Expression of stromal cell-derived factor-1 and CXCR4 chemokine receptor mRNAs in cultured rat glial and neuronal cells

Ohtani, Yoshikazu; Minami, Masabumi; Kawaguchi, Nami; Nishiyori, Atsushi; Yamamoto, Junki; Takami, Shinya; Satoh, Masamichi

doi:10.1016/s0168-0102(98)82046-4

Cited by 35 publications

(44 citation statements)

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“…Besides neurons, expression of CXCR4 is detected on the microglia and astrocytes in the mature CNS (Tanabe S et al, 1997;Ohtani Y et al, 1998). CXCL12 induces the migration of mouse microglial cells but not astrocytes (Tanabe S et al, 1997).…”

Section: Intercellular Communicationmentioning

confidence: 99%

Multiple roles of chemokine CXCL12 in the central nervous system: A migration from immunology to neurobiology

Ransohoff

2008

Progress in Neurobiology

302

245

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Chemotactic cytokines (chemokines) have been traditionally defined as small (10-14 kDa) secreted leukocyte chemoattractants. However, chemokines and their cognate receptors are constitutively expressed in the central nervous system (CNS) where immune activities are under stringent control. Why and how the CNS uses the chemokine system to carry out its complex physiological functions has intrigued neurobiologists. Here, we focus on chemokine CXCL12 and its receptor CXCR4 that have been widely characterized in peripheral tissues and delineate their main functions in the CNS. Extensive evidence supports CXCL12 as a key regulator for early development of the CNS. CXCR4 signaling is required for the migration of neuronal precursors, axon guidance/pathfinding and maintenance of neural progenitor cells (NPCs). In the mature CNS, CXCL12 modulates neurotransmission, neurotoxicity and neuroglial interactions. Thus, chemokines represent an inherent system that helps establish and maintain CNS homeostasis. In addition, growing evidence implicates altered expression of CXCL12 and CXCR4 in the pathogenesis of CNS disorders such as HIVassociated encephalopathy, brain tumor, stroke and multiple sclerosis (MS), making them the plausible targets for future pharmacological intervention.

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Section: Intercellular Communicationmentioning

confidence: 99%

Multiple roles of chemokine CXCL12 in the central nervous system: A migration from immunology to neurobiology

Ransohoff

2008

Progress in Neurobiology

302

245

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“…Following inflammation, cytokines are released in the blood and they can reach the brain, the blood-brain barrier permeability being increased. Cytokine stimulation could lead to higher levels of SDF-1a by activation of glial or endothelial cells that release chemokines (Meucci et al 1998, Ohtani et al 1998, Lee et al 2002. The released SDF1a could reach MCH neurons, bind CXCR4, and induce a change in the excitability of the neurons that could induce an adaptive answer to the inflammation and anorexia.…”

Section: Physiopathological Considerationsmentioning

confidence: 99%

Multiple actions of the chemokine stromal cell-derived factor-1α on neuronal activity

Guyon¹,

Nahon²

2007

Journal of Molecular Endocrinology

116

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The chemokine SDF-1a and its cognate receptor CXCR4 are expressed in several neuronal populations. This review focuses on our current knowledge about the actions of this chemokine on neuronal excitability, through CXCR4 or other yet unknown pathways. In various neuronal populations (CA1 neurons of the hippocampus, granular and Purkinje cells of the cerebellum, melanin-concentrating hormone neurons of the lateral hypothalamus, vasopressinergic neurons of the supraoptic and the paraventricular nucleus of the hypothalamus, and dopaminergic neurons of the substantia nigra), SDF-1a can modulate the activity of neurons by multiple regulatory pathways including and often combining: (i) modulation of voltage-dependent channels (sodium, potassium, and calcium), (ii) activation of the G-protein-activated inward rectifier potassium current, and (iii) increase in neurotransmitter release (gamma-amino butyric acid (GABA), glutamate, and dopamine), often through Ca-dependent mechanisms. The possible mechanisms underlying these effects and their consequences in terms of modulation of neuroendocrine systems and physiopathology are discussed.

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“…Thus, while astrocytes are unlikely to express CD4, the primary receptor for HIV-1 gp120 binding, other receptors probably serve this function. Possible candidates include the chemokine receptor CXCR4, which can serve as a coreceptor for HIV-1 gp120 (16,31) and is found on astrocytes (30,47,63). Such alternative HIV gp120 binding sites may prove to be pathophysiologically significant, since recent studies indicate that astrocytes can host nonproductive HIV-1 infection in vitro and in vivo (9).…”

Section: Vol 75 2001mentioning

confidence: 99%

Interferon-Independent, Human Immunodeficiency Virus Type 1 gp120-Mediated Induction of CXCL10/IP-10 Gene Expression by Astrocytes In Vivo and In Vitro

Asensio¹,

Maier²,

Milner³

et al. 2001

J Virol

122

102

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Expression of stromal cell-derived factor-1 and CXCR4 chemokine receptor mRNAs in cultured rat glial and neuronal cells

Cited by 35 publications

References 0 publications

Multiple roles of chemokine CXCL12 in the central nervous system: A migration from immunology to neurobiology

Multiple roles of chemokine CXCL12 in the central nervous system: A migration from immunology to neurobiology

Multiple actions of the chemokine stromal cell-derived factor-1α on neuronal activity

Interferon-Independent, Human Immunodeficiency Virus Type 1 gp120-Mediated Induction of CXCL10/IP-10 Gene Expression by Astrocytes In Vivo and In Vitro

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