ArticleAmerican journal of physiology. Renal physiology2018
Modulation of apolipoprotein L1-microRNA-193a axis prevents podocyte dedifferentiation in high-glucose milieu.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review.Cells · 2026Review
- APOL1 Dynamics in Diabetic Kidney Disease and Hypertension.Biomolecules · 2025Review
- APOL1 Modulates Renin-Angiotensin System.Biomolecules · 2024Article
- MicroRNA193a: An Emerging Mediator of Glomerular Diseases.Biomolecules · 2023Review
- Article
- Parietal Epithelial Cell Behavior and Its Modulation by microRNA-193a.Biomolecules · 2023Review
- Transcriptomic Analysis of Human PodocytesKidney international reports · 2023Article
- Menin Enhances Androgen Receptor-Independent Proliferation and Migration of Prostate Cancer Cells.Molecules and cells · 2022Article
- Podocyte Bioenergetics in the Development of Diabetic Nephropathy: The Role of Mitochondria.Endocrinology · 2022Review
- Pathogenic Role of MicroRNA Dysregulation in Podocytopathies.Frontiers in physiology · 2022Review
- Knockdown of lncRNA MALAT1 ameliorates acute kidney injury by mediating the miR-204/APOL1 pathway.Journal of clinical laboratory analysis · 2021Article
- Alterations in plasma membrane ion channel structures stimulate NLRP3 inflammasome activation in APOL1 risk milieu.The FEBS journal · 2020Article
- Urinary Exosomal MicroRNA Signatures in Nephrotic, Biopsy-Proven Diabetic Nephropathy.Journal of clinical medicine · 2020Article
- MiR193a Modulation and Podocyte Phenotype.Cells · 2020Article
- Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases.International journal of molecular sciences · 2020Review
- MicroRNAs in Podocyte Injury in Diabetic Nephropathy.Frontiers in genetics · 2020Review
- APOL1 and kidney cell function.American journal of physiology. Renal physiology · 2019Review
- Disrupted apolipoprotein L1-miR193a axis dedifferentiates podocytes through autophagy blockade in an APOL1 risk milieu.American journal of physiology. Cell physiology · 2019Article
- Disruption of APOL1-miR193a Axis Induces Disorganization of Podocyte Actin Cytoskeleton.Scientific reports · 2019Article
- Role of Apolipoprotein L1 in Human Parietal Epithelial Cell Transition.The American journal of pathology · 2018Article
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Authors and funding
16 authors at 6 institutions in 3 countries.
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Abstract
The loss of podocyte (PD) molecular phenotype is an important feature of diabetic podocytopathy. We hypothesized that high glucose (HG) induces dedifferentiation in differentiated podocytes (DPDs) through alterations in the apolipoprotein (APO) L1-microRNA (miR) 193a axis. HG-induced DPD dedifferentiation manifested in the form of downregulation of Wilms' tumor 1 (WT1) and upregulation of paired box 2 (PAX2) expression. WT1-silenced DPDs displayed enhanced expression of PAX2. Immunoprecipitation of DPD cellular lysates with anti-WT1 antibody revealed formation of WT1 repressor complexes containing Polycomb group proteins, enhancer of zeste homolog 2, menin, and DNA methyltransferase (DNMT1), whereas silencing of either WT1 or DNMT1 disrupted this complex with enhanced expression of PAX2. HG-induced DPD dedifferentiation was associated with a higher expression of miR193a, whereas inhibition of miR193a prevented DPD dedifferentiation in HG milieu. HG downregulated DPD expression of APOL1. miR193a-overexpressing DPDs displayed downregulation of APOL1 and enhanced expression of dedifferentiating markers; conversely, silencing of miR193a enhanced the expression of APOL1 and preserved DPD phenotype. Moreover, stably APOL1G0-overexpressing DPDs displayed the enhanced expression of WT1 but attenuated expression of miR193a; nonetheless, silencing of APOL1 reversed these effects. Since silencing of APOL1 enhanced miR193a expression as well as dedifferentiation in DPDs, it appears that downregulation of APOL1 contributed to dedifferentiation of DPDs through enhanced miR193a expression in HG milieu. Vitamin D receptor agonist downregulated miR193a, upregulated APOL1 expression, and prevented dedifferentiation of DPDs in HG milieu. These findings suggest that modulation of the APOL1-miR193a axis carries a potential to preserve DPD molecular phenotype in HG milieu.
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