The α-chemokine CXCL14 is up-regulated in the sciatic nerve of a mouse model of Charcot–Marie–Tooth disease type 1A and alters myelin gene expression in cultured Schwann cells

Barbaria, Elena M.; Kohl, Bianca; Buhren, Bettina Alexandra; Hasenpusch‐Theil, Kerstin; Kruse, Fabian; Küry, Patrick; Martini, Rudolf; Müller, Hans

doi:10.1016/j.nbd.2008.11.014

Cited by 20 publications

(13 citation statements)

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“…In a previous report, CXCL14 exerted a significant effect on the developmental control of nigral dopaminergic neuronal growth, proliferation, and survival62. In addition, CXCL14 modulated this proliferation in cultured Schwann cells81. In this study, we discovered that recombinant CXCL14 was able to reduce the infarct volume by increasing the expression of anti-apoptotic protein and diminishing the TUNEL + cells in the ischemic brain.…”

Section: Discussionmentioning

confidence: 53%

A Crucial Role of CXCL14 for Promoting Regulatory T Cells Activation in Stroke

Lee¹,

Liu²,

Lin³

et al. 2017

Theranostics

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Inflammatory processes have a detrimental role in the pathophysiology of ischemic stroke. However, little is known about the endogenous anti-inflammatory mechanisms in ischemic brain. Here, we identify CXCL14 as a critical mediator of these mechanisms. CXCL14 levels were upregulated in the ischemic brains of humans and rodents. Moreover, hypoxia inducible factor-1α (HIF-1α) drives hypoxia- or cerebral ischemia (CI)-dependent CXCL14 expression via directly binding to the CXCL14 promoter. Depletion of CXCL14 inhibited the accumulation of immature dendritic cells (iDC) or regulatory T cells (Treg) and increased the infarct volume, whereas the supplementation of CXCL14 had the opposite effects. CXCL14 promoted the adhesion, migration, and homing of circulating CD11c+ iDC to the ischemic tissue via the upregulation of the cellular prion protein (PrPC), PECAM-1, and MMPs. The accumulation of Treg in ischemic areas of the brain was mediated through a cooperative effect of CXCL14 and iDC-secreted IL-2-induced Treg differentiation. Interestingly, CXCL14 largely promoted IL-2-induced Treg differentiation. These findings indicate that CXCL14 is a critical immunomodulator involved in the stroke-induced inflammatory reaction. Passive CXCL14 supplementation provides a tractable path for clinical translation in the improvement of stroke-induced neuroinflammation.

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Section: Discussionmentioning

confidence: 53%

A Crucial Role of CXCL14 for Promoting Regulatory T Cells Activation in Stroke

Lee¹,

Liu²,

Lin³

et al. 2017

Theranostics

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“…Indeed, none of the previously described c-Jun target genes (41) were induced in the C22 model, indicating that other transcriptional programs were enacted by PMP22 overexpression in this model. Relatively few cytokines/chemokines were induced in the C22 model, with the exception of Cxcl14 (46), and immune cell markers were not an enriched gene ontology category with this data set (Supplemental Figure 2G).…”

Section: Resultsmentioning

confidence: 93%

PMP22 antisense oligonucleotides reverse Charcot-Marie-Tooth disease type 1A features in rodent models

Zhao¹,

Damle²,

Ikeda-Lee³

et al. 2017

Journal of Clinical Investigation

124

123

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“…As reported above for CXCL8, enhanced levels of CXCL13 have been found in active demyelination areas and presumably assist systemically injected neural precursor cells across the brain endothelium and favour functional recovery in animal models of MS (Weiss et al 2010;Bagaeva et al 2006). CXCL14 is also involved in myelination, is up-regulated in the sciatic nerve of a mouse model of Charcot-Marie-Tooth disease type 1A and alters myelin gene expression in cultured Schwann cells (Barbaria et al 2009). …”

Section: Cxcl13 Cxcl14 and Cxcl16mentioning

confidence: 81%

“…Moreover, CXCL1/CXCR2 signalling might play a role in oligodendrocyte proliferation and recruitment to demyelinated areas. Whereas CXCL14 alters myelin gene expression in cultured Schwann cells (Barbaria et al 2009), its role in the CNS is still unknown.…”

Section: Tissue Repairmentioning

confidence: 99%

Chemokines in CNS injury and repair

2012

Self Cite

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Recruitment of inflammatory cells is known to drive the secondary damage cascades that are common to injuries of the central nervous system (CNS). Cell activation and infiltration to the injury site is orchestrated by changes in the expression of chemokines, the chemoattractive cytokines. Reducing the numbers of recruited inflammatory cells by the blocking of the action of chemokines has turned out be a promising approach to diminish neuroinflammation and to improve tissue preservation and neovascularization. In addition, several chemokines have been shown to be essential for stem/progenitor cell attraction, their survival, differentiation and cytokine production. Thus, chemokines might indirectly participate in remyelination, neovascularization and neuroprotection, which are important prerequisites for CNS repair after trauma. Moreover, CXCL12 promotes neurite outgrowth in the presence of growth inhibitory CNS myelin and enhances axonal sprouting after spinal cord injury (SCI). Here, we review current knowledge about the exciting functions of chemokines in CNS trauma, including SCI, traumatic brain injury and stroke. We identify common principles of chemokine action and discuss the potentials and challenges of therapeutic interventions with chemokines.

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The α-chemokine CXCL14 is up-regulated in the sciatic nerve of a mouse model of Charcot–Marie–Tooth disease type 1A and alters myelin gene expression in cultured Schwann cells

Cited by 20 publications

References 50 publications

A Crucial Role of CXCL14 for Promoting Regulatory T Cells Activation in Stroke

A Crucial Role of CXCL14 for Promoting Regulatory T Cells Activation in Stroke

PMP22 antisense oligonucleotides reverse Charcot-Marie-Tooth disease type 1A features in rodent models

Chemokines in CNS injury and repair

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