miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation
Abstract As a global public health issue, intracerebral hemorrhage (ICH) is characterized by high morbidity and mortality. Brain injury following ICH is composed of primary and secondary injury, with the latter being more severe and resulting in increased apoptosis. Sox11 (sex-determining region Y-r...
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Nature Portfolio
2025-08-01
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| author | Tianyu Liang Yongchun Liu Renyang Liu Xianmei Shen Mingxia Xu |
| author_facet | Tianyu Liang Yongchun Liu Renyang Liu Xianmei Shen Mingxia Xu |
| author_sort | Tianyu Liang |
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| description | Abstract As a global public health issue, intracerebral hemorrhage (ICH) is characterized by high morbidity and mortality. Brain injury following ICH is composed of primary and secondary injury, with the latter being more severe and resulting in increased apoptosis. Sox11 (sex-determining region Y-related high-mobility-group 11), a vital member of the Sox gene family, is broadly discovered in the developing nervous system and may have a vital impact on neurogenesis, neuronal survival, and neurite outgrowth. The level and impacts of Sox11 in brain with ICH remain indistinct. The major objective of the current work was to explore the spatiotemporal expression of Sox11 and its roles in secondary brain injury under the ICH impairment. The ICH rat model was established by injecting autologous blood into the right basal ganglia of male Sprague–Dawley rats. It was observed that Sox11 expression was notably elevated in brain tissue after ICH. The enhancement of Sox11 expression through miR-221 reduced neuronal apoptosis and inflammation in the affected rats. Furthermore, overexpression of Sox11 mitigated ICH-induced brain edema, blood-brain barrier disruption, and cognitive impairments. In contrast, Sox11 knockdown resulted in opposing effects. These findings highlight the crucial role of Sox11 in alleviating secondary brain injury following ICH. Thus, upregulating Sox11 presents a promising therapeutic strategy to reduce secondary brain injury in clinical ICH cases. |
| format | Article |
| id | doaj-art-5d243cdbbe494d359a8174ac4e16cea1 |
| institution | Kabale University |
| issn | 2045-2322 |
| language | English |
| publishDate | 2025-08-01 |
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| spelling | doaj-art-5d243cdbbe494d359a8174ac4e16cea12025-08-20T03:45:52ZengNature PortfolioScientific Reports2045-23222025-08-0115111510.1038/s41598-025-15239-7miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammationTianyu Liang0Yongchun Liu1Renyang Liu2Xianmei Shen3Mingxia Xu4Emergency and Critical Care Center, Intensive Care Unit, Zhejiang Provincial People’s Hospital,（Affiliated People’s Hospital）Hangzhou Medical CollegeDepartment of Neurosurgery, Jiujiang People’s HospitalEmergency and Critical Care Center, Intensive Care Unit, Zhejiang Provincial People’s Hospital,（Affiliated People’s Hospital）Hangzhou Medical CollegeObstetrics and Gynecology, Haining Hospital of Traditional Chinese Medicine (Haining Cancer Hospital)Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery, Department of Nursing, Zhejiang Provincial People’s Hospital（Affiliated People’s Hospital）Hangzhou Medical CollegeAbstract As a global public health issue, intracerebral hemorrhage (ICH) is characterized by high morbidity and mortality. Brain injury following ICH is composed of primary and secondary injury, with the latter being more severe and resulting in increased apoptosis. Sox11 (sex-determining region Y-related high-mobility-group 11), a vital member of the Sox gene family, is broadly discovered in the developing nervous system and may have a vital impact on neurogenesis, neuronal survival, and neurite outgrowth. The level and impacts of Sox11 in brain with ICH remain indistinct. The major objective of the current work was to explore the spatiotemporal expression of Sox11 and its roles in secondary brain injury under the ICH impairment. The ICH rat model was established by injecting autologous blood into the right basal ganglia of male Sprague–Dawley rats. It was observed that Sox11 expression was notably elevated in brain tissue after ICH. The enhancement of Sox11 expression through miR-221 reduced neuronal apoptosis and inflammation in the affected rats. Furthermore, overexpression of Sox11 mitigated ICH-induced brain edema, blood-brain barrier disruption, and cognitive impairments. In contrast, Sox11 knockdown resulted in opposing effects. These findings highlight the crucial role of Sox11 in alleviating secondary brain injury following ICH. Thus, upregulating Sox11 presents a promising therapeutic strategy to reduce secondary brain injury in clinical ICH cases.https://doi.org/10.1038/s41598-025-15239-7Sox11MiR-221Secondary brain injuryIntracerebral hemorrhageNeuroinflammation |
| spellingShingle | Tianyu Liang Yongchun Liu Renyang Liu Xianmei Shen Mingxia Xu miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation Scientific Reports Sox11 MiR-221 Secondary brain injury Intracerebral hemorrhage Neuroinflammation |
| title | miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation |
| title_full | miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation |
| title_fullStr | miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation |
| title_full_unstemmed | miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation |
| title_short | miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation |
| title_sort | mir 221 activates sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation |
| topic | Sox11 MiR-221 Secondary brain injury Intracerebral hemorrhage Neuroinflammation |
| url | https://doi.org/10.1038/s41598-025-15239-7 |
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