ArticleAmerican journal of physiology. Renal physiology2018
Cells of NG2 lineage increase in glomeruli of mice following podocyte depletion.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- The UBR5 protein facilitates mesangial cell hypertrophy and glycolysis induced by high glucose by increasing the phosphorylation levels of AKT.Acta diabetologica · 2025Article
- Progression of albuminuria and podocyte injury in focal segmental glomerulosclerosis inhibited by enhanced glycosphingolipid GM3 via valproic acid.Scientific reports · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Glycosphingolipid GM3 prevents albuminuria and podocytopathy induced by anti-nephrin antibody.Scientific reports · 2022Article
- Protective effects of budesonide on LPS-induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence fromExperimental and therapeutic medicine · 2022Article
- Kidney repair and regeneration: perspectives of the NIDDK (Re)Building a Kidney consortium.Kidney international · 2022Article
- Global transcriptomic changes occur in aged mouse podocytes.Kidney international · 2020Article
- Inhibition of Renal Stellate Cell Activation Reduces Renal Fibrosis.Biomedicines · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Under certain circumstances, podocytes can be partially replaced following their loss in disease. The inability of podocytes to proliferate suggests that replacement derives from other cell types. Because neural/glial antigen 2 (NG2)-expressing cells can serve as progenitors in other organs and because herein we showed increased NG2 staining in podocytes following their loss in experimental focal segmental glomerulosclerosis, we used lineage tracing in NG2-CreER tdTomato mice to test the hypothesis that partial podocyte replacement might derive from this cell population. The percentage of glomeruli with red fluorescence protein (RFP)-labeled NG2 cells increased following podocyte depletion, which was augmented by enalapril. However, BrdU was not detected in RFP-labeled cells, consistent with the migration of these cells to the glomerulus. Within glomeruli, RFP-labeled cells did not coexpress podocyte proteins (p57, synaptopodin, nephrin, or podocin) but did coexpress markers for mesangial (α8 integrin, PDGFβ receptor) and parietal epithelial cells (PAX8, src-suppressed C-kinase substrate). These results suggest that following podocyte depletion, cells of NG2 lineage do not serve as adult podocyte progenitors but have the ability to transdifferentiate to mesangial and parietal epithelial cell fates.
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