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6 results on '"Essigke, Daniel"'

1. In mouse kidney endogenous transmembrane serine protease 2 (TMPRSS2) contributes to proteolytic processing and activation of the epithelial sodium channel (ENaC)

Author

Sure, Florian, primary, Afonso, Sara, additional, Schmidt, Paul, additional, Essigke, Daniel, additional, Kißler, Alicia, additional, Bertog, Marko, additional, Rinke, Ralf, additional, Wittmann, Sabine, additional, Gramberg, Thomas, additional, Artunc, Ferruh, additional, Korbmacher, Christoph, additional, and Ilyaskin, Alexandr, additional

Published
2023
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2. Untersuchung der Relevanz von Prostasin für die Regulation des Natrium- und Wasserhaushalts in vivo

Author

Essigke, Daniel Raphael and Artunc, Ferruh (Prof. Dr.)

Subjects
Prostasin, Triamteren, ENaC, Epithelialer Natriumkanal
Abstract

Trotz verschiedener in vitro Studien war die Relevanz der membranständigen Serinprotease Prostasin bei der Aktivierung des epithelialen Natriumkanals ENaC in vivo bisher noch unbekannt. Auf Grund der Letalität von Prostasin knock-out Mäusen, musste auf knock-in Mäuse ausgewichen werden. An Mauslinien mit nicht aktivierbarem Prostasin (Prss8-R44Q), proteolytisch inaktivem Prostasin (Prss8-S238A) und Wildtypprostasin (Prss8-wt) wurde die Rolle von Prostasin unter Niedrigsalzdiäten und unter diuretischen Behandlungen untersucht. Anhand des Modells eines Doxorubicin-induzierten nephrotisches Syndroms wurde dessen Verlauf im Vergleich der drei Genotypen untersucht. Prss8-S238A Mäuse zeigten unter Niedrigsalzdiäten und den Diuretika keinen Unterschied zum Wildtyp. Prss8-R44Q Mäuse entwickelten unter Niedrigsalzdiät einem kompensatorischen Hyperaldosteronismus und unter ENaC Blockade mit Triamteren ein dem renalen Pseudo-Hypoaldosteronismus (PHA) Typ 1 ähnliches Krankheitsbild. Bei allen Genotypen kam es nach Doxorubicin Injektion zu einem nephrotischen Syndrom mit renaler Natriumretention und Ödementstehung. Dies spricht dafür, dass die proteolytische Aktivität von Prostasin unter physiologischen Bedingungen keine Relevanz für die Aktivierung des ENaC hat und zeigt, dass die durch die Aktivierung an R44 ausgelöste Konfigurationsänderung von Prostasin in vivo relevant für die proteolytische Aktivierung von ENaC ist. Es ist davon auszugehen, dass Prostasin durch seine Membranbindung als Gerüst für eine noch nicht näher bekannte (Serin-)Protease dient, die den ENaC proteolytisch aktiviert, ohne ihn jedoch unter physiologischen Bedingungen selbst zu aktivieren. Abschließend zeigen die Daten, dass weder die proteolytische Aktivität noch die Tertiärstruktur von Prostasin in vivo eine Rolle bei der durch die proteolytischen Aktivierung des ENaC bedingten Natriumretention und der damit einhergehenden Ödembildung im experimentellen nephrotischen Syndrom spielen.

Published
2022

3. Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na+ channel in the mouse kidney

Author

Bohnert, Bernhard N., primary, Essigke, Daniel, additional, Janessa, Andrea, additional, Schneider, Jonas C., additional, Wörn, Matthias, additional, Kalo, M. Zaher, additional, Xiao, Mengyun, additional, Kong, Lingsi, additional, Omage, Kingsley, additional, Hennenlotter, Jörg, additional, Amend, Bastian, additional, Birkenfeld, Andreas L., additional, and Artunc, Ferruh, additional

Published
2021
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4. Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na + channel in the mouse kidney.

