ArticleThe Journal of clinical investigation2002
Diabetic LDL inhibits cell-cycle progression via STAT5B and p21(waf).
Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 26 citations in OpenAlex.
- The potential role of targeting the leptin receptor as a treatment for breast cancer in the context of hyperleptinemia: a literature review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Impaired adult hippocampal neurogenesis in a mouse model of familial hypercholesterolemia: A role for the LDL receptor and cholesterol metabolism in adult neural precursor cells.Molecular metabolism · 2019Article
- Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes Complications.Journal of diabetes research · 2015Review
- Gadd45α: a novel diabetes-associated gene potentially linking diabetic cardiomyopathy and baroreflex dysfunction.PloS one · 2012Article
- Unacylated ghrelin rescues endothelial progenitor cell function in individuals with type 2 diabetes.Diabetes · 2010Article
- Nox2 regulates endothelial cell cycle arrest and apoptosis via p21cip1 and p53.Free radical biology & medicine · 2007Article
- Identification of biomarkers, pathways, and potential therapeutic targets for heart failure using next-generation sequencing data and bioinformatics analysis.Therapeutic advances in cardiovascular diseaseArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modified LDL is a major cause of injury to the endothelium in diabetes. In the present study, we analyzed the effects on endothelial cells of LDL recovered from type 2 diabetic patients (dm-LDL) or from nondiabetic subjects (n-LDL). Treatment of human umbilical vein endothelial cells with dm-LDL, but not n-LDL, led to the accumulation of cells in G1. To dissect the molecular mechanisms of this effect, we analyzed the expression and function of the cyclin-dependent kinase inhibitor p21(waf), a cell cycle regulator known to be a target of the signal transducers and activators of transcription (STATs). dm-LDL led to transient STAT5 phosphorylation and the formation of a STAT5-containing complex and activated p21(waf) expression at the transcriptional level. Expression of the dominant-negative form of STAT5B, but not of STAT5A, significantly decreased both p21(waf) expression and the fraction of cells in G1. Finally, immunofluorescence analysis demonstrated that activated STAT5 is expressed in newly formed intraplaque vessels and in endothelial cells lining the luminal side of the plaque. Similarly, p21(waf) immunoreactivity was found in the neointimal vasculature. Our results suggest a role of STAT5B as a regulator of gene expression in diabetes-associated vascular disease.
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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.