Attractive guidance: How the chemokine SDF1/CXCL12 guides different cells to different locations

Lewellis, Stephen W.; Knaut, Holger

doi:10.1016/j.semcdb.2012.03.009

Cited by 53 publications

(47 citation statements)

References 86 publications

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“…4C). SDF1a is a migration signal for many cell types during both development and adulthood (42); neural progenitor cells have been shown to express the SDF1a receptor, CXCR4, as well as to exhibit migration in vitro and in vivo in response to SDF1a (43, 44). Accordingly, SDF1a was employed as a positive migration control.…”

Section: Collected From Pmn But Not Mf Promotes Hnsc Migrationmentioning

confidence: 99%

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

Hooshmand

Nguyen

Piltti

et al. 2017

The Journal of Immunology

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Inflammatory processes play a key role in pathophysiology of many neurologic diseases/trauma, but the effect of immune cells and factors on neurotransplantation strategies remains unclear. We hypothesized that cellular and humoral components of innate immunity alter fate and migration of human neural stem cells (hNSC). In these experiments, conditioned media collected from polymorphonuclear leukocytes (PMN) selectively increased hNSC astrogliogenesis and promoted cell migration in vitro. PMN were shown to generate C1q and C3a; exposure of hNSC to PMN-synthesized concentrations of these complement proteins promoted astrogliogenesis and cell migration. Furthermore, in vitro, Abs directed against C1q and C3a reversed the fate and migration effects observed. In a proof-of-concept in vivo experiment, blockade of C1q and C3a transiently altered hNSC migration and reversed astroglial fate after spinal cord injury. Collectively, these data suggest that modulation of the innate/humoral inflammatory microenvironment may impact the potential of cell-based therapies for recovery and repair following CNS pathology.

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Section: Collected From Pmn But Not Mf Promotes Hnsc Migrationmentioning

confidence: 99%

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

Hooshmand

Nguyen

Piltti

et al. 2017

The Journal of Immunology

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“…The chemokine CXCL12 regulates cell migration and homing processes in the immune system, hematopoietic system, brain, and other tissues (Stumm and Hollt, 2007;Miller et al, 2008;Tiveron and Cremer, 2008;Lewellis and Knaut, 2012). It mediates its effects through canonical G protein-coupled CXCR4 and through CXCR7 (Bleul et al, 1996;Oberlin et al, 1996;Balabanian et al, 2005;Burns et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

CXCR7 prevents excessive CXCL12-mediated downregulation of CXCR4 in migrating cortical interneurons

et al. 2014

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The CXCL12/CXCR4 signaling pathway is involved in the development of numerous neuronal and non-neuronal structures. Recent work established that the atypical second CXCL12 receptor, CXCR7, is essential for the proper migration of interneuron precursors in the developing cerebral cortex. Two CXCR7-mediated functions were proposed in this process: direct modulation of β-arrestin-mediated signaling cascades and CXCL12 scavenging to regulate local chemokine availability and ensure responsiveness of the CXCL12/ CXCR4 pathway in interneurons. Neither of these functions has been proven in the embryonic brain. Here, we demonstrate that migrating interneurons efficiently sequester CXCL12 through CXCR7. CXCR7 ablation causes excessive phosphorylation and downregulation of CXCR4 throughout the cortex in mice expressing CXCL12, but not in CXCL12-deficient animals. Cxcl12 −/− mice lack activated CXCR4 in embryonic brain lysates and display a similar interneuron positioning defect as Cxcr4−/− and Cxcl12 −/−;Cxcr7 −/− animals. Thus, CXCL12 is the only CXCR4-activating ligand in the embryonic brain and deletion of one of the CXCL12 receptors is sufficient to generate a migration phenotype that corresponds to the CXCL12-deficient pathway. Our findings imply that interfering with the CXCL12-scavenging activity of CXCR7 causes loss of CXCR4 function as a consequence of excessive CXCL12-mediated CXCR4 activation and degradation.

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“…These include hematopoietic stem/ progenitor cell (HSC/HPC) trafficking, immune surveillance, blood vessel, cardiac and central nervous system formation during development, revascularization at sites of tissue injury, and the initiation and metastatic spread of tumors [1][2][3][4][5][6][7][8][9]. CXCL12 plasma levels are rapidly elevated in response to tissue damage, with increased CXCL12 concentrations correlating with the severity of injury, increased vascular endothelial growth factor (VEGF) plasma levels, and the associated rapid mobilization of proangiogenic cells into the circulation [10,11].…”

Section: Introductionmentioning

confidence: 99%

The Hematopoietic Chemokine CXCL12 Promotes Integration of Human Endothelial Colony Forming Cell–Derived Cells into Immature Vessel Networks

Newey

Tsaknakis

Khoo

et al. 2014

Stem Cells and Development

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Attractive guidance: How the chemokine SDF1/CXCL12 guides different cells to different locations

Cited by 53 publications

References 86 publications

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

CXCR7 prevents excessive CXCL12-mediated downregulation of CXCR4 in migrating cortical interneurons

The Hematopoietic Chemokine CXCL12 Promotes Integration of Human Endothelial Colony Forming Cell–Derived Cells into Immature Vessel Networks

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