Traumatic brain injury in mice induces changes in the expression of the XCL1/XCR1 and XCL1/ITGA9 axes
| Autor: | Maria Grazia De Simoni, Katarzyna Popiolek-Barczyk, Marco Oggioni, Joanna Mika, Domenico Mercurio, Katarzyna Pawlik, Agata Ciechanowska, Katarzyna Ciapała |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
XCR1 Chemokine Traumatic brain injury Biology Article Chemokine receptor Astroglia Mice Downregulation and upregulation TBI Brain Injuries Traumatic medicine Animals Receptor Pharmacology XCL1 Microglia General Medicine medicine.disease Chemokines C Mice Inbred C57BL ITGA9 Disease Models Animal medicine.anatomical_structure Astrocytes biology.protein Disease Progression Receptors Chemokine Neuroscience Integrin alpha Chains |
| Zdroj: | Pharmacological Reports |
| ISSN: | 2299-5684 1734-1140 |
| Popis: | Background Every year, millions of people suffer from various forms of traumatic brain injury (TBI), and new approaches with therapeutic potential are required. Although chemokines are known to be involved in brain injury, the importance of X-C motif chemokine ligand 1 (XCL1) and its receptors, X-C motif chemokine receptor 1 (XCR1) and alpha-9 integrin (ITGA9), in the progression of TBI remain unknown. Methods Using RT-qPCR/Western blot/ELISA techniques, changes in the mRNA/protein levels of XCL1 and its two receptors, in brain areas at different time points were measured in a mouse model of TBI. Moreover, their cellular origin and possible changes in expression were evaluated in primary glial cell cultures. Results Studies revealed the spatiotemporal upregulation of the mRNA expression of XCL1, XCR1 and ITGA9 in all the examined brain areas (cortex, thalamus, and hippocampus) and at most of the evaluated stages after brain injury (24 h; 4, 7 days; 2, 5 weeks), except for ITGA9 in the thalamus. Moreover, changes in XCL1 protein levels occurred in all the studied brain structures; the strongest upregulation was observed 24 h after trauma. Our in vitro experiments proved that primary murine microglial and astroglial cells expressed XCR1 and ITGA9, however they seemed not to be a main source of XCL1. Conclusions These findings indicate that the XCL1/XCR1 and XCL1/ITGA9 axes may participate in the development of TBI. The XCL1 can be considered as one of the triggers of secondary injury, therefore XCR1 and ITGA9 may be important targets for pharmacological intervention after traumatic brain injury. Graphic abstract |
| Databáze: | OpenAIRE |
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