CXCR3-Dependent Microglial Recruitment Is Essential for Dendrite Loss after Brain Lesion

Rappert, Angelika; Bechmann, Ingo; Pivneva, T. A.; Mahlo, Jacqueline; Biber, Knut; Nolte, Christiané; Kovac, Adam D.; Gérard, Craig; Boddeke, Hendrikus; Nitsch, Robert; Kettenmann, Helmut

doi:10.1523/jneurosci.2451-04.2004

Cited by 232 publications

(222 citation statements)

References 62 publications

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“…2). The involvement of CXCL12/ CXCR4 signaling in hMSCs migration is consistent with findings in hypoglossal nerve injury (24), ischemic (63), and glioma (11) (6,45). In prion diseases, impairment of microglial migration, associated with the increased accumulation of PrP Sc but prolongation of survival, has been reported in CXCR3 gene deficient mice infected with prions (47).…”

Section: Discussionsupporting

confidence: 84%

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Song

Furuoka

Horiuchi

2011

J Virol

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Bone marrow-derived mesenchymal stem cells (MSCs) have been reported to migrate to brain lesions of neurodegenerative diseases; however, the precise mechanisms by which MSCs migrate remain to be elucidated. In this study, we carried out an in vitro migration assay to investigate the chemoattractive factors for MSCs in the brains of prion-infected mice. The migration of immortalized human MSCs (hMSCs) was reduced by their pretreatment with antibodies against the chemokine receptors, CCR3, CCR5, CXCR3, and CXCR4 and by pretreatment of brain extracts of prion-infected mice with antibodies against the corresponding ligands, suggesting the involvement of these receptors, and their ligands in the migration of hMSCs. In agreement with the results of an in vitro migration assay, hMSCs in the corpus callosum, which are considered to be migrating from the transplanted area toward brain lesions of prion-infected mice, expressed CCR3, CCR5, CXCR3, and CXCR4. The combined in vitro and in vivo analyses suggest that CCR3, CCR5, CXCR3, and CXCR4, and their corresponding ligands are involved in the migration of hMSCs to the brain lesions caused by prion propagation. In addition, hMSCs that had migrated to the right hippocampus of prion-infected mice expressed CCR1, CX3CR1, and CXCR4, implying the involvement of these chemokine receptors in hMSC functions after chemotactic migration. Further elucidation of the mechanisms that underlie the migration of MSCs may provide useful information regarding application of MSCs to the treatment of prion diseases.

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Section: Discussionsupporting

confidence: 84%

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Song

Furuoka

Horiuchi

2011

J Virol

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“…Estas modificaciones también podrían relacionarse con la presencia de microglías activadas muy tempranamente en la corteza motora tras la lesión. De hecho, se sabe que es necesario el reclutamiento y la proliferación de las microglías para que se produzcan alteraciones dendríticas neuronales después de una lesión (24).…”

Section: Discussionunclassified

“…Por otra parte, se sabe que, tras lesiones del sistema nervioso central, el árbol dendítrico de las neuronas sometidas a axotomía y de las 'denervadas' se remodela y se registra un aumento en la expresión de las quimiocinas, las cuales activan las células de la microglía residentes; se ha planteado que dicha activación es necesaria para que ocurra la remodelación neuronal después de una lesión (24,25). Es por esto que las células de la microglía se consideran los sensores más sensibles de alteraciones en el sistema nervioso central.…”

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Facial nerve injuries cause changes in central nervous system microglial cells

Cerón

Troncoso

2016

biomedica

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Introducción. El grupo de investigación del Laboratorio de Neurofisiología Comportamental de la Universidad Nacional de Colombia ha descrito modificaciones estructurales y electrofisiológicas en neuronas piramidales de la corteza motora producidas por la lesión del nervio facial contralateral en ratas. Sin embargo, poco se sabe sobre la posibilidad de que dichos cambios neuronales se acompañen también de modificaciones en las células gliales circundantes.Objetivo. Caracterizar el efecto de la lesión unilateral del nervio facial sobre la activación y proliferación de las células de la microglía en la corteza motora primaria contralateral en ratas.Materiales y métodos. Se hicieron pruebas de inmunohistoquímica para detectar las células de la microglía en el tejido cerebral de ratas sometidas a lesión del nervio facial, las cuales se sacrificaron en distintos momentos después de la intervención. Se infligieron dos tipos de lesiones: reversible (por compresión, lo cual permite la recuperación de la función) e irreversible (por corte, lo cual provoca parálisis permanente). Los tejidos cerebrales de los animales sin lesión (grupo de control absoluto) y de aquellos sometidos a falsa cirugía se compararon con los de los animales lesionados sacrificados 1, 2, 7, 21 y 35 días después de la lesión.Resultados. Las células de la microglía en la corteza motora de los animales lesionados irreversiblemente mostraron signos de proliferación y activación entre el tercero y séptimo días después de la lesión. La proliferación de las células de la microglía en animales con lesión reversible fue significativa solo a los tres días de infligida la lesión.Conclusiones. La lesión del nervio facial produce modificaciones en las células de la microglía de la corteza motora primaria. Estas modificaciones podrían estar involucradas en los cambios morfológicos y electrofisiológicos descritos en las neuronas piramidales de la corteza motora que comandan los movimientos faciales.

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“…CLN were isolated 24 h (n=5) and 72 h (n=5) after MCAO. Entorhinal cortex lesion (ECL) and facial nerve axotomy (FNA) were performed as described [32] in C57BL/6 mice (n=5 and n=3, respectively; Charles River). CLN were isolated 7 days later.…”

Section: Non-inflammatory Cns Damage Modelsmentioning

confidence: 99%

Brain antigens in functionally distinct antigen-presenting cell populations in cervical lymph nodes in MS and EAE

et al. 2008

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Drainage of central nervous system (CNS) antigens to the brain-draining cervical lymph nodes (CLN) is likely crucial in the initiation and control of autoimmune responses during multiple sclerosis (MS). We demonstrate neuronal antigens within CLN of MS patients. In monkeys and mice with experimental autoimmune encephalomyelitis (EAE) and in mouse models with non-inflammatory CNS damage, the type and extent of CNS damage was associated with the frequencies of CNS antigens within the cervical lymph nodes. In addition, CNS antigens drained to the spinal-cord-draining lumbar lymph nodes. In human MS CLN, neuronal antigens were present in pro-inflammatory antigen-presenting cells (APC), whereas the majority of myelin-containing cells were anti-inflammatory. This may reflect a different origin of the cells or different drainage mechanisms. Indeed, neuronal antigen-containing cells in J Mol Med (2009) human CLN did not express the lymph node homing receptor CCR7, whereas myelin antigen-containing cells in situ and in vitro did. Nevertheless, CLN from EAE-affected CCR7-deficient mice contained equal amounts of myelin and neuronal antigens as wild-type mice. We conclude that the type and frequencies of CNS antigens within the CLN are determined by the type and extent of CNS damage. Furthermore, the presence of myelin and neuronal antigens in functionally distinct APC populations within MS CLN suggests that differential immune responses can be evoked.

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CXCR3-Dependent Microglial Recruitment Is Essential for Dendrite Loss after Brain Lesion

Cited by 232 publications

References 62 publications

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Facial nerve injuries cause changes in central nervous system microglial cells

Brain antigens in functionally distinct antigen-presenting cell populations in cervical lymph nodes in MS and EAE

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