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Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis

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Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis. / Oh, Jun; Beckmann, Julia; Bloch, Jacek; Hettgen, Verena; Mueller, Julian; Li, Li; Hoemme, Meike; Gross, Marie-Luise; Penzel, Roland; Mundel, Peter; Schaefer, Franz; Schmitt, Claus P.

in: KIDNEY INT, Jahrgang 80, Nr. 5, 01.09.2011, S. 483-92.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Oh, J, Beckmann, J, Bloch, J, Hettgen, V, Mueller, J, Li, L, Hoemme, M, Gross, M-L, Penzel, R, Mundel, P, Schaefer, F & Schmitt, CP 2011, 'Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis', KIDNEY INT, Jg. 80, Nr. 5, S. 483-92. https://doi.org/10.1038/ki.2011.105

APA

Oh, J., Beckmann, J., Bloch, J., Hettgen, V., Mueller, J., Li, L., Hoemme, M., Gross, M-L., Penzel, R., Mundel, P., Schaefer, F., & Schmitt, C. P. (2011). Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis. KIDNEY INT, 80(5), 483-92. https://doi.org/10.1038/ki.2011.105

Vancouver

Oh J, Beckmann J, Bloch J, Hettgen V, Mueller J, Li L et al. Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis. KIDNEY INT. 2011 Sep 1;80(5):483-92. https://doi.org/10.1038/ki.2011.105

Bibtex

@article{0abf1b20c0bb468cb5083b85ce36c631,
title = "Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis",
abstract = "Calcimimetics increase the sensitivity of the parathyroid calcium-sensing receptor to extracellular calcium for efficient control of hyperparathyroidism. Recent studies suggest that there are beneficial effects of calcimimetics beyond the control of bone and mineral homeostasis. Here, we tested whether the calcium-sensing receptor is also expressed and functionally relevant in podocytes. Analysis of microarray data using Gene Set Enrichment Analysis found that the calcimimetic R-568 influenced various pathways related to oxidative stress, cytoskeletal regulation, cell proliferation, and survival in cultured podocytes. R-568 induced a dose- and time-dependent phosphorylation of the ERK1/2-P90RSK-CREB signaling cascade, and induced pro-survival phosphorylation of BAD and Bcl-xl, thus reducing puromycin aminonucleoside (PAN)-induced podocyte apoptosis by half. Moreover, R-568 preserved the actin cytoskeleton in podocytes exposed to PAN and improved recovery from exposure to cytochalasin D, a reversible inhibitor of actin polymerization. In rats, co-administration of R-568 prevented the proteinuria caused by a single dose of PAN and attenuated the glomerulosclerosis and loss of GFR caused by repetitive puromycin treatment. Hence, calcimimetics limit podocyte damage by antiapoptotic and cytoskeleton-stabilizing effects and may constitute a new approach in the prevention and treatment of glomerular disease.",
keywords = "Aniline Compounds, Animals, Calcimimetic Agents, Cell Survival, Cytoskeleton, Glomerulosclerosis, Focal Segmental, Podocytes, Rats, Receptors, Calcium-Sensing",
author = "Jun Oh and Julia Beckmann and Jacek Bloch and Verena Hettgen and Julian Mueller and Li Li and Meike Hoemme and Marie-Luise Gross and Roland Penzel and Peter Mundel and Franz Schaefer and Schmitt, {Claus P}",
year = "2011",
month = sep,
day = "1",
doi = "10.1038/ki.2011.105",
language = "English",
volume = "80",
pages = "483--92",
journal = "KIDNEY INT",
issn = "0085-2538",
publisher = "NATURE PUBLISHING GROUP",
number = "5",

}

RIS

TY - JOUR

T1 - Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis

AU - Oh, Jun

AU - Beckmann, Julia

AU - Bloch, Jacek

AU - Hettgen, Verena

AU - Mueller, Julian

AU - Li, Li

AU - Hoemme, Meike

AU - Gross, Marie-Luise

AU - Penzel, Roland

AU - Mundel, Peter

AU - Schaefer, Franz

AU - Schmitt, Claus P

PY - 2011/9/1

Y1 - 2011/9/1

N2 - Calcimimetics increase the sensitivity of the parathyroid calcium-sensing receptor to extracellular calcium for efficient control of hyperparathyroidism. Recent studies suggest that there are beneficial effects of calcimimetics beyond the control of bone and mineral homeostasis. Here, we tested whether the calcium-sensing receptor is also expressed and functionally relevant in podocytes. Analysis of microarray data using Gene Set Enrichment Analysis found that the calcimimetic R-568 influenced various pathways related to oxidative stress, cytoskeletal regulation, cell proliferation, and survival in cultured podocytes. R-568 induced a dose- and time-dependent phosphorylation of the ERK1/2-P90RSK-CREB signaling cascade, and induced pro-survival phosphorylation of BAD and Bcl-xl, thus reducing puromycin aminonucleoside (PAN)-induced podocyte apoptosis by half. Moreover, R-568 preserved the actin cytoskeleton in podocytes exposed to PAN and improved recovery from exposure to cytochalasin D, a reversible inhibitor of actin polymerization. In rats, co-administration of R-568 prevented the proteinuria caused by a single dose of PAN and attenuated the glomerulosclerosis and loss of GFR caused by repetitive puromycin treatment. Hence, calcimimetics limit podocyte damage by antiapoptotic and cytoskeleton-stabilizing effects and may constitute a new approach in the prevention and treatment of glomerular disease.

AB - Calcimimetics increase the sensitivity of the parathyroid calcium-sensing receptor to extracellular calcium for efficient control of hyperparathyroidism. Recent studies suggest that there are beneficial effects of calcimimetics beyond the control of bone and mineral homeostasis. Here, we tested whether the calcium-sensing receptor is also expressed and functionally relevant in podocytes. Analysis of microarray data using Gene Set Enrichment Analysis found that the calcimimetic R-568 influenced various pathways related to oxidative stress, cytoskeletal regulation, cell proliferation, and survival in cultured podocytes. R-568 induced a dose- and time-dependent phosphorylation of the ERK1/2-P90RSK-CREB signaling cascade, and induced pro-survival phosphorylation of BAD and Bcl-xl, thus reducing puromycin aminonucleoside (PAN)-induced podocyte apoptosis by half. Moreover, R-568 preserved the actin cytoskeleton in podocytes exposed to PAN and improved recovery from exposure to cytochalasin D, a reversible inhibitor of actin polymerization. In rats, co-administration of R-568 prevented the proteinuria caused by a single dose of PAN and attenuated the glomerulosclerosis and loss of GFR caused by repetitive puromycin treatment. Hence, calcimimetics limit podocyte damage by antiapoptotic and cytoskeleton-stabilizing effects and may constitute a new approach in the prevention and treatment of glomerular disease.

KW - Aniline Compounds

KW - Animals

KW - Calcimimetic Agents

KW - Cell Survival

KW - Cytoskeleton

KW - Glomerulosclerosis, Focal Segmental

KW - Podocytes

KW - Rats

KW - Receptors, Calcium-Sensing

U2 - 10.1038/ki.2011.105

DO - 10.1038/ki.2011.105

M3 - SCORING: Journal article

C2 - 21508926

VL - 80

SP - 483

EP - 492

JO - KIDNEY INT

JF - KIDNEY INT

SN - 0085-2538

IS - 5

ER -