ArticleCellular and molecular neurobiology2021
STAT3 Contributes to Intracranial Aneurysm Formation and Rupture by Modulating Inflammatory Response.
Article in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- Effects of KLF11 on Vascular Smooth Muscle Cells and its Underlying Mechanisms in Intracranial Aneurysm.Biochemical genetics · 2024Article
- Factors associated with early-onset intracranial aneurysms in patients with autosomal dominant polycystic kidney disease.Journal of nephrology · 2024Article
- Mutation Type and Intracranial Aneurysm Formation in Autosomal Dominant Polycystic Kidney Disease.Stroke (Hoboken, N.J.) · 2022Article
- High-Dimensional Immune Profiling by Mass Cytometry Revealed the Circulating Immune Cell Landscape in Patients With Intracranial Aneurysm.Frontiers in immunology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Intracranial aneurysm (IA) is a common type of refractory cerebrovascular diseases. Inflammatory responses have been reported to be associated with the pathogenesis of IA. We aimed to study the role of STAT3 on IA formation and inflammatory response. STAT3 expression and clinicopathological factors were analyzed in IA and normal cerebral arteries. mRNA level of STAT3 was detected in normal, unruptured, and ruptured IA tissues by RT-PCR and Western blot. Inflammatory cytokines were examined by ELISA in unruptured, ruptured IA tissues, as well as cells with STAT3 overexpression or knockdown. mRNA of phenotypic modulation-related factors was tested by RT-PCR in STAT3 overexpressing or knockdown VSMCs. STAT3 expression was upregulated in ruptured IA tissues and highly associated with IA diameter and IA type. Inflammatory cytokine secretion was increased in ruptured IA samples and positively correlated with STAT3 expression. STAT3 overexpression led to enhanced expression of SM-α actin, SM-MHC, MMP2, and MMP9, and increased secretion of inflammatory cytokines. Our findings have demonstrated that STAT3 is a key regulator in IA formation by modulating inflammatory cytokine expression.
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Registered trials
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