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Article ; Online: The ex vivo perfused mouse adrenal gland-a new model to study aldosterone secretion.

Plain, Allein / Knödl, Laura / Tegtmeier, Ines / Bandulik, Sascha / Warth, Richard

Pflugers Archiv : European journal of physiology

2024

Abstract: Aldosterone is a steroid hormone that is important for maintaining the volume and ionic composition of extracellular fluids and is produced in the zona glomerulosa of the adrenal cortex. The basic mechanisms controlling aldosterone secretion are known. ... ...

Abstract	Aldosterone is a steroid hormone that is important for maintaining the volume and ionic composition of extracellular fluids and is produced in the zona glomerulosa of the adrenal cortex. The basic mechanisms controlling aldosterone secretion are known. However, more detailed studies on the regulation of aldosterone secretion often fail due to the lack of suitable models: although secretion can be studied in cultured adrenocortical cells under defined conditions, the differentiation status of the cells is difficult to control and the complex anatomy of the adrenal cortex is lost. In living animals, the physiological context is intact, but the influences are manifold and the examination conditions cannot be sufficiently controlled. One method that closes the gap between cell models and studies in living animals is the isolated perfused adrenal gland. In the past, this method has provided important data on the pathophysiology of adrenal glands from larger animals, but the technique was not used in mice. Here, we developed a method for isolation and perfusion of the mouse adrenal gland to study aldosterone secretion. This technique preserves the complex anatomical and functional context of the mouse adrenal cortex, to ensure defined experimental conditions and to minimize extra-adrenal influences. Initial series of experiments with the ex vivo perfused mouse adrenal gland show that this model offers the possibility for unique insights into pathophysiological regulatory principles and is suitable for the use of genetically modified mouse models.
Language	English
Publishing date	2024-03-28
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/s00424-024-02950-z
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Article: A missense mutation in

Meindl, Katrin / Issler, Naomi / Afonso, Sara / Cebrian-Serrano, Alberto / Müller, Karin / Sterner, Christina / Othmen, Helga / Tegtmeier, Ines / Witzgall, Ralph / Klootwijk, Enriko / Davies, Benjamin / Kleta, Robert / Warth, Richard

Frontiers in cell and developmental biology

2023 Volume 11, Page(s) 1240558

Abstract: Normal function of the C-terminal Eps15 homology domain-containing protein 1 (EHD1) has previously been associated with endocytic vesicle trafficking, shaping of intracellular membranes, and ciliogenesis. We recently identified an autosomal recessive ... ...

Abstract	Normal function of the C-terminal Eps15 homology domain-containing protein 1 (EHD1) has previously been associated with endocytic vesicle trafficking, shaping of intracellular membranes, and ciliogenesis. We recently identified an autosomal recessive missense mutation c.1192C>T (p.R398W) of EHD1 in patients who had low molecular weight proteinuria (0.7-2.1 g/d) and high-frequency hearing loss. It was already known from
Language	English
Publishing date	2023-10-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1240558
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Article ; Online: Cellular Pathophysiology of Mutant Voltage-Dependent Ca2+ Channel CACNA1H in Primary Aldosteronism.

Gürtler, Florian / Jordan, Katrin / Tegtmeier, Ines / Herold, Janina / Stindl, Julia / Warth, Richard / Bandulik, Sascha

Endocrinology

2020 Volume 161, Issue 10

Abstract: The physiological stimulation of aldosterone production in adrenocortical glomerulosa cells by angiotensin II and high plasma K+ depends on the depolarization of the cell membrane potential and the subsequent Ca2+ influx via voltage-activated Ca2+ ... ...

