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 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.

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 Mechanisms of Scarring in Focal Segmental Glomerulosclerosis

2019 ◽  
Vol 67 (9) ◽  
pp. 623-632
Author(s):  
Jianyong Zhong ◽  
Jacob B. Whitman ◽  
Hai-Chun Yang ◽  
Agnes B. Fogo
Keyword(s):  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Genetic Mutation ◽  
Tubular Epithelial Cells ◽  
Podocyte Injury ◽  
Segmental Glomerulosclerosis ◽  
Initial Injury ◽  
Parietal Epithelial Cells ◽  
Initial Target ◽  
Increased Susceptibility

Focal segmental glomerulosclerosis (FSGS) presents with scar in parts of some glomeruli and often progresses to global and diffuse glomerulosclerosis. Podocyte injury is the initial target in primary FSGS, induced by a circulating factor. Several gene variants, for example, APOL1, are associated with increased susceptibility to FSGS. Primary FSGS may be due to genetic mutation in key podocyte genes. Increased work stress after loss of nephrons, epigenetic mechanisms, and various profibrotic pathways can contribute to progressive sclerosis, regardless of the initial injury. The progression of FSGS lesions also involves crosstalk between podocytes and other kidney cells, such as parietal epithelial cells, glomerular endothelial cells, and even tubular epithelial cells. New insights related to these mechanisms could potentially lead to new therapeutic strategies to prevent progression of FSGS.

scholarly journals The direction and role of phenotypic transition between podocytes and parietal epithelial cells in focal segmental glomerulosclerosis

2014 ◽  
Vol 306 (1) ◽  
pp. F98-F104 ◽  
Author(s):  
Kazuo Sakamoto ◽  
Toshiharu Ueno ◽  
Namiko Kobayashi ◽  
Satoshi Hara ◽  
Yasutoshi Takashima ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Wilms Tumor ◽  
Double Positive ◽  
Segmental Glomerulosclerosis ◽  
Injury Model ◽  
Major Direction ◽  
Parietal Epithelial Cell ◽  
Parietal Epithelial Cells ◽  
Phenotypic Transition

Focal segmental glomerulosclerosis (FSGS) is a podocyte disease. Among the various histologies of FSGS, active epithelial changes, hyperplasia, as typically seen in the collapsing variant, indicates disease progression. Using a podocyte-specific injury model of FSGS carrying a genetic podocyte tag combined with double immunostaining by different sets of podocytes and parietal epithelial cell (PEC) markers [nestin/Pax8, Wilms' tumor-1 (WT1)/claudin1, and podocalyxin/Pax2], we investigated the direction of epithelial phenotypic transition and its role in FSGS. FSGS mice showed progressive proteinuria and renal dysfunction often accompanied by epithelial hyperplasia, wherein 5-bromo-4-chloro-3-indoyl β-d-galactoside (X-gal)-positive podocyte-tagged cells were markedly decreased. The average numbers of double-positive cells in all sets of markers were significantly increased in the FSGS mice compared with the controls. In addition, the average numbers of double-positive cells for X-gal/Pax8, nestin/Pax8 and podocalyxin/Pax2 staining in the FSGS mice were comparable, whereas those of WT1/claudin1 were significantly increased. When we divided glomeruli from FSGS mice into those with FSGS lesions and those without, double-positive cells tended to be more closely associated with glomeruli without FSGS lesions compared with those with FSGS lesions. Moreover, the majority of double-positive cells appeared to be isolated and very rarely associated with FSGS lesions (1/1,997 glomeruli). This study is the first to show the incidence and localization of epithelial cells with phenotypical changes in FSGS using a genetic tag. The results suggest that the major direction of epithelial phenotypic transition in cellular FSGS is from podocytes to PECs and that these cells were less represented in the active lesions of FSGS.

scholarly journals Proliferating cells in HIV and pamidronate-associated collapsing focal segmental glomerulosclerosis are parietal epithelial cells

2006 ◽  
Vol 70 (2) ◽  
pp. 338-344 ◽  
Author(s):  
H.B.P.M. Dijkman ◽  
J.J. Weening ◽  
B. Smeets ◽  
K.C.N. Verrijp ◽  
T.H. van Kuppevelt ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Proliferating Cells ◽  
Segmental Glomerulosclerosis ◽  
Parietal Epithelial Cells

scholarly journals Aberrant Notch1-dependent effects on glomerular parietal epithelial cells promotes collapsing focal segmental glomerulosclerosis with progressive podocyte loss

2013 ◽  
Vol 83 (6) ◽  
pp. 1065-1075 ◽  
Author(s):  
Toshiharu Ueno ◽  
Namiko Kobayashi ◽  
Makiko Nakayama ◽  
Yasutoshi Takashima ◽  
Takamoto Ohse ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Focal Segmental Glomerulosclerosis ◽  
Segmental Glomerulosclerosis ◽  
Podocyte Loss ◽  
Parietal Epithelial Cells
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