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Book ; Online ; Thesis: Bedeutung der WNK3-Kinase für die Salz-, Wasser- und Blutdruckhomöostase in vivo

Mederle, Katharina / Wanke, Rüdiger

2013

Author's details	Katharina Mederle. Betreuer: Rüdiger Wanke
Language	German
Size	Online-Ressource
Publisher	Universitätsbibliothek der Ludwig-Maximilians-Universität
Publishing place	München
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	München, Ludwig-Maximilians-Universität, Diss., 2013
Database	Former special subject collection: coastal and deep sea fishing

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Book ; Thesis: Bedeutung der WNK3-Kinase für die Salz-, Wasser- und Blutdruckhomöostase in vivo

Mederle, Katharina Maria Theresa

2013

Author's details	von Katharina Maria Theresa Mederle
Language	German
Size	VIII, 115 S., Ill., graph. Darst.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Ludwig-Maximilians-Universität, Diss.--München, 2013
Database	Special collection on veterinary medicine and general parasitology

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Article ; Online: Inhibition of COX-1 attenuates the formation of thromboxane A2 and ameliorates the acute decrease in glomerular filtration rate in endotoxemic mice.

Mederle, Katharina / Meurer, Manuel / Castrop, Hayo / Höcherl, Klaus

American journal of physiology. Renal physiology

2015 Volume 309, Issue 4, Page(s) F332–40

Abstract: Thromboxane (Tx) A2 has been suggested to be involved in the development of sepsis-induced acute kidney injury (AKI). Therefore, we investigated the impact of cyclooxygenase (COX)-1 and COX-2 activity on lipopolysaccharide (LPS)-induced renal TxA2 ... ...

Abstract	Thromboxane (Tx) A2 has been suggested to be involved in the development of sepsis-induced acute kidney injury (AKI). Therefore, we investigated the impact of cyclooxygenase (COX)-1 and COX-2 activity on lipopolysaccharide (LPS)-induced renal TxA2 formation, and on endotoxemia-induced AKI in mice. Injection of LPS (3 mg/kg ip) decreased glomerular filtration rate (GFR) and the amount of thrombocytes to ∼50% of basal values after 4 h. Plasma and renocortical tissue levels of TxB2 were increased ∼10- and 1.7-fold in response to LPS, respectively. The COX-1 inhibitor SC-560 attenuated the LPS-induced fall in GFR and in platelet count to ∼75% of basal levels. Furthermore, SC-560 abolished the increase in plasma and renocortical tissue levels of TxB2 in response to LPS. The COX-2 inhibitor SC-236 further enhanced the LPS-induced decrease in GFR to ∼40% of basal values. SC-236 did not alter thrombocyte levels nor the LPS-induced increase in plasma and renocortical tissue levels of TxB2. Pretreatment with clopidogrel inhibited the LPS-induced drop in thrombocyte count, but did not attenuate the LPS-induced decrease in GFR and the increase in plasma TxB2 levels. This study demonstrates that endotoxemia-induced TxA2 formation depends on the activity of COX-1. Our study further indicates that the COX-1 inhibitor SC-560 has a protective effect on the decrease in renal function in response to endotoxin. Therefore, our data support a role for TxA2 in the development of AKI in response to LPS.
MeSH term(s)	Acute Kidney Injury/enzymology ; Acute Kidney Injury/etiology ; Acute Kidney Injury/physiopathology ; Acute Kidney Injury/prevention & control ; Animals ; Blood Platelets/drug effects ; Blood Platelets/enzymology ; Cyclooxygenase 1/metabolism ; Cyclooxygenase 2 Inhibitors/pharmacology ; Disease Models, Animal ; Down-Regulation ; Endotoxemia/chemically induced ; Endotoxemia/drug therapy ; Endotoxemia/enzymology ; Endotoxemia/physiopathology ; Endotoxins ; Glomerular Filtration Rate/drug effects ; Kidney/drug effects ; Kidney/enzymology ; Kidney/physiopathology ; Male ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/metabolism ; Mice, Inbred C57BL ; Platelet Aggregation Inhibitors/pharmacology ; Pyrazoles/pharmacology ; Signal Transduction/drug effects ; Thromboxane A2/metabolism ; Time Factors
Chemical Substances	Cyclooxygenase 2 Inhibitors ; Endotoxins ; Membrane Proteins ; Platelet Aggregation Inhibitors ; Pyrazoles ; SC 560 ; Thromboxane A2 (57576-52-0) ; endotoxin, Escherichia coli (67924-63-4) ; Cyclooxygenase 1 (EC 1.14.99.1) ; Ptgs1 protein, mouse (EC 1.14.99.1)
Language	English
Publishing date	2015-08-15
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.00567.2014
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Book ; Online ; Thesis: Bedeutung der WNK3-Kinase für die Salz-, Wasser- und Blutdruckhomöostase in vivo

Mederle, Katharina [Verfasser] / Wanke, Rüdiger [Akademischer Betreuer]

2013

Author's details	Katharina Mederle. Betreuer: Rüdiger Wanke
Keywords	Tiere (Zoologie) ; Animals (Zoology)
Subject code	sg590
Language	German
Publisher	Universitätsbibliothek der Ludwig-Maximilians-Universität
Publishing place	München
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: The angiotensin receptor-associated protein Atrap is a stimulator of the cardiac Ca2+-ATPase SERCA2a.