Abstract	The physiological stimulation of aldosterone production in adrenocortical glomerulosa cells by angiotensin II and high plasma K+ depends on the depolarization of the cell membrane potential and the subsequent Ca2+ influx via voltage-activated Ca2+ channels. Germline mutations of the low-voltage activated T-type Ca2+ channel CACNA1H (Cav3.2) have been found in patients with primary aldosteronism. Here, we investigated the electrophysiology and Ca2+ signaling of adrenal NCI-H295R cells overexpressing CACNA1H wildtype and mutant M1549V in order to understand how mutant CACNA1H alters adrenal cell function. Whole-cell patch-clamp measurements revealed a strong activation of mutant CACNA1H at the resting membrane potential of adrenal cells. Both the expression of wildtype and mutant CACNA1H led to a depolarized membrane potential. In addition, cells expressing mutant CACNA1H developed pronounced action potential-like membrane voltage oscillations. Ca2+ measurements showed an increased basal Ca2+ activity, an altered K+ sensitivity, and abnormal oscillating Ca2+ changes in cells with mutant CACNA1H. In addition, removal of extracellular Na+ reduced CACNA1H current, voltage oscillations, and Ca2+ levels in mutant cells, suggesting a role of the partial Na+ conductance of CACNA1H in cellular pathology. In conclusion, the pathogenesis of stimulus-independent aldosterone production in patients with CACNA1H mutations involves several factors: i) a loss of normal control of the membrane potential, ii) an increased Ca2+ influx at basal conditions, and iii) alterations in sensitivity to extracellular K+ and Na+. Finally, our findings underline the importance of CACNA1H in the control of aldosterone production and support the concept of the glomerulosa cell as an electrical oscillator.
MeSH term(s)	Adrenal Glands/metabolism ; Adrenal Glands/pathology ; Adrenal Glands/physiopathology ; Aldosterone/metabolism ; Animals ; CHO Cells ; Calcium/metabolism ; Calcium Channels, T-Type/genetics ; Calcium Channels, T-Type/metabolism ; Cricetinae ; Cricetulus ; Humans ; Hyperaldosteronism/genetics ; Hyperaldosteronism/metabolism ; Hyperaldosteronism/pathology ; Hyperaldosteronism/physiopathology ; Membrane Potentials ; Mutation ; Patch-Clamp Techniques ; Sodium/metabolism ; Tumor Cells, Cultured ; Zona Glomerulosa/metabolism ; Zona Glomerulosa/pathology ; Zona Glomerulosa/physiopathology
Chemical Substances	CACNA1H protein, human ; Calcium Channels, T-Type ; Aldosterone (4964P6T9RB) ; Sodium (9NEZ333N27) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-08-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqaa135
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Article ; Online: CLN7/MFSD8 may be an important factor for SARS-CoV-2 cell entry.

Heinl, Elena-Sofia / Lorenz, Sebastian / Schmidt, Barbara / Nasser M Laqtom, Nouf / Mazzulli, Joseph R / Francelle, Laetitia / Yu, Timothy W / Greenberg, Benjamin / Storch, Stephan / Tegtmeier, Ines / Othmen, Helga / Maurer, Katja / Steinfurth, Malin / Witzgall, Ralph / Milenkovic, Vladimir / Wetzel, Christian H / Reichold, Markus

iScience

2022 Volume 25, Issue 10, Page(s) 105082

Abstract: The SARS-CoV-2 virus has triggered a worldwide pandemic. According to the BioGrid database, CLN7 (MFSD8) is thought to interact with several viral proteins. The aim of this work was to investigate a possible involvement of CLN7 in the infection process. ... ...

Abstract	The SARS-CoV-2 virus has triggered a worldwide pandemic. According to the BioGrid database, CLN7 (MFSD8) is thought to interact with several viral proteins. The aim of this work was to investigate a possible involvement of CLN7 in the infection process. Experiments on a CLN7-deficient HEK293T cell line exhibited a 90% reduced viral load compared to wild-type cells. This observation may be linked to the finding that CLN7 ko cells have a significantly reduced GM1 content in their cell membrane. GM1 is found highly enriched in lipid rafts, which are thought to play an important role in SARS-CoV-2 infection. In contrast, overexpression of CLN7 led to an increase in viral load. This study provides evidence that CLN7 is involved in SARS-CoV-2 infection. This makes it a potential pharmacological target for drug development against COVID-19. Furthermore, it provides insights into the physiological function of CLN7 where still only little is known about.
Language	English
Publishing date	2022-09-06
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.105082
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Article ; Online: Abnormal respiration under hyperoxia in TASK-1/3 potassium channel double knockout mice.

Buehler, Philipp K / Bleiler, Doris / Tegtmeier, Ines / Heitzmann, Dirk / Both, Christian / Georgieff, Michael / Lesage, Florian / Warth, Richard / Thomas, Jörg

Respiratory physiology & neurobiology

2017 Volume 244, Page(s) 17–25

Abstract: Despite intensive research, the exact function of TASK potassium channels in central and peripheral chemoreception is still under debate. In this study, we investigated the respiration of unrestrained TASK-3 (TASK- ... ...