Author

Bohnert, Bernhard N., Essigke, Daniel, Janessa, Andrea, Schneider, Jonas C., W€orn, Matthias, Kalo, M. Zaher, Mengyun Xiao, Lingsi Kong, Omage, Kingsley, Hennenlotter, Jörg, Amend, Bastian, Birkenfeld, Andreas L., and Artunc, Ferruh

Subjects
*NEPHROTIC syndrome, *MINERALOCORTICOID receptors, *SALT-free diet, *KIDNEYS, *DOXORUBICIN, *BRUGADA syndrome
Abstract

Proteolytic activation of the renal epithelial Na+ channel (ENaC) involves cleavage events in its α- and γ-subunits and is thought to mediate Na+ retention in nephrotic syndrome (NS). However, the detection of proteolytically processed ENaC in kidney tissue from nephrotic mice has been elusive so far. We used a refined Western blot technique to reliably discriminate full-length α-ENaC and γ-ENaC and their cleavage products after proteolysis at their proximal and distal cleavage sites (designated from the NH2-terminus), respectively. Proteolytic ENaC activation was investigated in kidneys from mice with experimental NS induced by doxorubicin or inducible podocin deficiency with or without treatment with the serine protease inhibitor aprotinin. Nephrotic mice developed Na+ retention and increased expression of fragments of α-ENaC and γ-ENaC cleaved at both the proximal cleavage site and, more prominently, the distal cleavage site, respectively. Treatment with aprotinin but not with the mineralocorticoid receptor antagonist canrenoate prevented Na+ retention and upregulation of the cleavage products in nephrotic mice. Increased expression of cleavage products of α-ENaC and γ-ENaC was similarly found in healthy mice treated with a low-salt diet, sensitive to mineralocorticoid receptor blockade. In human nephrectomy specimens, γ-ENaC was found in the full-length form and predominantly cleaved at its distal cleavage site. In conclusion, murine experimental NS leads to aprotinin-sensitive proteolytic activation of ENaC at both proximal and, more prominently, distal cleavage sites of its α- and γ-subunit, most likely by urinary serine protease activity or proteasuria. [ABSTRACT FROM AUTHOR]

Published
2021
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6. Experimental nephrotic syndrome leads to proteolytic activation of the epithelial sodium channel (ENaC) in the mouse kidney

Author

Bohnert, Bernhard N., Essigke, Daniel, Janessa, Andrea, Schneider, Jonas C, Wörn, Matthias, Kalo, M. Zaher, Xiao, Mengyun, Kong, Lingsi, Omage, Kingsley, Hennenlotter, Joerg, Amend, Bastian, Birkenfeld, Andreas L., and Artunc, Ferruh

Abstract

Proteolytic activation of the renal epithelial sodium channel ENaC involves cleavage events in its α- and γ-subunits and is thought to mediate sodium retention in nephrotic syndrome (NS). However, detection of proteolytically processed ENaC in kidney tissue from nephrotic mice has been elusive so far. We used a refined Western blot technique to reliably discriminate full-length α- and γ-ENaC and their cleavage products after proteolysis at their proximal and distal cleavage sites (designated from the N-terminus), respectively. Proteolytic ENaC activation was investigated in kidneys from mice with experimental NS induced by doxorubicin or inducible podocin deficiency with or without treatment with the serine protease inhibitor aprotinin. Nephrotic mice developed sodium retention and increased expression of fragments of α- and γ-ENaC cleaved at both the proximal and more prominently at the distal cleavage site, respectively. Treatment with aprotinin but not with the mineralocorticoid receptor antagonist canrenoate prevented sodium retention and upregulation of the cleavage products in nephrotic mice. Increased expression of cleavage products of α- and γ-ENaC was similarly found in healthy mice treated with a low salt diet, sensitive to mineralocorticoid receptor blockade. In human nephrectomy specimens, γ-ENaC was found in the full-length form and predominantly cleaved at its distal cleavage site. In conclusion, murine experimental NS leads to aprotinin-sensitive proteolytic activation of ENaC at both proximal and more prominently distal cleavage sites of its α- and γ-subunit, most likely by urinary serine protease activity or proteasuria.

Published
2021
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