ArticleProceedings of the National Academy of Sciences of the United States of America2013
AMPKα2 exerts its anti-inflammatory effects through PARP-1 and Bcl-6.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
- Leveraging PARP-1/2 to Target Distant Metastasis.International journal of molecular sciences · 2024Review
- Mechanisms of endothelial activation, hypercoagulation and thrombosis in COVID-19: a link with diabetes mellitus.Cardiovascular diabetology · 2024Review
- Deficient leptin receptor signaling in T cells of human SLE.Frontiers in immunology · 2023Article
- Metformin: Activation of 5' AMP-activated protein kinase and its emerging potential beyond anti-hyperglycemic action.Frontiers in genetics · 2022Review
- Prevention of Hypertensive Disorders of Pregnancy-Is There a Place for Metformin?Journal of clinical medicine · 2021Review
- Macrophage Polarization and Plasticity in Systemic Lupus Erythematosus.Frontiers in immunology · 2021Review
- Metformin in cardiovascular diabetology: a focused review of its impact on endothelial function.Theranostics · 2021Review
- GLP-1-Induced AMPK Activation Inhibits PARP-1 and Promotes LXR-Mediated ABCA1 Expression to Protect Pancreatic β-Cells Against Cholesterol-Induced Toxicity Through Cholesterol Efflux.Frontiers in cell and developmental biology · 2021Article
- Can Metformin Exert as an Active Drug on Endothelial Dysfunction in Diabetic Subjects?Biomedicines · 2020Review
- AMPK, Mitochondrial Function, and Cardiovascular Disease.International journal of molecular sciences · 2020Review
- Review
- Endothelial mechanobiology.APL bioengineering · 2020Article
- Anti-inflammatory Property of AMP-activated Protein Kinase.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2020Review
- c-Abl-Mediated Tyrosine Phosphorylation of PARP1 Is Crucial for Expression of Proinflammatory Genes.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Nicotinamide Augments the Anti-Inflammatory Properties of Resveratrol through PARP1 Activation.Scientific reports · 2019Article
- Shear stress regulation of miR-93 and miR-484 maturation through nucleolin.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Insulin-like growth factor-1 activates AMPK to augment mitochondrial function and correct neuronal metabolism in sensory neurons in type 1 diabetes.Molecular metabolism · 2019Article
- Macrophage Polarization: Different Gene Signatures in M1(LPS+) vs. Classically and M2(LPS-) vs. Alternatively Activated Macrophages.Frontiers in immunology · 2019Review
- PARP1 and Poly(ADP-ribosyl)ation Signaling during Autophagy in Response to Nutrient Deprivation.Oxidative medicine and cellular longevity · 2019Review
- Improved Reperfusion and Vasculoprotection by the Poly(ADP-Ribose)Polymerase Inhibitor PJ34 After Stroke and Thrombolysis in Mice.Molecular neurobiology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
B-cell lymphoma-6 protein (Bcl-6) is a corepressor for inflammatory mediators such as vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 and -3, which function to recruit monocytes to vascular endothelial cells upon inflammation. Poly [ADP ribose] polymerase 1 (PARP-1) is proinflammatory, in part through its binding at the Bcl-6 intron 1 to suppress Bcl-6 expression. We investigated the mechanisms by which PARP-1 dissociates from the Bcl-6 intron 1, ultimately leading to attenuation of endothelial inflammation. Analysis of the PARP-1 primary sequence suggested that phosphorylation of PARP-1 Serine 177 (Ser-177) by AMP-activated protein kinase (AMPK) is responsible for the induction of Bcl-6. Our results show that AMPK activation with treatment of 5-aminoimidazole-4-carboxamide ribonucleotide, metformin, or pulsatile shear stress induces PARP-1 dissociation from the Bcl-6 intron 1, increases Bcl-6 expression, and inhibits expression of inflammatory mediators. Conversely, AMPKα suppression or knockdown produces the opposite effects. The results demonstrate an anti-infamatory pathway linking AMPK, PARP-1, and Bcl-6 in endothelial cells.
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Registered trials
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.