ArticleJournal of diabetes research2020
High Glucose Induces Endothelial COX2 and iNOS Expression via Inhibition of Monomethyltransferase SETD8 Expression.
Article in Journal of diabetes research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Uncovering endothelial to mesenchymal transition drivers in atherosclerosis via multi-omics analysis.BMC cardiovascular disorders · 2025Article
- Article
- Polydatin improves vascular endothelial function by maintaining mitochondrial homeostasis under high glucose conditions.Scientific reports · 2023Article
- Ultrastructural features mirror metabolic derangement in human endothelial cells exposed to high glucose.Scientific reports · 2023Article
- The protective roles of citrus flavonoids, naringenin, and naringin on endothelial cell dysfunction in diseases.Heliyon · 2023Review
- The Role of Histone Modifications in the Pathogenesis of Diabetic Kidney Disease.International journal of molecular sciences · 2023Review
- ESE-1 mediates lipopolysaccharide-induced BV2 cell inflammation via upregulation of HMGB1 expression.Journal of biosciences · 2023Article
- Article
- Propofol protects against high glucose-mediated endothelial injury via inhibition of COX2 and iNOS expressions.Acta biochimica et biophysica Sinica · 2022Article
- Methyltransferase SET domain family and its relationship with cardiovascular development and diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Article
- The SETD8/ELK1/bach1 complex regulates hyperglycaemia-mediated EndMT in diabetic nephropathy.Journal of translational medicine · 2022Article
- SETD8 cooperates with MZF1 to participate in hyperglycemia-induced endothelial inflammation via elevation of WNT5A levels in diabetic nephropathy.Cellular & molecular biology letters · 2022Article
- Network pharmacology and in vitro studies reveal the pharmacological effects and molecular mechanisms of Shenzhi Jiannao prescription against vascular dementia.BMC complementary medicine and therapies · 2022Article
- New insights into the role of melatonin in diabetic cardiomyopathy.Pharmacology research & perspectives · 2022Review
- Epigenetics in the pathogenesis of diabetic nephropathy.Acta biochimica et biophysica Sinica · 2022Review
- Article
- ets1 associates with KMT5A to participate in high glucose-mediated EndMT via upregulation of PFN2 expression in diabetic nephropathy.Molecular medicine (Cambridge, Mass.) · 2021Article
- The CREB/KMT5A complex regulates PTP1B to modulate high glucose-induced endothelial inflammatory factor levels in diabetic nephropathy.Cell death & disease · 2021Article
- A novel role of kallikrein-related peptidase 8 in the pathogenesis of diabetic cardiac fibrosis.Theranostics · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS) overexpression results in endothelial apoptosis, thus mediating vascular endothelial injury in hyperglycaemia. E26 transformation-specific sequence transcription factor-1 (ESE-1), which belongs to the E26 transformation-specific family of transcription factors, has been demonstrated to be involved in COX2 and iNOS gene transcription. Our previous study indicated that SET domain-containing protein 8 (SETD8) downregulation is involved in high glucose-mediated endothelial inflammation in human umbilical vein endothelial cells (HUVECs). Here, we report that SETD8 plays a major role in hyperglycaemia-induced COX2 and iNOS expression. In HUVECs, upregulation of ESE-1 expression was related to high glucose-mediated apoptosis and COX2 and iNOS expression. High glucose inhibited SETD8 expression, and overexpression of SETD8 diminished the effects of high glucose treatment. Consistently, RNA silencing of SETD8 led to the opposite effect. Furthermore, SETD8 was found to interact with specificity protein 1 (SP1). Blockade of SP1 protected against high glucose-mediated endothelial injury. Mechanistically, we showed that H4K20me1, a downstream target of SETD8, and SP1 were enriched at the ESE-1 promoter region by ChIP assay. Luciferase reporter assays indicated that SETD8 overexpression attenuated ESE-1 promoter activity and augmented the inhibitory effect of siSP1 on ESE-1 promoter activity. In general, our data indicate that SETD8 interacts with SP1 to coregulate ESE-1 expression, which is involved in hyperglycaemia-mediated endothelial apoptosis in HUVECs.
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