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

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.

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

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.

Dissociation of NEPH1 from nephrin is involved in development of a rat model of focal segmental glomerulosclerosis

2008 ◽  
Vol 295 (5) ◽  
pp. F1376-F1387 ◽  
Author(s):  
Yasuhiro Otaki ◽  
Naoko Miyauchi ◽  
Mutsumi Higa ◽  
Akira Takada ◽  
Takeshi Kuroda ◽  
...  
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Rat Model ◽  
Critical Role ◽  
Glomerular Capillary Wall ◽  
Morphological Alterations ◽  
Initiation Phase ◽  
Segmental Glomerulosclerosis ◽  
Glomerular Epithelial Cells ◽  
End Stage

Focal segmental glomerulosclerosis (FSGS) is a disease showing severe proteinuria, and the disease progresses to end-stage kidney failure in many cases. However, the pathogenic mechanism of FSGS is not well understood. The slit diaphragm (SD), which bridges the neighboring foot processes of glomerular epithelial cells, is understood to function as a barrier of the glomerular capillary wall. To investigate the role of SD dysfunction in the development of FSGS, we analyzed the expression of SD-associated molecules in rat adriamycin-induced nephropathy, a mimic of FSGS. The staining of the SD molecules nephrin, podocin, and NEPH1 had already shifted to a discontinuous dotlike pattern at the initiation phase of the disease, when neither proteinuria nor any morphological alterations were detected yet. The alteration of NEPH1 expression was the most evident among the molecules examined, and NEPH1 was dissociated from nephrin at the initiation phase. On day 28, when severe proteinuria was detected and sclerotic changes were already observed, alteration of the expressions of nephrin, podocin, and NEPH1 worsened, but no alteration in the expression of other SD-associated molecules or other podocyte molecules was detected. It is postulated that the dissociation of NEPH1 from nephrin initiates proteinuria and that the SD alteration restricted in these molecules plays a critical role in the development of sclerotic changes in FSGS.

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