ArticlePediatric research2011
Induction of podocyte-derived VEGF ameliorates podocyte injury and subsequent abnormal glomerular development caused by puromycin aminonucleoside.
Article in Pediatric research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Discovery of kidney disease targets using multimodal human podocyte injury models.Stem cell reports · 2026Article
- The effect of SGLT2 inhibitor and HIF-PHI on the podocyte-specific molecules and cytoskeleton of diabetic podocytes.BMC nephrology · 2025Article
- Mechanistic Insights Into Redox Damage of the Podocyte in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2025Review
- Low-Dose Erythropoietin Amplifies Beneficial Effects of Angiotensin II Blockade on Glomerulosclerosis.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- DMOG, a Prolyl Hydroxylase Inhibitor, Increases Hemoglobin Levels without Exacerbating Hypertension and Renal Injury in Salt-Sensitive Hypertensive Rats.The Journal of pharmacology and experimental therapeutics · 2020Article
- Lipoprotein modulation of proteinuric renal injury.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Kidney-derived c-kitScientific reports · 2018Article
- The role of survivin in podocyte injury induced by puromycin aminonucleoside.International journal of molecular sciences · 2014Article
- Yi qi qing re gao attenuates podocyte injury and inhibits vascular endothelial growth factor overexpression in puromycin aminonucleoside rat model.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- VEGF165b overexpression restores normal glomerular water permeability in VEGF164-overexpressing adult mice.American journal of physiology. Renal physiology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Our previous studies using puromycin aminonucleoside (PAN) established that podocyte damage leads to glomerular growth arrest during development and glomerulosclerosis later in life. This study examined the potential benefit of maintaining podocyte-derived VEGF in podocyte defense and survival after PAN injury using conditional transgenic podocytes and mice, in which human VEGF-A (hVEGF) transgene expression is controlled by tetracycline responsive element (TRE) promoter and reverse tetracycline transactivator (rtTA) in podocytes. In vitro experiments used primary cultured podocytes harvested from mice carrying podocin-rtTA and TRE-hVEGF transgenes, in which hVEGF can be induced selectively. Induction of VEGF in PAN-exposed podocytes resulted in preservation of intrinsic VEGF, α-actinin-4 and synaptopodin, antiapoptotic marker Bcl-xL/Bax, as well as attenuation in apoptotic marker cleaved/total caspase-3. In vivo, compared with genotype controls, PAN-sensitive neonatal mice with physiologically relevant levels of podocyte-derived VEGF showed significantly larger glomeruli. Furthermore, PAN-induced up-regulation of desmin, down-regulation of synaptopodin and nephrin, and disruption of glomerular morphology were significantly attenuated in VEGF-induced transgenic mice. Our data indicate that podocyte-derived VEGF provides self-preservation functions, which can rescue the cell after injury and preempt subsequent deterioration of the glomerulus in developing mice.
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Registered trials
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