Mederle, Katharina / Gess, Bernhard / Pluteanu, Florentina / Plackic, Jelena / Tiefenbach, Klaus-Jürgen / Grill, Alexandra / Kockskämper, Jens / Castrop, Hayo

Cardiovascular research

2016 Volume 110, Issue 3, Page(s) 359–370

Abstract: Aims: The angiotensin II type 1 receptor-associated protein (Atrap) is highly expressed in the heart, but its function in the heart is unknown. We hypothesized that cardiac Atrap may interact with proteins other than the AT1 receptor.: Methods and ... ...

Abstract	Aims: The angiotensin II type 1 receptor-associated protein (Atrap) is highly expressed in the heart, but its function in the heart is unknown. We hypothesized that cardiac Atrap may interact with proteins other than the AT1 receptor. Methods and results: To identify potential novel interacting partners of Atrap, pull-down assays were performed. Sequencing by MALDI-MS of the isolated complexes showed that Atrap interacts with the cardiac Ca(2+)-ATPase SERCA2a. The interaction between Atrap and SERCA2a was confirmed by co-immunoprecipitation and by surface plasmon resonance (SPR) spectroscopy. Atrap enhanced the SERCA-dependent Ca(2+) uptake in isolated SR membrane vesicles. Furthermore, sarcomere shortenings and [Ca(2+)]i transients (CaTs) were determined in ventricular myocytes isolated from Atrap-/- and wild-type (WT) mice. The amplitudes of CaTs and sarcomere shortenings were similar in Atrap-/- and WT myocytes. However, the CaT decay and sarcomere re-lengthening were prolonged in Atrap-/- myocytes. To further evaluate the functional relevance of the Atrap-SERCA2a interaction in vivo, left-ventricular function was assessed in WT and Atrap-/- mice. The heart rates (564 ± 10 b.p.m. vs. 560 ± 11 b.p.m.; P = 0.80) and ejection fractions (71.3 ± 1.3 vs. 72 ± 1.8%; P = 0.79) were similar in WT and Atrap-/- mice, respectively (n = 15 for each genotype). However, the maximum filling rate (dV/dtmax) was markedly decreased in Atrap-/- (725 ± 48 µL/s) compared with WT mice (1065 ± 122 µL/s; P = 0.01; n = 15). Conclusion: We identified Atrap as a novel regulatory protein of the cardiac Ca(2+)-ATPase SERCA2a. We suggest that Atrap enhances the activity of SERCA2a and, consequently, facilitates ventricular relaxation.
MeSH term(s)	Adaptor Proteins, Signal Transducing/deficiency ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Calcium Signaling ; Diastole ; Enzyme Activation ; HEK293 Cells ; Homeodomain Proteins/metabolism ; Humans ; Immunoprecipitation ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Cardiac/enzymology ; Protein Binding ; Proteomics/methods ; Sarcomeres/enzymology ; Sarcoplasmic Reticulum/enzymology ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Surface Plasmon Resonance ; Transfection ; Ventricular Function, Left
Chemical Substances	Adaptor Proteins, Signal Transducing ; Agtrap protein, mouse ; Homeodomain Proteins ; Tlx2 protein, mouse ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Atp2a2 protein, mouse (EC 7.2.2.10)
Language	English
Publishing date	2016-03-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvw064
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Article ; Online: Loss of WNK3 is compensated for by the WNK1/SPAK axis in the kidney of the mouse.

Mederle, Katharina / Mutig, Kerim / Paliege, Alexander / Carota, Isabel / Bachmann, Sebastian / Castrop, Hayo / Oppermann, Mona

American journal of physiology. Renal physiology

2013 Volume 304, Issue 9, Page(s) F1198–209

Abstract: WNK3 kinase is expressed throughout the nephron and acts as a positive regulator of NKCC2 and NCC in vitro. Here we addressed the in vivo relevance of WNK3 using WNK3-deficient mice. WNK3-/- mice were viable and showed no gross abnormalities. The net ... ...

