ArticlePediatric nephrology (Berlin, Germany)2007
Pax-2 and N-myc regulate epithelial cell proliferation and apoptosis in a positive autocrine feedback loop.
Article in Pediatric nephrology (Berlin, Germany), 2007. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- The Role of the PAX Genes in Renal Cell Carcinoma.International journal of molecular sciences · 2024Review
- ATDiabetologia · 2021Article
- MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis.Cell journal · 2020Article
- Maternal diabetes modulates kidney formation in murine progeny: the role of hedgehog interacting protein (HHIP).Diabetologia · 2014Article
- MicroRNAs: potential regulators of renal development genes that contribute to CAKUT.Pediatric nephrology (Berlin, Germany) · 2014Review
- Article
- Deficiency of intrarenal angiotensin II type 2 receptor impairs paired homeo box-2 and N-myc expression during nephrogenesis.Pediatric nephrology (Berlin, Germany) · 2008Article
- Effect of in utero and early-life conditions on adult health and disease.The New England journal of medicine · 2008Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both paired homeo box-2 (Pax-2) and N-myc genes play pivotal roles in renal morphogenesis via their effects on cell proliferation and differentiation, but whether and how they interact have not been addressed. In the present study, we investigated such a potential interaction using embryonic renal cells in vitro. Mouse embryonic mesenchymal (MK4) cells stably transfected with Pax-2 cDNA in sense (+) or antisense (-) orientation were used for experiments. Pax-2 promoter activity was monitored by luciferase assay. Reactive oxygen species (ROS) generation, cell proliferation, and cell apoptosis were evaluated. We found that Pax-2 and N-myc gene expression were upregulated and downregulated in Pax-2 (+) and Pax-2 (-) stable transformants, respectively. ROS generation and apoptosis were significantly reduced both in Pax-2 (+) transformants compared with Pax-2 (-) transformants and in naïve MK4 cells cultured in either normal- (5 mM) or high-glucose (25 mM) medium. Transient transfection of N-myc cDNA into Pax-2 (-) stable transformants restored Pax-2 gene expression and prevented ROS generation induced by high glucose. Our data demonstrate that Pax-2 gene overexpression prevents hyperglycemia-induced apoptosis, and N-myc appears to provide a positive autocrine feedback on Pax-2 gene expression in embryonic mesenchymal cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.