Abstract	Despite intensive research, the exact function of TASK potassium channels in central and peripheral chemoreception is still under debate. In this study, we investigated the respiration of unrestrained TASK-3 (TASK-3
Language	English
Publishing date	2017-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2077867-3
ISSN	1878-1519 ; 1569-9048
ISSN (online)	1878-1519
ISSN	1569-9048
DOI	10.1016/j.resp.2017.06.009
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Article ; Online: Sex-dependent differences in the in vivo respiratory phenotype of the TASK-1 potassium channel knockout mouse.

Jungbauer, Stefan / Buehler, Philipp Karl / Neubauer, Jacqueline / Haas, Cordula / Heitzmann, Dirk / Tegtmeier, Ines / Sterner, Christina / Barhanin, Jacques / Georgieff, Michael / Warth, Richard / Thomas, Jörg

Respiratory physiology & neurobiology

2017 Volume 245, Page(s) 13–28

Abstract: TASK-1 potassium channels have been implicated in central and peripheral chemoreception; however, the precise contribution of TASK-1 for the control of respiration is still under debate. Here, we investigated the respiration of unrestrained adult and ... ...

Abstract	TASK-1 potassium channels have been implicated in central and peripheral chemoreception; however, the precise contribution of TASK-1 for the control of respiration is still under debate. Here, we investigated the respiration of unrestrained adult and neonatal TASK-1 knockout mice (TASK-1
MeSH term(s)	Aging/metabolism ; Anesthetics, Inhalation/pharmacology ; Animals ; Animals, Newborn ; Cohort Studies ; Female ; Humans ; Hypercapnia/physiopathology ; Infant ; Isoflurane/pharmacology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins/deficiency ; Nerve Tissue Proteins/genetics ; Plethysmography, Whole Body ; Potassium Channels, Tandem Pore Domain/deficiency ; Potassium Channels, Tandem Pore Domain/genetics ; Respiration/drug effects ; Sex Characteristics ; Sudden Infant Death/genetics ; Tidal Volume/physiology
Chemical Substances	Anesthetics, Inhalation ; Nerve Tissue Proteins ; Potassium Channels, Tandem Pore Domain ; potassium channel subfamily K member 3 ; Isoflurane (CYS9AKD70P)
Language	English
Publishing date	2017
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2077867-3
ISSN	1878-1519 ; 1569-9048
ISSN (online)	1878-1519
ISSN	1569-9048
DOI	10.1016/j.resp.2016.11.005
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Article ; Online: Dynamics of renal electrolyte excretion in growing mice.

Schmidt, Katharina / Ripper, Maria / Tegtmeier, Ines / Humberg, Evelyn / Sterner, Christina / Reichold, Markus / Warth, Richard / Bandulik, Sascha

Nephron. Physiology

2013 Volume 124, Issue 3-4, Page(s) 7–13

Abstract: Genetically modified mice represent important models for elucidating renal pathophysiology, but gene deletions frequently cause severe failure to thrive. In such cases, the analysis of the phenotype is often limited to the first weeks of life when renal ... ...

Abstract	Genetically modified mice represent important models for elucidating renal pathophysiology, but gene deletions frequently cause severe failure to thrive. In such cases, the analysis of the phenotype is often limited to the first weeks of life when renal excretory function undergoes dramatic physiological changes. Here, we investigated the postnatal dynamics of urinary ion excretion in mice. The profiles of urinary electrolyte excretion of mice were examined from birth until after weaning using an automated ion chromatography system. Postnatally, mice grew about 0.4 g/day, except during two phases with slower weight gain: (i) directly after birth during adaptation to extrauterine conditions (P0-P2) and (ii) during the weaning period (P15-P21), when nutrition changed from mother's milk to solid chow and water. During the first 3 days after birth, remarkable changes in urinary Na(+), Ca(2+), Mg(2+), and phosphate concentrations occurred, whereas K(+) and Cl(-) concentrations hardly changed. From days 4-14 after birth, Na(+), Ca(2+), Mg(2+), K(+), and Cl(-) concentrations remained relatively stable at low levels. Urinary concentrations of creatinine, NH4(+), phosphate, and sulfate constantly increased from birth until after weaning. Profiles of salt excretion in KCNJ10(-/-) mice exemplified the relevance of age-dependent analysis of urinary excretion. In conclusion, the most critical phases for analysis of renal ion excretion during the first weeks of life are directly after birth and during the weaning period. The age dependence of urinary excretion varies for the different ions. This should be taken into consideration when the renal phenotype of mice is investigated during the first weeks of life.
MeSH term(s)	Age Factors ; Animals ; Animals, Newborn/growth & development ; Chromatography, Ion Exchange ; Creatinine/urine ; Ions/urine ; Kidney/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Weaning
Chemical Substances	Ions ; Creatinine (AYI8EX34EU)
Language	English
Publishing date	2013
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207121-6
ISSN	1660-2137 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2137 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000356816
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Article ; Online: A Founder Mutation in

