ArticleBMC nephrology2014
The glomerular parietal epithelial cell's responses are influenced by SM22 alpha levels.
Article in BMC nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
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- Decreased GM3 correlates with proteinuria in minimal change nephrotic syndrome and focal segmental glomerulosclerosis.Clinical and experimental nephrology · 2022Article
- Screening prognostic genes related to leucovorin, fluorouracil, and irinotecan treatment sensitivity by performing co-expression network analysis for colon cancer.Frontiers in genetics · 2022Article
- Chronic Kidney Allograft Disease: New Concepts and Opportunities.Frontiers in medicine · 2021Review
- CD44 impacts glomerular parietal epithelial cell changes in the aged mouse kidney.Physiological reports · 2020Article
- Dual lineage tracing shows that glomerular parietal epithelial cells can transdifferentiate toward the adult podocyte fate.Kidney international · 2019Article
- Cells of NG2 lineage increase in glomeruli of mice following podocyte depletion.American journal of physiology. Renal physiology · 2018Article
- The Presence of Urinary Renal Progenitor Cells in Stable Kidney Transplant Recipients Anticipates Allograft Deterioration.Frontiers in physiology · 2018Article
- Gas1 expression in parietal cells of Bowman's capsule in experimental diabetic nephropathy.Histochemistry and cell biology · 2017Article
- Article
- Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys.American journal of physiology. Renal physiology · 2016Article
- Changes in glomerular parietal epithelial cells in mouse kidneys with advanced age.American journal of physiology. Renal physiology · 2015Article
- Transgelin gene is frequently downregulated by promoter DNA hypermethylation in breast cancer.Clinical epigenetics · 2015Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundStudies have shown in several diseases initially affecting podocytes, that the neighboring glomerular parietal epithelial cells (PECs) are secondarily involved. The PEC response might be reparative under certain circumstances, yet injurious under others. The factors governing these are not well understood. We have shown that SM22α, an actin-binding protein considered a marker of smooth muscle differentiation, is upregulated in podocytes and PECs in several models of podocyte disease. However, the impact of SM22α levels on PECs is not known.
methodsExperimental glomerular disease, characterized by primary podocyte injury, was induced in aged-matched SM22α+/+ and SM22α-/-mice by intraperitoneal injection of sheep anti-rabbit glomeruli antibody. Immunostaining methods were employed on days 7 and 14 of disease.
resultsThe number of PEC transition cells, defined as cells co-expressing a PEC protein (PAX2) and podocyte protein (Synaptopodin) was higher in diseased SM22α-/-mice compared with SM22α+/+mice. WT1 staining along Bowman's capsule is higher in diseased SM22α-/-mice. This was accompanied by increased PEC proliferation (measured by ki-67 staining), and an increase in immunostaining for the progenitor marker NCAM, in a subpopulation of PECs in diseased SM22α-/-mice. In addition, immunostaining for vimentin and alpha smooth muscle actin, markers of epithelial-to-mesenchymal transition (EMT), was lower in diseased SM22α-/-mice compared to diseased SM22α+/+mice.
conclusionSM22α levels may impact how PECs respond following a primary podocyte injury in experimental glomerular disease. Absent/lower levels favor an increase in PEC transition cells and PECs expressing a progenitor marker, and a lower EMT rate compared to SM22α+/+mice, where SM22 levels are markedly increased in PECs.
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