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  • Review Article
  • Published:

The emergence of the glomerular parietal epithelial cell

Nature Reviews Nephrology volume 10, pages 158–173 (2014)Cite this article

Subjects

Key Points

  • Parietal epithelial cells (PECs) are the predominant cell type in glomerular crescents

  • When activated in focal segmental glomerulosclerosis, PECs migrate to the glomerular tuft and produce Bowman's basement membrane matrix proteins, leading to segmental scarring

  • Different PEC subpopulations have been identified under normal conditions

  • In humans, but not mice, a subset of PECs express markers characteristics of stem or progenitor cells

  • Filtered albumin injures PECs by inducing apoptosis, and limits PEC progenitors from undergoing regeneration

Abstract

Glomerular diseases are the leading causes of chronic and end-stage kidney disease. In the 1980s and 1990s, attention was focused on the biology and role of glomerular endothelial and mesangial cells. For the past two decades, seminal discoveries have been made in podocyte biology in health and disease. More recently, the glomerular parietal epithelial cell (PEC)—the fourth resident glomerular cell type—has been under active study, leading to a better understanding and definition of how these cells behave normally, and their potential roles in glomerular disease. Accordingly, this Review will focus on our current knowledge of PECs, in both health and disease. We discuss model systems to study PECs, how PECs might contribute to glomerulosclerosis, crescent and pseudocrescent formation and how PECs handle filtered albumin. These events have consequences on PEC structure and function, and PECs have potential roles as stem or progenitor cells for podocytes in glomerular regeneration, which will also be described.

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Figure 1: Terminology for cells on Bowman's capsule.
Figure 2: Selected methods used to study PECs.
Figure 3: How PECs might contribute to glomerular disease.
Figure 4: Phenotype of aPECs.
Figure 5: Schematic for the evolution of cellular crescents.

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Acknowledgements

M. J. Moeller is supported by the TP17 SFB/Transregio 57 of the Deutsche Forschungsgemeinschaft (DFG) and B. Smeets by a grant by the DFG (BO 3755/1-1). M. J. Moeller is also supported by the European Research Projects on Rare Diseases (E-Rare), Project Rare-G # 01 GM 1208A and is a member of the SFB/Transregio 57 DFG consortium “Mechanisms of organ fibrosis”. S. J. Shankland is supported by grants from the NIH and the American Heart Association (DK056799, DK083391).

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Authors and Affiliations

  1. Division of Nephrology, University of Washington, 1959 North East Pacific Avenue, Box 356521, Room BB1269, Seattle, 98195-6521, WA, USA

    Stuart J. Shankland & Jeffrey W. Pippin

  2. Nephrology and Clinical Immunology, University Hospital of the RWTH Aachen University, Pauwelsstraße 30, 52074, Aachen, Germany

    Bart Smeets & Marcus J. Moeller

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All authors researched data for the article, made a substantial contribution to a discussion of the content and wrote and edited the manuscript.

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Shankland, S., Smeets, B., Pippin, J. et al. The emergence of the glomerular parietal epithelial cell. Nat Rev Nephrol 10, 158–173 (2014). https://doi.org/10.1038/nrneph.2014.1

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