Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury
Traumatic brain injury (TBI) is one of the major health problems worldwide that causes death or permanent disability through primary and secondary damages in the brain. TBI causes primary brain damage and activates glial cells and immune and inflammatory cells, including mast cells in the brain asso...
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2020/4243953 |
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| author | Duraisamy Kempuraj Mohammad Ejaz Ahmed Govindhasamy Pushpavathi Selvakumar Ramasamy Thangavel Sudhanshu P. Raikwar Smita A. Zaheer Shankar S. Iyer Casey Burton Donald James Asgar Zaheer |
| author_facet | Duraisamy Kempuraj Mohammad Ejaz Ahmed Govindhasamy Pushpavathi Selvakumar Ramasamy Thangavel Sudhanshu P. Raikwar Smita A. Zaheer Shankar S. Iyer Casey Burton Donald James Asgar Zaheer |
| author_sort | Duraisamy Kempuraj |
| collection | DOAJ |
| description | Traumatic brain injury (TBI) is one of the major health problems worldwide that causes death or permanent disability through primary and secondary damages in the brain. TBI causes primary brain damage and activates glial cells and immune and inflammatory cells, including mast cells in the brain associated with neuroinflammatory responses that cause secondary brain damage. Though the survival rate and the neurological deficiencies have shown significant improvement in many TBI patients with newer therapeutic options, the underlying pathophysiology of TBI-mediated neuroinflammation, neurodegeneration, and cognitive dysfunctions is understudied. In this study, we analyzed mast cells and neuroinflammation in weight drop-induced TBI. We analyzed mast cell activation by toluidine blue staining, serum chemokine C-C motif ligand 2 (CCL2) level by enzyme-linked immunosorbent assay (ELISA), and proteinase-activated receptor-2 (PAR-2), a mast cell and inflammation-associated protein, vascular endothelial growth factor receptor 2 (VEGFR2), and blood-brain barrier tight junction-associated claudin 5 and Zonula occludens-1 (ZO-1) protein expression in the brains of TBI mice. Mast cell activation and its numbers increased in the brains of 24 h and 72 h TBI when compared with sham control brains without TBI. Mouse brains after TBI show increased CCL2, PAR-2, and VEGFR2 expression and derangement of claudin 5 and ZO-1 expression as compared with sham control brains. TBI can cause mast cell activation, neuroinflammation, and derangement of tight junction proteins associated with increased BBB permeability. We suggest that inhibition of mast cell activation can suppress neuroimmune responses and glial cell activation-associated neuroinflammation and neurodegeneration in TBI. |
| format | Article |
| id | doaj-art-4cb671a6f59742f0b29426dde0a9bec7 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-4cb671a6f59742f0b29426dde0a9bec72025-02-03T01:05:21ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/42439534243953Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain InjuryDuraisamy Kempuraj0Mohammad Ejaz Ahmed1Govindhasamy Pushpavathi Selvakumar2Ramasamy Thangavel3Sudhanshu P. Raikwar4Smita A. Zaheer5Shankar S. Iyer6Casey Burton7Donald James8Asgar Zaheer9Department of Neurology, School of Medicine, University of Missouri, Columbia, MO, USADepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USADepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USADepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USADepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USADepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USADepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USAPhelps Health, Rolla, MO, USAPhelps Health, Rolla, MO, USADepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USATraumatic brain injury (TBI) is one of the major health problems worldwide that causes death or permanent disability through primary and secondary damages in the brain. TBI causes primary brain damage and activates glial cells and immune and inflammatory cells, including mast cells in the brain associated with neuroinflammatory responses that cause secondary brain damage. Though the survival rate and the neurological deficiencies have shown significant improvement in many TBI patients with newer therapeutic options, the underlying pathophysiology of TBI-mediated neuroinflammation, neurodegeneration, and cognitive dysfunctions is understudied. In this study, we analyzed mast cells and neuroinflammation in weight drop-induced TBI. We analyzed mast cell activation by toluidine blue staining, serum chemokine C-C motif ligand 2 (CCL2) level by enzyme-linked immunosorbent assay (ELISA), and proteinase-activated receptor-2 (PAR-2), a mast cell and inflammation-associated protein, vascular endothelial growth factor receptor 2 (VEGFR2), and blood-brain barrier tight junction-associated claudin 5 and Zonula occludens-1 (ZO-1) protein expression in the brains of TBI mice. Mast cell activation and its numbers increased in the brains of 24 h and 72 h TBI when compared with sham control brains without TBI. Mouse brains after TBI show increased CCL2, PAR-2, and VEGFR2 expression and derangement of claudin 5 and ZO-1 expression as compared with sham control brains. TBI can cause mast cell activation, neuroinflammation, and derangement of tight junction proteins associated with increased BBB permeability. We suggest that inhibition of mast cell activation can suppress neuroimmune responses and glial cell activation-associated neuroinflammation and neurodegeneration in TBI.http://dx.doi.org/10.1155/2020/4243953 |
| spellingShingle | Duraisamy Kempuraj Mohammad Ejaz Ahmed Govindhasamy Pushpavathi Selvakumar Ramasamy Thangavel Sudhanshu P. Raikwar Smita A. Zaheer Shankar S. Iyer Casey Burton Donald James Asgar Zaheer Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury Mediators of Inflammation |
| title | Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury |
| title_full | Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury |
| title_fullStr | Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury |
| title_full_unstemmed | Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury |
| title_short | Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury |
| title_sort | mast cell activation neuroinflammation and tight junction protein derangement in acute traumatic brain injury |
| url | http://dx.doi.org/10.1155/2020/4243953 |
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