ArticleAmerican journal of physiology. Renal physiology2019
Podocyte-specific expression of Cre recombinase promotes glomerular basement membrane thickening.
Article in American journal of physiology. Renal physiology, 2019. 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, 22 citations in OpenAlex.
- Podocyte-derived endothelin-1 and endothelial cell endothelin A receptors are essential for glomerular injury in mouse models of focal segmental glomerulosclerosis.Kidney international · 2026Article
- A guide to cell-type-specific Cre mouse models in atherosclerosis: from background strains to future directions.Frontiers in cardiovascular medicine · 2026Review
- Protective Effect of Neochlorogenic Acid on Diabetic Nephropathy via Inflammation and Pyroptosis Suppression.Journal of agricultural and food chemistry · 2025Article
- Podocyte-Specific Expression of the Stress Response Protein REDD1 Is Necessary for Diabetes-Induced Podocytopenia.Diabetes · 2025Article
- Interrelation of Natural Polyphenol and Fibrosis in Diabetic Nephropathy.Molecules (Basel, Switzerland) · 2024Review
- COL4A3 Mutation Induced Podocyte Apoptosis by Dysregulation of NADPH Oxidase 4 and MMP-2.Kidney international reports · 2023Article
- Cre toxicity in mouse models of cardiovascular physiology and disease.Nature cardiovascular research · 2022Article
- Heterozygous expression of Cre recombinase in podocytes has no impact on the anti-glomerular basement membrane glomerulonephritis model in C57BL/6J mice.Physiological reports · 2022Article
- Measuring cardiomyocyte cell-cycle activity and proliferation in the age of heart regeneration.American journal of physiology. Heart and circulatory physiology · 2022Review
- Loss of CLDN5 in podocytes deregulates WIF1 to activate WNT signaling and contributes to kidney disease.Nature communications · 2022Article
- Erythroid-specific inactivation of Slc12a6/Kcc3 by EpoR promoter-driven Cre expression reduces K-Cl cotransport activity in mouse erythrocytes.Physiological reports · 2022Article
- UAB-UCSD O'Brien Center for Acute Kidney Injury Research.American journal of physiology. Renal physiology · 2021Review
- Know Your Model: Recombinase-expressing mice.Lab animal · 2020Article
- The Cre/lox system: Cre-ating unintended damage.American journal of physiology. Renal physiology · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Conditional gene targeting using Cre recombinase has offered a powerful tool to modify gene function precisely in defined cells/tissues and at specific times. However, in mammalian cells, Cre recombinase can be genotoxic. The importance of including Cre-expressing control mice to avoid misinterpretation and to maximize the validity of the experimental results has been increasingly recognized. While studying the role of podocytes in the pathogenesis of glomerular basement membrane (GBM) thickening, we used Cre recombinase driven by the podocyte-specific podocin promoter (NPHS2-Cre) to generate a conditional knockout. By conventional structural and functional measures (histology by periodic acid-Schiff staining, albuminuria, and plasma creatinine), we did not detect significant differences between NPHS2-Cre transgenic and wild-type control mice. However, surprisingly, the group that expressed Cre transgene alone developed signs of podocyte toxicity, including marked GBM thickening, loss of normal foot process morphology, and reduced Wilms tumor 1 expression. GBM thickening was characterized by altered expression of core structural protein laminin isoform α
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