ArticleArteriosclerosis, thrombosis, and vascular biology2013
Adenosine monophosphate-activated protein kinase-α2 deficiency promotes vascular smooth muscle cell migration via S-phase kinase-associated protein 2 upregulation and E-cadherin downregulation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- lncRNA H19 facilitates vascular neointima formation by targeting miR-125a-3p/FLT1 axis.Acta biochimica et biophysica Sinica · 2024Article
- The Recent Research Progress of NF-κB Signaling on the Proliferation, Migration, Invasion, Immune Escape and Drug Resistance of Glioblastoma.International journal of molecular sciences · 2023Review
- Deletion ofAutophagy · 2021Article
- Tertiary butylhydroquinone alleviated liver steatosis and increased cell survival via β-arrestin-2/PI3K/AKT pathway.Iranian journal of basic medical sciences · 2021Article
- Metformin in patients with and without diabetes: a paradigm shift in cardiovascular disease management.Cardiovascular diabetology · 2019Review
- AMP-Activated Protein Kinase: An Ubiquitous Signaling Pathway With Key Roles in the Cardiovascular System.Circulation research · 2017Review
- Pioglitazone Attenuates Injury-Induced Neointima Formation in Mouse Femoral Artery Partially through the Activation of AMP-Activated Protein Kinase.Pharmacology · 2017Article
- Functional characterization of AMP-activated protein kinase signaling in tumorigenesis.Biochimica et biophysica acta · 2016Review
- AMP-Activated Protein Kinase Alpha 2 Deletion Induces VSMC Phenotypic Switching and Reduces Features of Atherosclerotic Plaque Stability.Circulation research · 2016Article
- Time and flow-dependent changes in the p27(kip1) gene network drive maladaptive vascular remodeling.Journal of vascular surgery · 2015Article
- Activation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo.Nature medicine · 2015Article
- Minireview: hey U(PS): metabolic and proteolytic homeostasis linked via AMPK and the ubiquitin proteasome system.Molecular endocrinology (Baltimore, Md.) · 2014Review
- Redox regulation of endothelial cell fate.Cellular and molecular life sciences : CMLS · 2014Article
Corrections and comments
- Correction · 2019-10-23Error in Image · Updated to Retraction ·
- Retraction · 2022-10-13Concerns/Issues about Data · Concerns/Issues about Image · Investigation by Company/Institution · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) ·
- Erratum issued
- Erratum issued
- RetractedRetraction.2022
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveAbnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are critical events in the progression of several vasculopathologies. Adenosine monophosphate-activated protein kinase (AMPK) has been shown to play a pivotal role in cellular proliferation and migration. However, the roles of AMPK in VSMC migration and its underlying molecular mechanisms remain elusive. APPROACH AND
resultsVSMC migration and the neointima formation were studied in cultured mouse VSMCs or in carotid artery ligation of wild-type C57BL/6J mice, AMPKα2, AMPKα1 homozygous-deficient (AMPKα2(-/-), AMPKα1(-/-)) mice. Deletion of AMPKα2, but not AMPKα1, led to increased phosphorylation of both IкB kinase α and its downstream target nuclear factor кB2/p100 at serine 866/870. Consequently, phosphor-p100 at S866/870 bound with E3 ubiquitin ligase β-transducin repeat-containing protein resulting in the proteolytic processing of the p100 precursor and nuclear factor кB2/p52 induction. Interestingly, acetylation of histone H3 at lysine 56 mediated by histone deacetylase-3 reduction was enhanced significantly in AMPKα2(-/-) VSMCs compared with wild-type or AMPKα1(-/-) VSMCs. Moreover, the augmented association of p52/acetylation of histone H3 at lysine 56 with the promoter of ubiquitin E3 ligase, S-phase kinase-associated protein 2, was shown in AMPKα2(-/-) VSMCs by chromatin immunoprecipitation assay. Furthermore, AMPKα2 deletion caused S-phase kinase-associated protein 2-mediated E-cadherin downregulation. S-Phase kinase-associated protein 2 siRNA abolished the increased migration of AMPKα2(-/-) VSMCs via E-cadherin upregulation. Finally, neointima formation after ligation of carotid artery was increased in AMPKα2(-/-), but not AMPKα1(-/-), mice.
conclusionsWe conclude that deletion of AMPKα2 causes aberrant VSMC migration with accelerated neointima formation in vivo.
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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.