scholarly journals Parietal epithelial cells maintain the epithelial cell continuum forming Bowman's space in focal segmental glomerulosclerosis

2021 ◽  
Author(s):  
Laura Miesen ◽  
Péter Bándi ◽  
Brigith Willemsen ◽  
Fieke Mooren ◽  
Thiago Strieder ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Glomerular Epithelial Cell ◽  
Segmental Glomerulosclerosis ◽  
Glomerular Epithelial Cells ◽  
Tubular System ◽  
Sclerotic Lesions ◽  
Parietal Epithelial Cells ◽  
Glomerular Tuft

In the glomerulus, Bowman's space is formed by a continuum of glomerular epithelial cells. In focal segmental glomerulosclerosis (FSGS), glomeruli show segmental scarring, a result of activated PECs invading the glomerular tuft. The segmental scars interrupt the epithelial continuum. However, non-sclerotic segments seem to be preserved even in glomeruli with advanced lesions. We studied the histology of the segmental pattern in Munich Wistar Frömter (MWF) rats, a model for secondary FSGS. Our results showed that matrix layers lined with PECs cover the sclerotic lesions. These PECs formed contacts with podocytes of the uninvolved tuft segments, restoring the epithelial continuum. Formed Bowman's spaces were still connected to the tubular system. Furthermore, in biopsies of patients with secondary FSGS we also detected matrix layers formed by PECs, separating the uninvolved from the sclerotic glomerular segments. While PECs have a major role in the formation of glomerulosclerosis, we showed that in FSGS, PECs also restore the glomerular epithelial cell continuum that surrounds Bowman's space. This process may be beneficial and indispensable for glomerular filtration in the uninvolved segments of sclerotic glomeruli.

scholarly journals Cre recombinase toxicity in podocytes: a novel genetic model for FSGS in adolescent mice

2019 ◽  
Vol 317 (5) ◽  
pp. F1375-F1382 ◽  
Author(s):  
Madeleine Frahsek ◽  
Kevin Schulte ◽  
Arnaldo Chia-Gil ◽  
Sonja Djudjaj ◽  
Herdit Schueler ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Genetic Model ◽  
Transgenic Animals ◽  
Cre Recombinase ◽  
Young Age ◽  
Podocyte Injury ◽  
Sclerotic Lesions ◽  
Parietal Epithelial Cells ◽  
Time Point

Here, we show that inducible overexpression of Cre recombinase in glomerular podocytes but not in parietal epithelial cells may trigger focal segmental glomerulosclerosis (FSGS) in juvenile transgenic homocygous Pod-rtTA/LC1 mice. Administration of doxycycline shortly after birth, but not at any other time point later in life, resulted in podocyte injury and development of classical FSGS lesions in these mice. Sclerotic lesions were formed as soon as 3 wk of age, and FSGS progressed with low variability until 13 wk of age. In addition, our experiments identified Cre toxicity as a potentially relevant limitation for studies in podocytes of transgenic animals. In summary, our study establishes a novel genetic model for FSGS in mice, which exhibits low variability and manifests already at a young age.

Up-Regulation of CD74 Expression in Parietal Epithelial Cells in a Mouse Model of Focal Segmental Glomerulosclerosis

Nephron ◽  
2016 ◽  
Vol 134 (4) ◽  
pp. 238-252 ◽  
Author(s):  
Takeshi Yamazaki ◽  
Satoshi Sasaki ◽  
Takayuki Okamoto ◽  
Yasuyuki Sato ◽  
Asako Hayashi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mouse Model ◽  
Focal Segmental Glomerulosclerosis ◽  
Segmental Glomerulosclerosis ◽  
Parietal Epithelial Cells

scholarly journals Common histological patterns in glomerular epithelial cells in secondary focal segmental glomerulosclerosis

2015 ◽  
Vol 88 (5) ◽  
pp. 990-998 ◽  
Author(s):  
Christoph Kuppe ◽  
Hermann-Josef Gröne ◽  
Tammo Ostendorf ◽  
Toin H. van Kuppevelt ◽  
Peter Boor ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Segmental Glomerulosclerosis ◽  
Glomerular Epithelial Cells

Is CD44 in glomerular parietal epithelial cells a pathological marker of renal function deterioration in primary focal segmental glomerulosclerosis?

