ArticleMolecular and cellular biochemistry2008
Transcriptional regulation of plasminogen activator inhibitor-1 in vascular endothelial cells induced by oxidized very low density lipoproteins.
Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 18 citations in OpenAlex.
- Modified Lipoproteins Induce Arterial Wall Inflammation During Atherogenesis.Frontiers in cardiovascular medicine · 2022Review
- Plasminogen activator inhibitor links obesity and thrombotic cerebrovascular diseases: The roles of PAI-1 and obesity on stroke.Metabolic brain disease · 2017Review
- Proteotoxic stress of cancer: implication of the heat-shock response in oncogenesis.Journal of cellular physiology · 2012Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated levels of triglycerides and very low density lipoproteins (VLDL) are biochemical markers of metabolic syndrome and diabetes. VLDL from hypertriglyceridemic or diabetic patients increased the generation of plasminogen activator inhibitor-1 (PAI-1) from cultured vascular endothelial cells (EC). Susceptibility of VLDL to peroxidation was increased in diabetic patients. Heat shock factor-1 (HSF1) is implicated in the transcriptional regulation of PAI-1 induced by glycated low density lipoprotein (LDL). The present study examined the effects of oxidized VLDL (oxVLDL) on the expression of PAI-1 and HSF1 in cultured human EC and mouse embryo fibroblasts (MEF). OxVLDL modified by copper or iron ions increased the expression of PAI-1 and HSF1 in EC compared to VLDL or LDL. Butylated hydroxytulene inhibited oxVLDL-induced expression of PAI-1 and HSF1 in EC. OxVLDL increased the binding of HSF1 to PAI-1 promoter. Short interference RNA for HSF1 inhibited oxVLDL-induced PAI-1 expression in EC. OxVLDL stimulated the expression of PAI-1 from MEF of wild-type mice, but failed to increase PAI-1 expression in MEF of HSF1-knockout mice. The results indicate that oxVLDL increased PAI-1 expression, and HSF1 mediates the transcription of PAI-1 in cultured vascular EC or fibroblasts.
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