Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBI
Traumatic brain injury (TBI) is a global public health problem. As an important cause of secondary injury, cerebrovascular reaction can cause secondary bleeding, venous sinus thrombosis, and malignant brain swelling. Recent clinical studies have confirmed that intracranial venous return disorder is...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-11-01
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| Series: | Brain Research Bulletin |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0361923023002290 |
| _version_ | 1827753373292560384 |
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| author | Cheng Wang Liang Xian Shaorui Zheng Jun Li Xiangrong Chen Shousen Wang |
| author_facet | Cheng Wang Liang Xian Shaorui Zheng Jun Li Xiangrong Chen Shousen Wang |
| author_sort | Cheng Wang |
| collection | DOAJ |
| description | Traumatic brain injury (TBI) is a global public health problem. As an important cause of secondary injury, cerebrovascular reaction can cause secondary bleeding, venous sinus thrombosis, and malignant brain swelling. Recent clinical studies have confirmed that intracranial venous return disorder is closely related to the prognosis of patients, yet the specific molecular mechanism involved in this process is still unclear. This study used an acute subdural hematoma (ASDH) model with cranial venous outflow obstruction (CVO) to explore how CVO aggravates the pathological process after TBI, especially for inflammation and tissue damage. The results suggest that intracranial venous return disorder exacerbates neurological deficits and brain edema in rats with ASDH by aggravating the destruction of endothelial cell tight junctions (TJs) proteins and promoting the expression of inflammatory factors, the activation of microglia and expression of recombinant A disintegrin and metalloprotease 17 (ADAM17) as well as the secretion of solTNF-α, a soluble form of tumor necrosis factor-alpha (TNFα), which in turn increase IκB-α ((inhibitor of the transcription factor nuclear factor-κB) and NF-κB p65. Our study revealed a molecular basis of how CVO aggravates inflammation and tissue damage. |
| first_indexed | 2024-03-11T07:35:16Z |
| format | Article |
| id | doaj.art-d2198a7b67bf4ebba49cfd3000fe5400 |
| institution | Directory Open Access Journal |
| issn | 1873-2747 |
| language | English |
| last_indexed | 2024-03-11T07:35:16Z |
| publishDate | 2023-11-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Brain Research Bulletin |
| spelling | doaj.art-d2198a7b67bf4ebba49cfd3000fe54002023-11-17T05:25:01ZengElsevierBrain Research Bulletin1873-27472023-11-01204110804Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBICheng Wang0Liang Xian1Shaorui Zheng2Jun Li3Xiangrong Chen4Shousen Wang5Department of Neurosurgery, The First Affiliated Hospital of Wannan Medical College, Wuhu, PR China; Fuzong Clinical Medical College of Fujian Medical University, Fuzhou, PR ChinaFuzong Clinical Medical College of Fujian Medical University, Fuzhou, PR ChinaFuzong Clinical Medical College of Fujian Medical University, Fuzhou, PR ChinaDepartment of Neurosurgery, 900th Hospital, Fuzhou, PR ChinaDepartment of Neurosurgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, PR China; Corresponding author.Fuzong Clinical Medical College of Fujian Medical University, Fuzhou, PR China; Department of Neurosurgery, 900th Hospital, Fuzhou, PR China; Corresponding author at: Fuzong Clinical Medical College of Fujian Medical University, Fuzhou, PR China.Traumatic brain injury (TBI) is a global public health problem. As an important cause of secondary injury, cerebrovascular reaction can cause secondary bleeding, venous sinus thrombosis, and malignant brain swelling. Recent clinical studies have confirmed that intracranial venous return disorder is closely related to the prognosis of patients, yet the specific molecular mechanism involved in this process is still unclear. This study used an acute subdural hematoma (ASDH) model with cranial venous outflow obstruction (CVO) to explore how CVO aggravates the pathological process after TBI, especially for inflammation and tissue damage. The results suggest that intracranial venous return disorder exacerbates neurological deficits and brain edema in rats with ASDH by aggravating the destruction of endothelial cell tight junctions (TJs) proteins and promoting the expression of inflammatory factors, the activation of microglia and expression of recombinant A disintegrin and metalloprotease 17 (ADAM17) as well as the secretion of solTNF-α, a soluble form of tumor necrosis factor-alpha (TNFα), which in turn increase IκB-α ((inhibitor of the transcription factor nuclear factor-κB) and NF-κB p65. Our study revealed a molecular basis of how CVO aggravates inflammation and tissue damage.http://www.sciencedirect.com/science/article/pii/S0361923023002290Cerebral venous circulationTraumatic brain injuryNeuroinflammationSolTNF-αNF-κB |
| spellingShingle | Cheng Wang Liang Xian Shaorui Zheng Jun Li Xiangrong Chen Shousen Wang Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBI Brain Research Bulletin Cerebral venous circulation Traumatic brain injury Neuroinflammation SolTNF-α NF-κB |
| title | Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBI |
| title_full | Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBI |
| title_fullStr | Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBI |
| title_full_unstemmed | Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBI |
| title_short | Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBI |
| title_sort | cranial venous outflow obstruction promotes neuroinflammation via adam17 soltnf α nf κb pathway following experimental tbi |
| topic | Cerebral venous circulation Traumatic brain injury Neuroinflammation SolTNF-α NF-κB |
| url | http://www.sciencedirect.com/science/article/pii/S0361923023002290 |
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