ArticleExperimental & molecular medicine2011
Inhibition of NF-κB prevents high glucose-induced proliferation and plasminogen activator inhibitor-1 expression in vascular smooth muscle cells.
Article in Experimental & molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
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- Integrative analysis of gene expression, protein abundance, and metabolomic profiling elucidates complex relationships in chronic hyperglycemia-induced changes in human aortic smooth muscle cells.Journal of biological engineering · 2024Article
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- Diabetes-Associated Hyperglycemia Causes Rapid-Onset Ocular Surface Damage.Investigative ophthalmology & visual science · 2023Article
- Focal adhesion kinase-related pathways may be suppressed by metformin in vascular smooth muscle cells in high glucose conditions.Endocrinology, diabetes & metabolism · 2022Article
- Metabolomic Analysis of Serum and Tear Samples from Patients with Obesity and Type 2 Diabetes Mellitus.International journal of molecular sciences · 2022Article
- Zinc Ameliorates the Osteogenic Effects of High Glucose in Vascular Smooth Muscle Cells.Cells · 2021Article
- High Glucose and Advanced Glycation End Products Induce CD147-Mediated MMP Activity in Human Adipocytes.Cells · 2021Article
- Diabetes Mellitus Promotes Smooth Muscle Cell Proliferation in Mouse Ureteral Tissue through the P-ERK/P-JNK/VEGF/PKC Signaling Pathway.Medicina (Kaunas, Lithuania) · 2021Article
- Yixintongmai Inhibits Proliferation and Migration and Promotes Apoptosis of Vascular Smooth Muscle Cells Cultured with High Glucose.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Role of SGK1 in the Osteogenic Transdifferentiation and Calcification of Vascular Smooth Muscle Cells Promoted by Hyperglycemic Conditions.International journal of molecular sciences · 2020Article
- Inhibition of Notch Signaling Alleviated Diabetic Macrovasculopathy in an In Vitro Model.Acta Cardiologica Sinica · 2020Article
- MiR145-5p inhibits proliferation of PMVECs via PAI-1 in experimental hepatopulmonary syndrome rat pulmonary microvascular hyperplasia.Biology open · 2019Article
- Chicoric acid prevents PDGF-BB-induced VSMC dedifferentiation, proliferation and migration by suppressing ROS/NFκB/mTOR/P70S6K signaling cascade.Redox biology · 2018Article
- Gene expression profiles and signaling mechanisms in αBMC systems biology · 2017Article
- NF-κβ: A Potential Target in the Management of Vascular Complications of Diabetes.Frontiers in pharmacology · 2017Review
- Role of βInternational journal of clinical and experimental pathology · 2017Article
- Article
- Inhibition of TLR4 attenuates vascular dysfunction and oxidative stress in diabetic rats.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Subcellular proteomic approach for identifying the signaling effectors of protein kinase C-β₂ under high glucose conditions in human umbilical vein endothelial cells.Molecular medicine reports · 2015Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent epidemiologic studies clearly showed that early intensive glucose control has a legacy effect for preventing diabetic macrovascular complications. However, the cellular and molecular processes by which high glucose leads to macrovascular complications are poorly understood. Vascular smooth muscle cell (VSMC) dysfunction due to high glucose is a characteristic of diabetic vascular complications. Activation of nuclear factor-κB (NF-κB) may play a key role in the regulation of inflammation and proliferation of VSMCs. We examined whether VSMC proliferation and plasminogen activator inhibitor-1 (PAI-1) expression induced by high glucose were mediated by NF-κB activation. Also, we determined whether selective inhibition of NF-κB would inhibit proliferation and PAI-1 expression in VSMCs. VSMCs of the aorta of male SD rats were treated with various concentrations of glucose (5.6, 11.1, 16.7, and 22.2 mM) with or without an inhibitor of NF-κB or expression of a recombinant adenovirus vector encoding an IκB-α mutant (Ad-IκBαM). VSMC proliferation was examined using an MTT assay. PAI-1 expression was assayed by real-time PCR and PAI-1 protein in the media was measured by ELISA. NF-κB activation was determined by immunohistochemical staining, NF-κB reporter assay, and immunoblotting. We found that glucose stimulated VSMC proliferation and PAI-1 expression in a dose-dependent manner up to 22.2 mM. High glucose (22.2 mM) alone induced an increase in NF-κB activity. Treatment with inhibitors of NF-κB such as MG132, PDTC or expression of Ad-IκB-αM in VSMCs prevented VSMC proliferation and PAI-1 expression induced by high glucose. In conclusion, inhibition of NF-κB activity prevented high glucose-induced VSMC proliferation and PAI-1 expression.
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