Abstract	WNK3 kinase is expressed throughout the nephron and acts as a positive regulator of NKCC2 and NCC in vitro. Here we addressed the in vivo relevance of WNK3 using WNK3-deficient mice. WNK3-/- mice were viable and showed no gross abnormalities. The net tubular function was similar in wild-type (WT) and WNK3-/- mice as assessed by determination of 24-h urine output (1.63 ± .06 in WT and 1.55 ± .1 ml in WNK3-/-, n=16; P=0.42) and ambient urine osmolarity (1,804 ± 62 in WT vs. 1,819 ± 61 mosmol/kg in WNK3-/-, n=40; P=0.86). Water restriction (48 h) increased urine osmolarity similarly in both genotypes to 3,440 ± 220 and 3,200 ± 180 mosmol/kg in WT and WNK3-/- mice, respectively (n=11; P=0.41). The glomerular filtration rate (343 ± 22 vs. 315 ± 13 ml/min), renal blood flow (1.35 ± 0.1 vs. 1.42 ± 0.04 ml), and plasma renin concentration (94 ± 18 vs. 80 ± 13 ng ANG I·ml(-1)·h(-1)) were similar between WT and WNK3-/- mice (n=13; P=0.54). WNK1 was markedly upregulated in WNK3-deficient mice, whereas the expression of WNK4 was similar in both genotypes. When the mice were fed a salt-restricted diet [0.02% NaCl (wt/wt)] the levels of pSPAK/OSR1, pNKCC2, and pNCC were enhanced in both genotypes compared with the baseline conditions, with the levels in WNK3-/- exceeding those in WT mice. The upregulation of pSPAK/OSR1, pNKCC2, and pNCC in WNK3-/- mice relative to the levels in WT mice when fed a low-salt diet was paralleled by an increased diuresis in response to hydrochlorothiazide. In summary, the overall relevance of WNK3 for the renal reabsorption of NaCl appears to be limited and can be largely compensated for by the activation of WNK3-independent pathways. Consequently, our data suggest that WNK3 may serve as a member of a kinase network that facilitates the fine-tuning of renal transepithelial NaCl transport.
MeSH term(s)	Animals ; Biological Transport/physiology ; Female ; Glomerular Filtration Rate/physiology ; Kidney/blood supply ; Kidney/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Minor Histocompatibility Antigens ; Models, Animal ; Protein-Serine-Threonine Kinases/deficiency ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/physiology ; Regional Blood Flow/physiology ; Signal Transduction/physiology ; Sodium Chloride/metabolism ; Sodium-Potassium-Chloride Symporters/physiology ; Solute Carrier Family 12, Member 1 ; WNK Lysine-Deficient Protein Kinase 1
Chemical Substances	Minor Histocompatibility Antigens ; Slc12a1 protein, mouse ; Sodium-Potassium-Chloride Symporters ; Solute Carrier Family 12, Member 1 ; Sodium Chloride (451W47IQ8X) ; Stk39 protein, mouse (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; WNK Lysine-Deficient Protein Kinase 1 (EC 2.7.11.1) ; Wnk1 protein, mouse (EC 2.7.11.1) ; Wnk3 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2013-05-01
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.00288.2012
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Article ; Online: The angiotensin II AT1 receptor-associated protein Arap1 is involved in sepsis-induced hypotension.

Mederle, Katharina / Schweda, Frank / Kattler, Veronika / Doblinger, Elisabeth / Miyata, Keishi / Höcherl, Klaus / Oike, Yuichi / Castrop, Hayo

Critical care (London, England)

2013 Volume 17, Issue 4, Page(s) R130

Abstract: Introduction: Hypotension in septic patients results from hypovolemia, vasodilatation and hyporeactivity to vasoconstrictors, such as angiotensin II. The AT1 receptor-associated protein 1 (Arap1) is expressed in vascular smooth muscle cells and ... ...

