ArticleJournal of neuroinflammation2018
β-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke.
Article in Journal of neuroinflammation, 2018. 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, 26 citations in OpenAlex.
- Advances in stroke-associated pneumonia in the era of revascularization therapy.Chinese medical journal · 2026Review
- Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway.iScience · 2026Article
- Identifying the shared genes and their related microRNAs, metabolites, and pathways in ischemic stroke and epilepsy.Scientific reports · 2026Article
- Beyond the usual suspects: rethinking post-stroke immunosuppression.Frontiers in immunology · 2026Review
- Serum IL-6 and functional outcome after endovascular therapy: the mediating role of infarct volume growth in acute ischemic stroke.Frontiers in immunology · 2026Article
- Autonomic dysfunction and treatment strategies in intracerebral hemorrhage.CNS neuroscience & therapeutics · 2024Review
- NDUFA11 may be the disulfidptosis-related biomarker of ischemic stroke based on integrated bioinformatics, clinical samples, and experimental analyses.Frontiers in neuroscience · 2024Article
- How S100B crosses brain barriers and why it is considered a peripheral marker of brain injury.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Friends or foes: The mononuclear phagocyte system in ischemic stroke.Brain pathology (Zurich, Switzerland) · 2023Review
- Premorbid Use of Beta-Blockers or Angiotensin-Converting Enzyme Inhibitors/Angiotensin Receptor Blockers in Patients with Acute Ischemic Stroke.Oxidative medicine and cellular longevity · 2023Article
- Article
- Clenbuterol, a Selective β2-Adrenergic Receptor Agonist, Inhibits or Limits Post-Stroke Pneumonia, but Increases Infarct Volume in MCAO Mice.Journal of inflammation research · 2022Article
- Kisspeptin-54 attenuates oxidative stress and neuronal apoptosis in early brain injury after subarachnoid hemorrhage in rats via GPR54/ARRB2/AKT/GSK3β signaling pathway.Free radical biology & medicine · 2021Article
- Targeting the Angiotensin II Type 1 Receptor in Cerebrovascular Diseases: Biased Signaling Raises New Hopes.International journal of molecular sciences · 2021Review
- Stroke-induced immunosuppression: implications for the prevention and prediction of post-stroke infections.Journal of neuroinflammation · 2021Review
- Inflammatory Factors as Potential Markers of Early Neurological Deterioration in Acute Ischemic Stroke Patients Receiving Endovascular Therapy - The AISRNA Study.Journal of inflammation research · 2021Article
- β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion.Nature communications · 2020Article
- Histone deacetylase 6 interference protects mice against experimental stroke-induced brain injury via activating Nrf2/HO-1 pathway.Animal cells and systems · 2019Article
- Augmented β2-adrenergic signaling dampens the neuroinflammatory response following ischemic stroke and increases stroke size.Journal of neuroinflammation · 2019Article
- β-arrestin-2 in PAR-1-biased signaling has a crucial role in endothelial function via PDGF-β in stroke.Cell death & disease · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundStroke-induced immunodeficiency syndrome (SIDS) is regarded as a protective mechanism for secondary inflammatory injury as well as a contributor to infection complications. Although stroke-induced hyperactivation of the sympathetic system is proved to facilitate SIDS, the involved endogenous factors and pathways are largely elusive. In this study, we aim to investigate the function of beta-arrestin-2 (ARRB2) in the sympathetic-mediated SIDS.
methodsSplenic ARRB2 expression and the sympathetic system activity were detected after establishing transient models of middle cerebral artery occlusion (MCAO). In addition, a correlation between ARRB2 expression and the sympathetic system activity was analyzed using a linear correlation analysis. Any SIDS reflected in monocyte dysfunction was investigated by measuring inflammatory cytokine secretion and neurological deficit scores and infarct volume were tested to assess neurological outcome. Further, ARRB2 expression in the monocytes was knocked down in vitro by siRNAs. Following the stimulation of noradrenaline and lipopolysaccharide, cytokine secretion and the nuclear factor-κB (NF-κB) pathway were evaluated to gain insight into the mechanisms related to the contribution of ARRB2 to adrenergic-induced monocyte dysfunction.
resultsSplenic ARRB2 expression was significantly increased after stroke and also showed a significant positive correlation with the sympathetic system activity. Stroke-induced monocyte dysfunction resulted in an increase of the interleukin-10 (IL-10) level as well as a decrease of the interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels. Also, blockade of adrenergic-activity significantly reversed these cytokine levels, and blockade of adrenergic-activity improved stroke-induced neurological results. However, the improved neurological results had no significant correlation with ARRB2 expression. Furthermore, the in vitro results showed that the deficiency of ARRB2 dramatically repealed adrenergic-induced monocyte dysfunction and the inhibition of NF-κB signaling phosphorylation activity.
conclusionsARRB2 is implicated in the sympathetic-triggered SIDS, in particular, monocyte dysfunction after stroke. Accordingly, ARRB2 may be a promising therapeutic target for the immunological management of stroke in a clinic.
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