/- ). NS was induced after oral doxycycline treatment for 14 days and mice were followed for subsequent 14 days.
RESULTS: Uninduced nphs2Δipod *plg-/- mice had normal kidney function and sodium handling. After induction, proteinuria increased similarly in both nphs2Δipod *plg+/+ and nphs2Δipod *plg-/- mice. Western blot revealed the urinary excretion of plasminogen and plasmin in nphs2Δipod *plg+/+ mice which were absent in nphs2Δipod *plg-/- mice. After the onset of proteinuria, amiloride-sensitive natriuresis was increased compared to the uninduced state in both genotypes. Subsequently, urinary sodium excretion dropped in both genotypes leading to an increase in body weight and development of ascites. Treatment with the serine protease inhibitor aprotinin prevented sodium retention in both genotypes.
CONCLUSIONS: This study shows that mice lacking urinary plasminogen are not protected from ENaC-mediated sodium retention in experimental NS. This points to an essential role of other urinary serine proteases in the absence of plasminogen.
© 2020 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

Entities:  

Keywords:  epithelial sodium channel; nephrotic syndrome; plasminogen; proteasuria; sodium retention

Mesh:

Substances:

Year:  2020        PMID: 32455507      PMCID: PMC7688481          DOI: 10.1111/apha.13512

Source DB:  PubMed          Journal:  Acta Physiol (Oxf)        ISSN: 1748-1708            Impact factor:   6.311


  42 in total

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Review 2.  ENaC at the cutting edge: regulation of epithelial sodium channels by proteases.

Authors:  Thomas R Kleyman; Marcelo D Carattino; Rebecca P Hughey
Journal:  J Biol Chem       Date:  2009-04-28       Impact factor: 5.157

3.  Sodium retention by uPA in nephrotic syndrome?

Authors:  Heimo Ehmke
Journal:  Acta Physiol (Oxf)       Date:  2019-10-12       Impact factor: 6.311

4.  Urokinase-type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)-mediated sodium retention in experimental nephrotic syndrome.

Authors:  Bernhard N Bohnert; Sophie Daiminger; Matthias Wörn; Florian Sure; Tobias Staudner; Alexandr V Ilyaskin; Firas Batbouta; Andrea Janessa; Jonas C Schneider; Daniel Essigke; Sandip Kanse; Silke Haerteis; Christoph Korbmacher; Ferruh Artunc
Journal:  Acta Physiol (Oxf)       Date:  2019-05-20       Impact factor: 6.311

5.  Plasmin activates epithelial Na+ channels by cleaving the gamma subunit.

Authors:  Christopher J Passero; Gunhild M Mueller; Helbert Rondon-Berrios; Stevan P Tofovic; Rebecca P Hughey; Thomas R Kleyman
Journal:  J Biol Chem       Date:  2008-11-03       Impact factor: 5.157

6.  Serum- and glucocorticoid-inducible kinase 1 in doxorubicin-induced nephrotic syndrome.

Authors:  Ferruh Artunc; Omaima Nasir; Kerstin Amann; Krishna M Boini; Hans-Ulrich Häring; Teut Risler; Florian Lang
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7.  Association of Plasminuria with Overhydration in Patients with CKD.

Authors:  Anja Schork; Matthias Woern; Hubert Kalbacher; Wolfgang Voelter; Regina Nacken; Marko Bertog; Silke Haerteis; Christoph Korbmacher; Nils Heyne; Andreas Peter; Hans-Ulrich Häring; Ferruh Artunc
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8.  Cholesterol depletion of the plasma membrane prevents activation of the epithelial sodium channel (ENaC) by SGK1.

Authors:  Bettina Krueger; Silke Haerteis; Limin Yang; Andrea Hartner; Robert Rauh; Christoph Korbmacher; Alexei Diakov
Journal:  Cell Physiol Biochem       Date:  2009-11-04

9.  Cathepsin B increases ENaC activity leading to hypertension early in nephrotic syndrome.

Authors:  Alexey Larionov; Eileen Dahlke; Madlen Kunke; Luis Zanon Rodriguez; Ina M Schiessl; Jean-Luc Magnin; Ursula Kern; Abdel A Alli; Geraldine Mollet; Oliver Schilling; Hayo Castrop; Franziska Theilig
Journal:  J Cell Mol Med       Date:  2019-07-31       Impact factor: 5.310

10.  Regulation of ENaC trafficking in rat kidney.

Authors:  Gustavo Frindt; Diego Gravotta; Lawrence G Palmer
Journal:  J Gen Physiol       Date:  2016-02-15       Impact factor: 4.086

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Journal:  Int J Mol Sci       Date:  2022-06-16       Impact factor: 6.208

2.  Cleavage state of γENaC in mouse and rat kidneys.

Authors:  Gustavo Frindt; Shujie Shi; Thomas R Kleyman; Lawrence G Palmer
Journal:  Am J Physiol Renal Physiol       Date:  2021-02-01

3.  Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice.

Authors:  Daniel Essigke; Alexandr V Ilyaskin; Matthias Wörn; Bernhard N Bohnert; Mengyun Xiao; Christoph Daniel; Kerstin Amann; Andreas L Birkenfeld; Roman Szabo; Thomas H Bugge; Christoph Korbmacher; Ferruh Artunc
Journal:  Acta Physiol (Oxf)       Date:  2021-03-11       Impact factor: 7.523

4.  The Deleterious Effects of Impaired Fibrinolysis on Skeletal Development Are Dependent on Fibrin(ogen), but Independent of Interlukin-6.

Authors:  Heather A Cole; Stephanie N Moore-Lotridge; Gregory D Hawley; Richard Jacobson; Masato Yuasa; Leslie Gewin; Jeffry S Nyman; Matthew J Flick; Jonathan G Schoenecker
Journal:  Front Cardiovasc Med       Date:  2021-12-06

5.  Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity.

Authors:  Daniel Essigke; Bernhard N Bohnert; Andrea Janessa; Matthias Wörn; Kingsley Omage; Hubert Kalbacher; Andreas L Birkenfeld; Thomas H Bugge; Roman Szabo; Ferruh Artunc
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6.  Essential role of DNA-PKcs and plasminogen for the development of doxorubicin-induced glomerular injury in mice.

Authors:  Bernhard N Bohnert; Irene Gonzalez-Menendez; Thomas Dörffel; Jonas C Schneider; Mengyun Xiao; Andrea Janessa; M Zaher Kalo; Birgit Fehrenbacher; Martin Schaller; Nicolas Casadei; Kerstin Amann; Christoph Daniel; Andreas L Birkenfeld; Florian Grahammer; Lahoucine Izem; Edward F Plow; Leticia Quintanilla-Martinez; Ferruh Artunc
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Review 7.  ENaC activation by proteases.

Authors:  Deepika Anand; Edith Hummler; Olivia J Rickman
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