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Traumatic brain injury in mice induces changes in the expression of the XCL1/XCR1 and XCL1/ITGA9 axes

Authors
  • Ciechanowska, Agata1
  • Popiolek-Barczyk, Katarzyna1
  • Ciapała, Katarzyna1
  • Pawlik, Katarzyna1
  • Oggioni, Marco2
  • Mercurio, Domenico2
  • de Simoni, Maria-Grazia2
  • Mika, Joanna1
  • 1 Polish Academy of Sciences,
  • 2 Istituto di Ricerche Farmacologiche Mario Negri IRCCS,
Type
Published Article
Journal
Pharmacological Reports
Publisher
Springer International Publishing
Publication Date
Nov 13, 2020
Volume
72
Issue
6
Pages
1579–1592
Identifiers
DOI: 10.1007/s43440-020-00187-y
PMID: 33185818
PMCID: PMC7704520
Source
PubMed Central
Keywords
Disciplines
  • Article
License
Unknown

Abstract

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

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