2017 ◽  
Vol 32 (11) ◽  
pp. 2165-2169 ◽  
Author(s):  
Brunna Pinto Froes ◽  
Stanley de Almeida Araújo ◽  
Eduardo Alves Bambirra ◽  
Eduardo Araújo Oliveira ◽  
Ana Cristina Simões e Silva ◽  
...  
Keyword(s):  
Renal Function ◽  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Segmental Glomerulosclerosis ◽  
Renal Function Deterioration ◽  
Parietal Epithelial Cells

scholarly journals Glomerular parietal epithelial cells contribute to adult podocyte regeneration in experimental focal segmental glomerulosclerosis

2015 ◽  
Vol 88 (5) ◽  
pp. 999-1012 ◽  
Author(s):  
Diana G. Eng ◽  
Maria W. Sunseri ◽  
Natalya V. Kaverina ◽  
Sebastian S. Roeder ◽  
Jeffrey W. Pippin ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Segmental Glomerulosclerosis ◽  
Parietal Epithelial Cells ◽  
Podocyte Regeneration

scholarly journals Mechanisms of Scarring in Focal Segmental Glomerulosclerosis

2021 ◽  
pp. 1-9
Author(s):  
Ke Sun ◽  
Qionghong Xie ◽  
Chuan-Ming Hao
Keyword(s):  
Epithelial Cells ◽  
Influencing Factors ◽  
Focal Segmental Glomerulosclerosis ◽  
Therapeutic Strategies ◽  
Podocyte Injury ◽  
Segmental Glomerulosclerosis ◽  
Potential Sources ◽  
Histologic Pattern ◽  
Parietal Epithelial Cells

<b><i>Background:</i></b> Focal segmental glomerulosclerosis (FSGS) is a histologic pattern characterized by focal glomerular scarring, which often progresses to systemic and diffuse glomerulosclerosis. Previous studies have emphasized that the initiation of classic FSGS occurs in podocytes. The dysfunction and loss of podocytes have been associated with the development of proteinuria and the progression of various diseases. In addition, primary, secondary, and genetic FSGS are caused by different mechanisms of podocyte injury. <b><i>Summary:</i></b> The potential sources and mechanism of podocyte supplementation are the focus of our current research. Increasing attention has been paid to the role played by parietal epithelial cells (PECs) during the progression of FSGS. PECs are not only the primary influencing factors in glomerulosclerosis lesions but also have repair abilities, which remain a focus of debate. Notably, other resident glomerular cells also play significant roles in the progression of this disease. <b><i>Key Message:</i></b> In this review, we focus on the mechanism of scarring in FSGS and discuss current and potential therapeutic strategies.

scholarly journals Puromycin Aminonucleoside Suppresses Integrin Expression in Cultured Glomerular Epithelial Cells

2001 ◽  
Vol 12 (4) ◽  
pp. 758-766 ◽  
Author(s):  
UMA KRISHNAMURTI ◽  
BING ZHOU ◽  
WEI-WEI FAN ◽  
EFFIE TSILIBARY ◽  
ELIZABETH WAYNER ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Type Iv Collagen ◽  
Cell Detachment ◽  
Puromycin Aminonucleoside ◽  
Glomerular Epithelial Cell ◽  
Type Iv ◽  
Glomerular Epithelial Cells

Abstract. Puromycin aminonucleoside (PAN)-induced nephrosis is a well-described model of human idiopathic nephrotic syndrome, but the mechanism of PAN's effect is not completely understood. Because PAN injection into rats results in retraction of glomerular epithelial cell foot processes and glomerular epithelial cell detachment, it was hypothesized that PAN might alter the contacts between these cells and the glomerular basement membrane. The major integrin expressed by glomerular epithelial cells is α3β1, which mediates attachment of these cells to extracellular matrix proteins including type IV collagen. T-SV 40 immortalized human glomerular epithelial cells were used to study PAN's effects on α3β1 expression, as well as that of podocalyxin and the slit diaphragm component ZO-1. Glomerular epithelial cells were seeded into plastic flasks and allowed to attach and proliferate for 48 h. The cells were then incubated for another 48 h in media containing 0, 0.5, or 5.0 μg/ml PAN. PAN exposure resulted in dose-dependent decreases in α3 and β1 expression, both at the protein level and at the mRNA level. This was accompanied by a significant decrease in the adhesion of glomerular epithelial cells to type IV collagen. PAN did not affect ZO-1 protein expression. Treatment with PAN increased the expression of podocalyxin at the protein and mRNA levels. Reduced glomerular epithelial cell expression of α3β1 integrins and impaired adhesion to type IV collagen may contribute to the glomerular epithelial cell detachment from glomerular basement membrane seen in the PAN nephrosis model.

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