STAT3 Contributes to Intracranial Aneurysm Formation and Rupture by Modulating Inflammatory Response
© 2020. Springer Science+Business Media, LLC, part of Springer Nature..
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:41 |
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| Enthalten in: |
Cellular and molecular neurobiology - 41(2021), 8 vom: 17. Nov., Seite 1715-1725 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Jiang, Zhixian [VerfasserIn] |
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| Links: |
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| Themen: |
Inflammatory response |
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| Anmerkungen: |
Date Completed 01.02.2022 Date Revised 01.02.2022 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1007/s10571-020-00941-z |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM313789037 |
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| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Inflammatory response | |
| 650 | 4 | |a Intracranial aneurysms | |
| 650 | 4 | |a STAT3 | |
| 650 | 4 | |a Vascular smooth muscle cell | |
| 650 | 7 | |a STAT3 Transcription Factor |2 NLM | |
| 650 | 7 | |a STAT3 protein, human |2 NLM | |
| 700 | 1 | |a Huang, Jiaxin |e verfasserin |4 aut | |
| 700 | 1 | |a You, Lingtong |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Jinning |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Bingyu |e verfasserin |4 aut | |
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