Single and Transient Ca2+ Peaks in Podocytes do not induce Changes in Glomerular Filtration and Perfusion

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Single and Transient Ca2+ Peaks in Podocytes do not induce Changes in Glomerular Filtration and Perfusion. / Koehler, Sybille; Brähler, Sebastian; Kuczkowski, Alexander; Binz, Julia; Hackl, Matthias J; Hagmann, Henning; Höhne, Martin; Vogt, Merly C; Wunderlich, Claudia M; Wunderlich, F Thomas; Schweda, Frank; Schermer, Bernhard; Benzing, Thomas; Brinkkoetter, Paul T.

In: SCI REP-UK, Vol. 6, 19.10.2016, p. 35400.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Koehler, S, Brähler, S, Kuczkowski, A, Binz, J, Hackl, MJ, Hagmann, H, Höhne, M, Vogt, MC, Wunderlich, CM, Wunderlich, FT, Schweda, F, Schermer, B, Benzing, T & Brinkkoetter, PT 2016, 'Single and Transient Ca2+ Peaks in Podocytes do not induce Changes in Glomerular Filtration and Perfusion', SCI REP-UK, vol. 6, pp. 35400. https://doi.org/10.1038/srep35400

APA

Koehler, S., Brähler, S., Kuczkowski, A., Binz, J., Hackl, M. J., Hagmann, H., Höhne, M., Vogt, M. C., Wunderlich, C. M., Wunderlich, F. T., Schweda, F., Schermer, B., Benzing, T., & Brinkkoetter, P. T. (2016). Single and Transient Ca2+ Peaks in Podocytes do not induce Changes in Glomerular Filtration and Perfusion. SCI REP-UK, 6, 35400. https://doi.org/10.1038/srep35400

Vancouver

Bibtex

@article{3c5162318d564e3abe8c4a8adf3581d7,
title = "Single and Transient Ca2+ Peaks in Podocytes do not induce Changes in Glomerular Filtration and Perfusion",
abstract = "Chronic alterations in calcium (Ca2+) signalling in podocytes have been shown to cause proteinuria and progressive glomerular diseases. However, it is unclear whether short Ca2+ peaks influence glomerular biology and cause podocyte injury. Here we generated a DREADD (Designer Receptor Exclusively Activated by a Designer Drug) knock-in mouse line to manipulate intracellular Ca2+ levels. By mating to a podocyte-specific Cre driver we are able to investigate the impact of Ca2+ peaks on podocyte biology in living animals. Activation of the engineered G-protein coupled receptor with the synthetic compound clozapine-N-oxide (CNO) evoked a short and transient Ca2+ peak in podocytes immediately after CNO administration in vivo. Interestingly, this Ca2+ peak did neither affect glomerular perfusion nor filtration in the animals. Moreover, no obvious alterations in the glomerular morphology could be observed. Taken together, these in vivo findings suggest that chronic alterations and calcium overload rather than an induction of transient Ca2+ peaks contribute to podocyte disease.",
author = "Sybille Koehler and Sebastian Br{\"a}hler and Alexander Kuczkowski and Julia Binz and Hackl, {Matthias J} and Henning Hagmann and Martin H{\"o}hne and Vogt, {Merly C} and Wunderlich, {Claudia M} and Wunderlich, {F Thomas} and Frank Schweda and Bernhard Schermer and Thomas Benzing and Brinkkoetter, {Paul T}",
year = "2016",
month = oct,
day = "19",
doi = "10.1038/srep35400",
language = "English",
volume = "6",
pages = "35400",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Single and Transient Ca2+ Peaks in Podocytes do not induce Changes in Glomerular Filtration and Perfusion

AU - Koehler, Sybille

AU - Brähler, Sebastian

AU - Kuczkowski, Alexander

AU - Binz, Julia

AU - Hackl, Matthias J

AU - Hagmann, Henning

AU - Höhne, Martin

AU - Vogt, Merly C

AU - Wunderlich, Claudia M

AU - Wunderlich, F Thomas

AU - Schweda, Frank

AU - Schermer, Bernhard

AU - Benzing, Thomas

AU - Brinkkoetter, Paul T

PY - 2016/10/19

Y1 - 2016/10/19

N2 - Chronic alterations in calcium (Ca2+) signalling in podocytes have been shown to cause proteinuria and progressive glomerular diseases. However, it is unclear whether short Ca2+ peaks influence glomerular biology and cause podocyte injury. Here we generated a DREADD (Designer Receptor Exclusively Activated by a Designer Drug) knock-in mouse line to manipulate intracellular Ca2+ levels. By mating to a podocyte-specific Cre driver we are able to investigate the impact of Ca2+ peaks on podocyte biology in living animals. Activation of the engineered G-protein coupled receptor with the synthetic compound clozapine-N-oxide (CNO) evoked a short and transient Ca2+ peak in podocytes immediately after CNO administration in vivo. Interestingly, this Ca2+ peak did neither affect glomerular perfusion nor filtration in the animals. Moreover, no obvious alterations in the glomerular morphology could be observed. Taken together, these in vivo findings suggest that chronic alterations and calcium overload rather than an induction of transient Ca2+ peaks contribute to podocyte disease.

AB - Chronic alterations in calcium (Ca2+) signalling in podocytes have been shown to cause proteinuria and progressive glomerular diseases. However, it is unclear whether short Ca2+ peaks influence glomerular biology and cause podocyte injury. Here we generated a DREADD (Designer Receptor Exclusively Activated by a Designer Drug) knock-in mouse line to manipulate intracellular Ca2+ levels. By mating to a podocyte-specific Cre driver we are able to investigate the impact of Ca2+ peaks on podocyte biology in living animals. Activation of the engineered G-protein coupled receptor with the synthetic compound clozapine-N-oxide (CNO) evoked a short and transient Ca2+ peak in podocytes immediately after CNO administration in vivo. Interestingly, this Ca2+ peak did neither affect glomerular perfusion nor filtration in the animals. Moreover, no obvious alterations in the glomerular morphology could be observed. Taken together, these in vivo findings suggest that chronic alterations and calcium overload rather than an induction of transient Ca2+ peaks contribute to podocyte disease.

U2 - 10.1038/srep35400

DO - 10.1038/srep35400

M3 - SCORING: Journal article

C2 - 27759104

VL - 6

SP - 35400

JO - SCI REP-UK

JF - SCI REP-UK

SN - 2045-2322

ER -