ArticleStroke2016
Recombinant Osteopontin Stabilizes Smooth Muscle Cell Phenotype via Integrin Receptor/Integrin-Linked Kinase/Rac-1 Pathway After Subarachnoid Hemorrhage in Rats.
Article in Stroke, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
- Review
- Vagus nerve stimulation inhibits pyroptosis and improves outcome of cerebral ischemic stroke by upregulating osteopontin (SPP1) to disturb ASC oligomerization.BMC medicine · 2025Article
- Increased Plasma Levels of Thrombin-Cleaved Osteopontin in Patients with Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2025Article
- The vasoprotective role of IGF-1 signaling in the cerebral microcirculation: prevention of cerebral microhemorrhages in aging.GeroScience · 2025Review
- Neural repair function of osteopontin in stroke and stroke‑related diseases (Review).Experimental and therapeutic medicine · 2024Review
- The Modulation of Septic Shock: A Proteomic Approach.International journal of molecular sciences · 2024Article
- IGF1R deficiency in vascular smooth muscle cells impairs myogenic autoregulation and cognition in mice.Frontiers in aging neuroscience · 2024Article
- Pathogenic mechanisms and therapeutic implications of extracellular matrix remodelling in cerebral vasospasm.Fluids and barriers of the CNS · 2023Review
- Thymosin β4 preserves vascular smooth muscle phenotype in atherosclerosis via regulation of low density lipoprotein related protein 1 (LRP1).International immunopharmacology · 2023Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Peroxisome proliferator‑activated receptor β/δ regulates cerebral vasospasm after subarachnoid hemorrhage via modulating vascular smooth muscle cells phenotypic conversion.Molecular medicine reports · 2021Article
- Higher Plasma Osteopontin Concentrations Associated with Subsequent Development of Chronic Shunt-Dependent Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage.Translational stroke research · 2021Article
- TheNeural regeneration research · 2021Review
- Thymosin β4 protects against aortic aneurysm via endocytic regulation of growth factor signaling.The Journal of clinical investigation · 2021Article
- Cerebrovascular pathophysiology of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.Histology and histopathology · 2021Review
- Exendin-4 Preserves Blood-Brain Barrier IntegrityFrontiers in molecular neuroscience · 2021Article
- Osteopontin as a candidate of therapeutic application for the acute brain injury.Journal of cellular and molecular medicine · 2020Review
- Acute intranasal osteopontin treatment in male rats following TBI increases the number of activated microglia but does not alter lesion characteristics.Journal of neuroscience research · 2020Article
- Osteopontin attenuates early brain injury through regulating autophagy-apoptosis interaction after subarachnoid hemorrhage in rats.CNS neuroscience & therapeutics · 2019Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
background and purposeRecombinant osteopontin (rOPN) has been reported to be neuroprotective in stroke animal models. The purpose of this study is to investigate a potential role and mechanism of nasal administration of rOPN on preserving the vascular smooth muscle phenotype in early brain injury after subarachnoid hemorrhage (SAH).
methodsOne hundred and ninety-two male adult Sprague-Dawley rats were used. The SAH model was induced by endovascular perforation. Integrin-linked kinase small interfering RNA was intracerebroventricularly injected 48 hours before SAH. The integrin receptor antagonist fibronectin-derived peptide Gly-Arg-Gly-Asp-Ser-Pro (GRGDSP), focal adhesion kinase inhibitor Fib-14, and Rac-1 inhibitor NSC23766 were administered 1 hour before SAH induction. rOPN was administered via the intracerebroventricular and nasal route after SAH. SAH grade, neurological scores, brain water content, brain swelling, hematoxylin and eosin staining, India ink angiography, Western blots, and immunofluorescence were used to study the mechanisms of rOPN on the vascular smooth muscle phenotypic transformation.
resultsThe marker proteins of vascular smooth muscle phenotypic transformation α-smooth muscle actin decreased and embryonic smooth muscle myosin heavy chain (SMemb) increased significantly at 24 and 72 hours in the cerebral arteries after SAH. rOPN prevented the changes of α-smooth muscle actin and SMemb and significantly alleviated neurobehavioral dysfunction, increased the cross-sectional area and the lumen diameter of the cerebral arteries, reduced the brain water content and brain swelling, and improved the wall thickness of cerebral arteries. These effects of rOPN were abolished by GRGDSP, integrin-linked kinase small interfering RNA, and NSC23766. Intranasal application of rOPN at 3 hours after SAH also reduced neurological deficits.
conclusionsrOPN prevented the vascular smooth muscle phenotypic transformation and improved the neurological outcome, which was possibly mediated by the integrin receptor/integrin-linked kinase/Rac-1 pathway.
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