ArticleAmerican journal of physiology. Renal physiology2014
The direction and role of phenotypic transition between podocytes and parietal epithelial cells in focal segmental glomerulosclerosis.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Pathogenesis of Focal Segmental Glomerulosclerosis and Related Disorders.Annual review of pathology · 2025Review
- Transplantation of decellularized porcine kidney grafts repopulated with primary human cells demonstrates filtration function in pigs.Communications medicine · 2024Article
- Diabetic nephropathy with marked extra-capillary cell proliferation: a case report.BMC nephrology · 2023Article
- Collapsing glomerulopathy: unraveling varied pathogeneses.Current opinion in nephrology and hypertension · 2023Review
- Digital spatial profiling of collapsing glomerulopathy.Kidney international · 2022Article
- Cell Hypertrophy: A "Biophysical Roadblock" to Reversing Kidney Injury.Frontiers in cell and developmental biology · 2022Article
- Morphological Features of Minimal Change Disease and Focal Segmental Glomerulosclerosis Using Repeat Biopsy and Parietal Epithelial Cell Marker.Kidney diseases (Basel, Switzerland) · 2020Article
- Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
- APOL1 and kidney cell function.American journal of physiology. Renal physiology · 2019Review
- Parietal cells-new perspectives in glomerular disease.Cell and tissue research · 2017Article
- Collapsing glomerulopathy, the Saudi Arabian scenario. A study of 31 cases and a review of literature.Saudi medical journal · 2017Review
- Can podocytes be regenerated in adults?Current opinion in nephrology and hypertension · 2017Review
- Glomerular epithelial CD44 expression and segmental sclerosis in IgA nephropathy.Clinical and experimental nephrology · 2016Article
- Partial podocyte replenishment in experimental FSGS derives from nonpodocyte sources.American journal of physiology. Renal physiology · 2016Article
- Glomerular parietal epithelial cells contribute to adult podocyte regeneration in experimental focal segmental glomerulosclerosis.Kidney international · 2015Article
- The phenotypes of podocytes and parietal epithelial cells may overlap in diabetic nephropathy.Kidney international · 2015Article
- Cells of renin lineage are adult pluripotent progenitors in experimental glomerular disease.American journal of physiology. Renal physiology · 2015Article
- The use of lineage tracing to study kidney injury and regeneration.Nature reviews. Nephrology · 2015Review
- ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2015Article
- MicroRNA-193a Regulates the Transdifferentiation of Human Parietal Epithelial Cells toward a Podocyte Phenotype.Journal of the American Society of Nephrology : JASN · 2015Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
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.
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