ArticleThe Journal of biological chemistry2013
AMP-dependent kinase inhibits oxidative stress-induced caveolin-1 phosphorylation and endocytosis by suppressing the dissociation between c-Abl and Prdx1 proteins in endothelial cells.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Caveolin-1 regulates inflammatory mediators in retinal endothelial cells.Molecular vision · 2024Article
- Review
- Suppressive effects of quercetin on hydrogen peroxide-induced caveolin-1 phosphorylation in endothelial cells.Journal of clinical biochemistry and nutrition · 2021Article
- Caveolae and lipid sorting: Shaping the cellular response to stress.The Journal of cell biology · 2020Review
- Alpha-synuclein-induced mitochondrial dysfunction is mediated via a sirtuin 3-dependent pathway.Molecular neurodegeneration · 2020Article
- Acadesine suppresses TNF-α induced complement component 3 (C3), in retinal pigment epithelial (RPE) cells.PloS one · 2020Article
- Structural and Functional Remodeling of the Brain Vasculature Following Stroke.Frontiers in physiology · 2020Review
- Abl family tyrosine kinases govern IgG extravasation in the skin in a murine pemphigus model.Nature communications · 2019Article
- Peroxiredoxins in Cancer and Response to Radiation Therapies.Antioxidants (Basel, Switzerland) · 2019Review
- A review of the role of cav-1 in neuropathology and neural recovery after ischemic stroke.Journal of neuroinflammation · 2018Review
- Canagliflozin inhibits interleukin-1β-stimulated cytokine and chemokine secretion in vascular endothelial cells by AMP-activated protein kinase-dependent and -independent mechanisms.Scientific reports · 2018Article
- AICAR suppresses TNF-α-induced complement factor B in RPE cells.Scientific reports · 2017Article
- Article
- A concise review on advances in development of small molecule anti-inflammatory therapeutics emphasising AMPK: An emerging target.International journal of immunopathology and pharmacology · 2016Review
- Roles of peroxiredoxins in cancer, neurodegenerative diseases and inflammatory diseases.Pharmacology & therapeutics · 2016Review
- AMPK-Activated Protein Kinase Suppresses Ccr2 Expression by Inhibiting the NF-κB Pathway in RAW264.7 Macrophages.PloS one · 2016Article
- Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease.Free radical biology & medicine · 2015Review
- Human podocytes perform polarized, caveolae-dependent albumin endocytosis.American journal of physiology. Renal physiology · 2014Article
- Effects of selenoprotein S on oxidative injury in human endothelial cells.Journal of translational medicine · 2013Article
- Neoatherosclerosis after Drug-Eluting Stent Implantation: Roles and Mechanisms.Oxidative medicine and cellular longevityReview
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Caveolin-1 is the primary structural component of endothelial caveolae that is essential for transcellular trafficking of albumin and is also a critical scaffolding protein that regulates the activity of signaling molecules in caveolae. Phosphorylation of caveolin-1 plays a fundamental role in the mechanism of oxidant-induced vascular hyper permeability. However, the regulatory mechanism of caveolin-1 phosphorylation remains unclear. Here we identify a previously unexpected role for AMPK in inhibition of caveolin-1 phosphorylation under oxidative stress. A pharmacological activator of AMPK, 5-amino-4-imidazole carboxamide riboside (AICAR), inhibited oxidative stress-induced phosphorylation of both caveolin-1 and c-Abl, which is the major kinase of caveolin-1, and endocytosis of albumin in human umbilical vein endothelial cell. These effects were abolished by treatment with two specific inhibitors of AICAR, dipyridamole, and 5-iodotubericidin. Consistently, knockdown of the catalytic AMPKα subunit by siRNA abolished the inhibitory effect of AICAR on oxidant-induced phosphorylation of both caveolin-1 and c-Abl. Pretreatment with specific c-Abl inhibitor, imatinib mesylate, and knock down of c-Abl significantly decreased the caveolin-1 phosphorylation after H2O2 exposure and abolished the inhibitory effect of AICAR on the caveolin-1 phosphorylation. Interestingly, knockdown of Prdx-1, an antioxidant enzyme associated with c-Abl, increased phosphorylation of both caveolin-1 and c-Abl and abolished the inhibitory effect of AICAR on the caveolin-1 phosphorylation. Furthermore, co-immunoprecipitation experiment showed that AICAR suppressed the oxidant-induced dissociation between c-Abl and Prdx1. Overall, our results suggest that activation of AMPK inhibits oxidative stress-induced caveolin-1 phosphorylation and endocytosis, and this effect is mediated in part by stabilizing the interaction between c-Abl and Prdx-1.
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