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aPKCλ/ι and aPKCζ contribute to podocyte differentiation and glomerular maturation

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aPKCλ/ι and aPKCζ contribute to podocyte differentiation and glomerular maturation. / Hartleben, Björn; Widmeier, Eugen; Suhm, Martina; Worthmann, Kirstin; Schell, Christoph; Helmstädter, Martin; Wiech, Thorsten; Walz, Gerd; Leitges, Michael; Schiffer, Mario; Huber, Tobias B.

In: J AM SOC NEPHROL, Vol. 24, No. 2, 01.02.2013, p. 253-67.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Hartleben, B, Widmeier, E, Suhm, M, Worthmann, K, Schell, C, Helmstädter, M, Wiech, T, Walz, G, Leitges, M, Schiffer, M & Huber, TB 2013, 'aPKCλ/ι and aPKCζ contribute to podocyte differentiation and glomerular maturation', J AM SOC NEPHROL, vol. 24, no. 2, pp. 253-67. https://doi.org/10.1681/ASN.2012060582

APA

Hartleben, B., Widmeier, E., Suhm, M., Worthmann, K., Schell, C., Helmstädter, M., Wiech, T., Walz, G., Leitges, M., Schiffer, M., & Huber, T. B. (2013). aPKCλ/ι and aPKCζ contribute to podocyte differentiation and glomerular maturation. J AM SOC NEPHROL, 24(2), 253-67. https://doi.org/10.1681/ASN.2012060582

Vancouver

Hartleben B, Widmeier E, Suhm M, Worthmann K, Schell C, Helmstädter M et al. aPKCλ/ι and aPKCζ contribute to podocyte differentiation and glomerular maturation. J AM SOC NEPHROL. 2013 Feb 1;24(2):253-67. https://doi.org/10.1681/ASN.2012060582

Bibtex

@article{9dca2485763040faa883b52a94d20edd,
title = "aPKCλ/ι and aPKCζ contribute to podocyte differentiation and glomerular maturation",
abstract = "Precise positioning of the highly complex interdigitating podocyte foot processes is critical to form the normal glomerular filtration barrier, but the molecular programs driving this process are unknown. The protein atypical protein kinase C (aPKC)--a component of the Par complex, which localizes to tight junctions and interacts with slit diaphragm proteins--may play a role. Here, we found that the combined deletion of the aPKCλ/ι and aPKCζ isoforms in podocytes associated with incorrectly positioned centrosomes and Golgi apparatus and mislocalized molecules of the slit diaphragm. Furthermore, aPKC-deficient podocytes failed to form the normal network of foot processes, leading to defective glomerular maturation with incomplete capillary formation and mesangiolysis. Our results suggest that aPKC isoforms orchestrate the formation of the podocyte processes essential for normal glomerular development and kidney function. Defective aPKC signaling results in a dramatically simplified glomerular architecture, causing severe proteinuria and perinatal death.",
keywords = "Animals, Capillaries, Cell Differentiation, Centrosome, Female, Golgi Apparatus, Isoenzymes, Kidney Glomerulus, Male, Mice, Mice, Knockout, Microscopy, Electron, Podocytes, Protein Kinase C, Proteinuria, Signal Transduction, Tight Junctions",
author = "Bj{\"o}rn Hartleben and Eugen Widmeier and Martina Suhm and Kirstin Worthmann and Christoph Schell and Martin Helmst{\"a}dter and Thorsten Wiech and Gerd Walz and Michael Leitges and Mario Schiffer and Huber, {Tobias B}",
year = "2013",
month = feb,
day = "1",
doi = "10.1681/ASN.2012060582",
language = "English",
volume = "24",
pages = "253--67",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "2",

}

RIS

TY - JOUR

T1 - aPKCλ/ι and aPKCζ contribute to podocyte differentiation and glomerular maturation

AU - Hartleben, Björn

AU - Widmeier, Eugen

AU - Suhm, Martina

AU - Worthmann, Kirstin

AU - Schell, Christoph

AU - Helmstädter, Martin

AU - Wiech, Thorsten

AU - Walz, Gerd

AU - Leitges, Michael

AU - Schiffer, Mario

AU - Huber, Tobias B

PY - 2013/2/1

Y1 - 2013/2/1

N2 - Precise positioning of the highly complex interdigitating podocyte foot processes is critical to form the normal glomerular filtration barrier, but the molecular programs driving this process are unknown. The protein atypical protein kinase C (aPKC)--a component of the Par complex, which localizes to tight junctions and interacts with slit diaphragm proteins--may play a role. Here, we found that the combined deletion of the aPKCλ/ι and aPKCζ isoforms in podocytes associated with incorrectly positioned centrosomes and Golgi apparatus and mislocalized molecules of the slit diaphragm. Furthermore, aPKC-deficient podocytes failed to form the normal network of foot processes, leading to defective glomerular maturation with incomplete capillary formation and mesangiolysis. Our results suggest that aPKC isoforms orchestrate the formation of the podocyte processes essential for normal glomerular development and kidney function. Defective aPKC signaling results in a dramatically simplified glomerular architecture, causing severe proteinuria and perinatal death.

AB - Precise positioning of the highly complex interdigitating podocyte foot processes is critical to form the normal glomerular filtration barrier, but the molecular programs driving this process are unknown. The protein atypical protein kinase C (aPKC)--a component of the Par complex, which localizes to tight junctions and interacts with slit diaphragm proteins--may play a role. Here, we found that the combined deletion of the aPKCλ/ι and aPKCζ isoforms in podocytes associated with incorrectly positioned centrosomes and Golgi apparatus and mislocalized molecules of the slit diaphragm. Furthermore, aPKC-deficient podocytes failed to form the normal network of foot processes, leading to defective glomerular maturation with incomplete capillary formation and mesangiolysis. Our results suggest that aPKC isoforms orchestrate the formation of the podocyte processes essential for normal glomerular development and kidney function. Defective aPKC signaling results in a dramatically simplified glomerular architecture, causing severe proteinuria and perinatal death.

KW - Animals

KW - Capillaries

KW - Cell Differentiation

KW - Centrosome

KW - Female

KW - Golgi Apparatus

KW - Isoenzymes

KW - Kidney Glomerulus

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Microscopy, Electron

KW - Podocytes

KW - Protein Kinase C

KW - Proteinuria

KW - Signal Transduction

KW - Tight Junctions

U2 - 10.1681/ASN.2012060582

DO - 10.1681/ASN.2012060582

M3 - SCORING: Journal article

C2 - 23334392

VL - 24

SP - 253

EP - 267

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 2

ER -