Issler, Naomi / Afonso, Sara / Weissman, Irith / Jordan, Katrin / Cebrian-Serrano, Alberto / Meindl, Katrin / Dahlke, Eileen / Tziridis, Konstantin / Yan, Guanhua / Robles-López, José M / Tabernero, Lydia / Patel, Vaksha / Kesselheim, Anne / Klootwijk, Enriko D / Stanescu, Horia C / Dumitriu, Simona / Iancu, Daniela / Tekman, Mehmet / Mozere, Monika /

Jaureguiberry, Graciana / Outtandy, Priya / Russell, Claire / Forst, Anna-Lena / Sterner, Christina / Heinl, Elena-Sofia / Othmen, Helga / Tegtmeier, Ines / Reichold, Markus / Schiessl, Ina Maria / Limm, Katharina / Oefner, Peter / Witzgall, Ralph / Fu, Lifei / Theilig, Franziska / Schilling, Achim / Shuster Biton, Efrat / Kalfon, Limor / Fedida, Ayalla / Arnon-Sheleg, Elite / Ben Izhak, Ofer / Magen, Daniella / Anikster, Yair / Schulze, Holger / Ziegler, Christine / Lowe, Martin / Davies, Benjamin / Böckenhauer, Detlef / Kleta, Robert / Falik Zaccai, Tzipora C / Warth, Richard

Journal of the American Society of Nephrology : JASN

2022 Volume 33, Issue 4, Page(s) 732–745

Abstract: Background: The endocytic reabsorption of proteins in the proximal tubule requires a complex machinery and defects can lead to tubular proteinuria. The precise mechanisms of endocytosis and processing of receptors and cargo are incompletely understood. ... ...

Abstract	Background: The endocytic reabsorption of proteins in the proximal tubule requires a complex machinery and defects can lead to tubular proteinuria. The precise mechanisms of endocytosis and processing of receptors and cargo are incompletely understood. EHD1 belongs to a family of proteins presumably involved in the scission of intracellular vesicles and in ciliogenesis. However, the relevance of EHD1 in human tissues, in particular in the kidney, was unknown. Methods: Genetic techniques were used in patients with tubular proteinuria and deafness to identify the disease-causing gene. Diagnostic and functional studies were performed in patients and disease models to investigate the pathophysiology. Results: We identified six individuals (5-33 years) with proteinuria and a high-frequency hearing deficit associated with the homozygous missense variant c.1192C>T (p.R398W) in Conclusions: A homozygous missense variant of
MeSH term(s)	Adolescent ; Adult ; Animals ; Child ; Child, Preschool ; Deafness/genetics ; Endocytosis ; Humans ; Kidney Tubules, Proximal/metabolism ; Low Density Lipoprotein Receptor-Related Protein-2/genetics ; Low Density Lipoprotein Receptor-Related Protein-2/metabolism ; Mice ; Mutation ; Proteinuria/metabolism ; Vesicular Transport Proteins/genetics ; Young Adult ; Zebrafish/metabolism
Chemical Substances	EHD1 protein, human ; Low Density Lipoprotein Receptor-Related Protein-2 ; Vesicular Transport Proteins
Language	English
Publishing date	2022-02-11
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.2021101312
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Article: Dynamics of Renal Electrolyte Excretion in Growing Mice

Schmidt, Katharina / Ripper, Maria / Tegtmeier, Ines / Humberg, Evelyn / Sterner, Christina / Reichold, Markus / Warth, Richard / Bandulik, Sascha

