ArticleMedical science monitor : international medical journal of experimental and clinical research2016
Silencing of Transient Receptor Potential Channel 4 Alleviates oxLDL-induced Angiogenesis in Human Coronary Artery Endothelial Cells by Inhibition of VEGF and NF-κB.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Endothelial Transient Receptor Potential Canonical Channel Regulates Angiogenesis and Promotes Recovery After Myocardial Infarction.Journal of the American Heart Association · 2022Article
- Endothelial Colony-Forming Cells Dysfunctions Are Associated with Arterial Hypertension in a Rat Model of Intrauterine Growth Restriction.International journal of molecular sciences · 2021Article
- Endothelial Progenitor Cells Dysfunctions and Cardiometabolic Disorders: From Mechanisms to Therapeutic Approaches.International journal of molecular sciences · 2021Review
- Transient Receptor Potential Canonical (TRPC) Channels as Modulators of Migration and Invasion.International journal of molecular sciences · 2020Review
- TRPC Channels: Dysregulation and CaCells · 2020Review
- Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular CaFrontiers in physiology · 2019Review
- 17β-Estradiol Promotes Angiogenesis of Rat Cardiac Microvascular Endothelial Cells In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- TRPM8 Activation via 3-Iodothyronamine Blunts VEGF-Induced Transactivation of TRPV1 in Human Uveal Melanoma Cells.Frontiers in pharmacology · 2018Article
- Tetramethylpyrazine and Paeoniflorin Inhibit Oxidized LDL-Induced Angiogenesis in Human Umbilical Vein Endothelial Cells via VEGF and Notch Pathways.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- TRP Channels in Angiogenesis and Other Endothelial Functions.Frontiers in physiology · 2018Review
- Metastasis-Associated Protein 1 Deficiency Results in Compromised Pulmonary Alveolar Capillary Angiogenesis in Mice.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- C1q/TNF-Related Protein-9 Ameliorates Ox-LDL-Induced Endothelial Dysfunction via PGC-1α/AMPK-Mediated Antioxidant Enzyme Induction.International journal of molecular sciences · 2017Article
- MiR-206 Suppresses the Progression of Coronary Artery Disease by Modulating Vascular Endothelial Growth Factor (VEGF) Expression.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTransient receptor potential channel 4 (TRPC4) plays central roles in endothelial cell function. The aim of this study was to investigate the silencing effects of TRPC4 on oxidized low-density lipoprotein (oxLDL)-induced angiogenesis in human coronary artery endothelial cells (HCAECs), as well as the underlying molecular mechanism involved in this process. MATERIAL/
methodsHCAECs were transfected with small interfering RNA (siRNA) targeting TRPC4 (TRPC4-siRNA) or with a negative control (NC)-siRNA. The expression of TRPC4 was confirmed by real-time polymerase chain reaction (RT-PCR) and Western blotting. After the siRNA transfection, oxLDL was added to the medium. Cell proliferation, migration, and in vitro angiogenesis were determined by bromodeoxyuridine (BrdU) enzyme-linked immunosorbent assay (ELISA), Transwell assay and scratch-wound assay, respectively, and tube formation on Matrigel. Expression of vascular endothelial growth factor (VEGF) and nuclear factor (NF)-κB p65 were assessed by Western blotting.
resultsBoth the mRNA and protein levels of TRPC4 were significantly reduced by transfection with TRPC4-siRNA compared to the control group or NC-siRNA group (P<0.05). Silencing of TRPC4 significantly decreased the cell proliferation, migration, and tube formation (all P<0.05). Furthermore, the expression levels of VEGF and NF-κB p65 were markedly lowered by silencing of TRPC4 in HCAECs.
conclusionsThese results suggest that silencing of TRPC4 alleviates angiogenesis induced by oxLDL in HCAECs through inactivation of VEGF and NF-κB. Suppression of TRPC4 might be an alternative therapeutic strategy for atherosclerotic neovascularization.
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