Abstract	Introduction: Hypotension in septic patients results from hypovolemia, vasodilatation and hyporeactivity to vasoconstrictors, such as angiotensin II. The AT1 receptor-associated protein 1 (Arap1) is expressed in vascular smooth muscle cells and increases the surface expression of the AT1-receptor in vitro. We hypothesized that dysregulation of Arap1 may contribute to vascular hyporeactivity to angiotensin II during endotoxemia. Methods: Arap1-deficient mice were used to assess the role of Arap1 in sepsis-induced hypotension. The isolated perfused kidney was used as an in vitro model to determine the relevance of Arap1 for vascular resistance and sensitivity to angiotensin II. Results: During endotoxemia, mean arterial blood pressure (MAP) decreased in both genotypes, with the time course of sepsis-induced hypotension being markedly accelerated in Arap1-/- compared to +/+ mice. However, baseline MAP was similar in Arap1-/- and wildtype mice (102 ± 2 vs.103 ± 2 mmHg; telemetry measurements; n = 10; P = 0.66). Following lipopolysaccharide (LPS) injections (3 mg/kg), Arap1 expression was successively down-regulated in the wildtype mice, reaching levels below 10% of baseline expression. The endotoxemia-related decline in Arap1 expression could be recapitulated in cultured mesangial cells by incubation with pro-inflammatory cytokines, such as tumor necrosis factor α and interferon γ. Plasma renin concentration was increased in Arap1-/- mice compared to wildtype mice (66 ± 6 vs. 41 ± 4 ng AngI/ml/h; n = 23; P = 0.001), presumably contributing to preserved MAP under baseline conditions. The sensitivity of the vasculature to angiotensin II was reduced in Arap1-/- compared to +/+ mice, as determined in the isolated perfused kidney. Conclusions: Our data suggest that down-regulation of Arap1 expression during sepsis contributes to the development of hypotension by causing reduced vascular sensitivity to angiotensin II.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Blood Pressure ; Down-Regulation ; Hypotension/etiology ; Hypotension/metabolism ; Kidney/metabolism ; Lipopolysaccharides ; Male ; Mice ; Renin/metabolism ; Renin-Angiotensin System/physiology ; Sepsis/chemically induced ; Sepsis/physiopathology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Agtrap protein, mouse ; Lipopolysaccharides ; Renin (EC 3.4.23.15)
Language	English
Publishing date	2013-07-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2041406-7
ISSN	1466-609X ; 1364-8535
ISSN (online)	1466-609X
ISSN	1364-8535
DOI	10.1186/cc12809
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Article ; Online: Angiotensin AT1 receptor-associated protein Arap1 in the kidney vasculature is suppressed by angiotensin II.

Doblinger, Elisabeth / Höcherl, Klaus / Mederle, Katharina / Kattler, Veronika / Walter, Steen / Hansen, Pernille B / Jensen, Boye / Castrop, Hayo

American journal of physiology. Renal physiology

2012 Volume 302, Issue 10, Page(s) F1313–24

Abstract: Arap1 is a protein that interacts with angiotensin II type 1 (AT(1)) receptors and facilitates increased AT(1) receptor surface expression in vitro. In the present study, we assessed the tissue localization and regulation of Arap1 in vivo. Arap1 was ... ...

Abstract	Arap1 is a protein that interacts with angiotensin II type 1 (AT(1)) receptors and facilitates increased AT(1) receptor surface expression in vitro. In the present study, we assessed the tissue localization and regulation of Arap1 in vivo. Arap1 was found in various mouse organs, with the highest expression in the heart, kidney, aorta, and adrenal gland. Renal Arap1 protein was restricted to the vasculature and to glomerular mesangial cells and was absent from tubular epithelia. A similar localization was found in human kidneys. To test the hypothesis that angiotensin II may control renal Arap1 expression, mice were subjected to various conditions to alter the activity of the renin-angiotensin system. A high-salt diet (4% NaCl, 7 days) upregulated Arap1 expression in mice by 47% compared with controls (0.6% NaCl, P = 0.03). Renal artery stenosis (7 days) or water restriction (48 h) suppressed Arap1 levels compared with controls (-64 and -62% in the clipped and contralateral kidney, respectively; and -50% after water restriction, P < 0.01). Angiotensin II infusion (2 μg·kg(-1)·min(-1), 7 days) reduced Arap1 mRNA levels compared with vehicle by 29% (P < 0.01), whereas AT(1) antagonism (losartan, 30 mg·kg(-1)·day(-1), 7 days) enhanced Arap1 mRNA expression by 52% (P < 0.01); changes in mRNA were paralleled by Arap1 protein abundance. Experiments with hydralazine and epithelial nitric oxide synthase-/- mice further suggested that Arap1 expression changed in parallel with angiotensin II, rather than with blood pressure per se. Similar to in vivo, Arap1 mRNA and protein were suppressed by angiotensin II in a time- and dose-dependent manner in cultured mesangial cells. In summary, Arap1 is highly expressed in the renal vasculature, and its expression is suppressed by angiotensin II. Thus Arap1 may serve as a local modulator of vascular AT(1) receptor function in vivo.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Angiotensin II/pharmacology ; Animals ; Blood Vessels/physiology ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Humans ; Male ; Mesangial Cells/physiology ; Mice ; Mice, Inbred C57BL ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Receptor, Angiotensin, Type 1/metabolism ; Renal Circulation/drug effects ; Renal Circulation/physiology ; Renin/metabolism ; Vasoconstrictor Agents/pharmacology
Chemical Substances	ARAP1 protein, human ; Adaptor Proteins, Signal Transducing ; Agtrap protein, mouse ; Carrier Proteins ; GTPase-Activating Proteins ; Receptor, Angiotensin, Type 1 ; Vasoconstrictor Agents ; Angiotensin II (11128-99-7) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39) ; Renin (EC 3.4.23.15)
Language	English
Publishing date	2012-05-15
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.00620.2011
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