Nephron Physiology

2013 Volume 124, Issue 3-4, Page(s) 7–13

Institution	Medical Cell Biology, University of Regensburg, Regensburg, Germany
Abstract	Genetically modified mice represent important models for elucidating renal pathophysiology, but gene deletions frequently cause severe failure to thrive. In such cases, the analysis of the phenotype is often limited to the first weeks of life when renal excretory function undergoes dramatic physiological changes. Here, we investigated the postnatal dynamics of urinary ion excretion in mice. The profiles of urinary electrolyte excretion of mice were examined from birth until after weaning using an automated ion chromatography system. Postnatally, mice grew about 0.4 g/day, except during two phases with slower weight gain: (i) directly after birth during adaptation to extrauterine conditions (P0-P2) and (ii) during the weaning period (P15-P21), when nutrition changed from mother's milk to solid chow and water. During the first 3 days after birth, remarkable changes in urinary Na, Ca2+, Mg2+, and phosphate concentrations occurred, whereas K and Cl concentrations hardly changed. From days 4-14 after birth, Na, Ca2+, Mg2+, K, and Cl concentrations remained relatively stable at low levels. Urinary concentrations of creatinine, NH4, phosphate, and sulfate constantly increased from birth until after weaning. Profiles of salt excretion in KCNJ10 mice exemplified the relevance of age-dependent analysis of urinary excretion. In conclusion, the most critical phases for analysis of renal ion excretion during the first weeks of life are directly after birth and during the weaning period. The age dependence of urinary excretion varies for the different ions. This should be taken into consideration when the renal phenotype of mice is investigated during the first weeks of life.
Keywords	Renal electrolyte excretion ; Growing mice ; Postnatal dynamics ; Genetically modified mice
Language	English
Publishing date	2013-11-26
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
ZDB-ID	207121-6
ISSN	1660-2137 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2137 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000356816
Database	Karger publisher's database

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Article ; Online: Dynamics of Renal Electrolyte Excretion in Growing Mice

Schmidt, Katharina / Ripper, Maria / Tegtmeier, Ines / Humberg, Evelyn / Sterner, Christina / Reichold, Markus / Warth, Richard / Bandulik, Sascha

Nephron Physiology

2013 Volume 124, Issue 3-4, Page(s) 13–17

Abstract	Genetically modified mice represent important models for elucidating renal pathophysiology, but gene deletions frequently cause severe failure to thrive. In such cases, the analysis of the phenotype is often limited to the first weeks of life when renal excretory function undergoes dramatic physiological changes. Here, we investigated the postnatal dynamics of urinary ion excretion in mice. The profiles of urinary electrolyte excretion of mice were examined from birth until after weaning using an automated ion chromatography system. Postnatally, mice grew about 0.4 g/day, except during two phases with slower weight gain: (i) directly after birth during adaptation to extrauterine conditions (P0-P2) and (ii) during the weaning period (P15-P21), when nutrition changed from mother's milk to solid chow and water. During the first 3 days after birth, remarkable changes in urinary Na+, Ca2+, Mg2+, and phosphate concentrations occurred, whereas K+ and Cl- concentrations hardly changed. From days 4-14 after birth, Na+, Ca2+, Mg2+, K+, and Cl- concentrations remained relatively stable at low levels. Urinary concentrations of creatinine, NH4+, phosphate, and sulfate constantly increased from birth until after weaning. Profiles of salt excretion in KCNJ10-/- mice exemplified the relevance of age-dependent analysis of urinary excretion. In conclusion, the most critical phases for analysis of renal ion excretion during the first weeks of life are directly after birth and during the weaning period. The age dependence of urinary excretion varies for the different ions. This should be taken into consideration when the renal phenotype of mice is investigated during the first weeks of life.© 2013 S. Karger AG, Basel
Keywords	Genetically modified mice ; Growing mice ; Postnatal dynamics ; Renal electrolyte excretion
Language	English
Publisher	S. Karger AG
Publishing place	Basel
Publishing country	Switzerland
Document type	Article ; Online
ZDB-ID	207121-6
ISSN	1660-2137 ; 1423-0186 ; 0028-2766 ; 1660-2137 ; 0028-2766
ISSN (online)	1660-2137 ; 1423-0186
ISSN	1660-2137 ; 0028-2766
DOI	10.1159/000356816
Database	Karger publisher's database

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