A Novel Role for Lymphotactin (XCL1) Signaling in the Nervous System: XCL1 Acts via its Receptor XCR1 to Increase Trigeminal Neuronal Excitability

Bird, Emma V.; Iannitti, Tommaso; Christmas, Claire R.; Obara, Ilona; Andreev, Veselin I.; King, Anne E.; Boissonade, Fiona M.

doi:10.1016/j.neuroscience.2018.03.030

Cited by 13 publications

(29 citation statements)

References 65 publications

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“…The findings can be explained by the fact that chemokines are able to promote migration and fusion of the monocyte lineage in vitro through increasing the of integrin α9β1( 2 ). Another possibility to explain the promoted osteoclastogenesis in our study might be that activation of XCL1-XCR1 axis initiates PI3K/AKT, MEK, and JNK signaling pathways in a variety of cells ( 25 , 26 ). These signaling pathways are involved in regulation of osteoclasts differentiation and bone resorption activity.…”

Section: Discussionmentioning

confidence: 89%

Blockade of XCL1/Lymphotactin Ameliorates Severity of Periprosthetic Osteolysis Triggered by Polyethylene-Particles

et al. 2020

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Tian et al. XCL1/Lymphotactin in Periprosthetic Osteolysis inflammatory and osteoclastogenic factors, including IL-6, IL-8, and RANKL in human differentiated osteoblasts. Together, these results suggested the potential role of XCL1 in the pathogenesis of periprosthetic osteolysis and aseptic loosening. Our data broaden knowledge of the pathogenesis of aseptic prosthesis loosening and highlight a novel molecular target for therapeutic intervention.

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Section: Discussionmentioning

confidence: 89%

Blockade of XCL1/Lymphotactin Ameliorates Severity of Periprosthetic Osteolysis Triggered by Polyethylene-Particles

et al. 2020

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“…Based on their analysis, XCL1-XCR1 axis is involved in the peripheral and central trigeminal pain pathway. In other words, induction of c-FOS, extracellular signal-regulated kinase, and PP38 expression and also hyper-excitability within the trigeminal subnucleus caudalis nociceptive circuitry compose the possible proposed mechanism (Bird et al, 2018).…”

Section: )mentioning

confidence: 99%

Introducing Critical Pain Related Genes: A System Biology Approach

Tavirani

Zadeh-Esmaeel

et al. 2018

Basic Clin. Neurosci. J.

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Pain is valuable in diagnosis and also warning of the patients. Many molecular reagents are introduced which are related to pain. In this research, the pain-related genes are screened to identify the critical ones. Methods: First, the pain-related genes were pulling out from the STRING database, and Cytoscape software was used to make the interactome unit. Then the central genes and their neighbors were analyzed. Finally, the genes were clustered, and the essential genes were introduced. Results: After analyzing 159 genes of the network, FOS, IL6, TNF, TAC1, IL8, and KNG1 were identified as the essential genes. Further analysis revealed that 88 genes are directly connected to the central genes. More resolution led to ignoring TNF and IL8 and considering SCN-alpha and PAICS as additional critical nodes. Conclusion: Six critical genes related to pain were identified. They can be potentially considered as new drug targets. Further investigation is required to introduce the central genes as a pain killer.

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“…Similar results were obtained in rodent models of TBI, and recent experimental studies have shown significant changes in some chemokines, e.g., CCL2, CCL3, CCL4, CCL9, CCL11, CX3CL1, and CXCL5 [ 1 , 7 , 8 ], however, there is still a lack of knowledge about X-C motif chemokine ligand 1 (XCL1, also known as lymphotactin and SCM-1alpha). XCL1 acts through X-C motif chemokine receptor 1 (XCR1), which is a G-protein coupled receptor [ 9 ] that has been detected in neurons [ 10 , 11 ]. It was shown that after mental nerve damage the XCR1 is upregulated at the site of the injury—the authors proposed XCL1 as an excitability factor in orofacial pain [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

“…XCL1 acts through X-C motif chemokine receptor 1 (XCR1), which is a G-protein coupled receptor [ 9 ] that has been detected in neurons [ 10 , 11 ]. It was shown that after mental nerve damage the XCR1 is upregulated at the site of the injury—the authors proposed XCL1 as an excitability factor in orofacial pain [ 11 ]. Importantly, XCL1 is produced not only by immune cells [ 12 ], but also by neurons [ 10 , 11 , 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

“…It was shown that after mental nerve damage the XCR1 is upregulated at the site of the injury—the authors proposed XCL1 as an excitability factor in orofacial pain [ 11 ]. Importantly, XCL1 is produced not only by immune cells [ 12 ], but also by neurons [ 10 , 11 , 13 , 14 ]. Therefore, the role of XCL1 in TBI is particularly interesting.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2020

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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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A Novel Role for Lymphotactin (XCL1) Signaling in the Nervous System: XCL1 Acts via its Receptor XCR1 to Increase Trigeminal Neuronal Excitability

Cited by 13 publications

References 65 publications

Blockade of XCL1/Lymphotactin Ameliorates Severity of Periprosthetic Osteolysis Triggered by Polyethylene-Particles

Blockade of XCL1/Lymphotactin Ameliorates Severity of Periprosthetic Osteolysis Triggered by Polyethylene-Particles

Introducing Critical Pain Related Genes: A System Biology Approach

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

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