Chemokines released from astrocytes promote chemokine receptor 5-mediated neuronal cell differentiation

Park, Mi Hee; Lee, Yong Kyung; Lee, Yeon Hee; Kim, Yun-Bae; Yun, Young Won; Nam, Sang Yoon; Hwang, Se Jin; Han, Seok‐Youn; Kim, Seung Up; Hong, Jin Tae

doi:10.1016/j.yexcr.2009.06.017

Cited by 32 publications

(23 citation statements)

References 37 publications

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“…6.389 2.56 × 10 -5 Regulates neurite outgrowth/brain circuitry; implicated in schizophrenia; knockout mice exhibit abberrant neuronal connectivity [44][45][46][47][48][49][50][51][52][53][54][55] CCL5 (chemokine [C-C motif] ligand 5 [RANTES]) 1.614 3.07 × 10 -5 Chemoattractant for blood monocytes, memory T-helper cells and eosinophils; suggested plasma marker for depression and schizophrenia [59,60] FLT1 (FMS-related tyrosine kinase 1) 3.348 1.14 × 10 -4 VEGF receptor implicated in synaptic transmission [61,62] ENPP2 (ectonucleotide pyrophosphatase/ phosphodiesterase 2) 2.450 1.55 × 10 -4 Regulates myelin formation [70] GAP43 (growth-associated protein 43) 1.797 1.78 × 10 -4 Regulates neurite outgrowth and plasticity [56][57][58] DDX60 (DEAD [Asp-Glu-Ala-Asp] box polypeptide 60)…”

Section: Methodsmentioning

confidence: 99%

“…GAP43 is expressed in neuronal growth cones and is crucial for neuronal plasticity and axonal guidance [56,57] and GAP43 deficient mice express extreme stress sensitivity and autistic-like features [58]. CCL5 is implicated in neuronal survival [59] and in astrocyte-mediated neuronal differentiation [60]. FLT1 is involved in hippocampal neurogenesis [61] and in astroglial remodeling after brain injury [62].…”

Section: Chl1 and Paroxetine Sensitivitymentioning

confidence: 99%

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Genome-wide Expression Profiling of Human Lymphoblastoid Cell Lines Identifies CHL1 as a Putative SSRI Antidepressant Response Biomarker

et al. 2011

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Section: Methodsmentioning

confidence: 99%

Section: Chl1 and Paroxetine Sensitivitymentioning

confidence: 99%

Genome-wide Expression Profiling of Human Lymphoblastoid Cell Lines Identifies CHL1 as a Putative SSRI Antidepressant Response Biomarker

et al. 2011

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“…Concordant with their known role in the periphery, chemokines are up regulated during inflammation, and contribute to brain immunity and neuroprotection (Cartier et al, 2005;Glass et al, 2005;Madrigal et al, 2009;Omari et al, 2009). They are also involved in progenitor cell migration towards brain tumors (Magge et al, 2009), and participate in brain development and neuronal cell differentiation (Zou et al, 1998;Park et al, 2009). They are even distributed in neurons as neuromodulators are, and modify release of neurotransmitters or neuropeptides (Rostene et al, 2007).…”

Section: The Small Molecule Competitively Binds To the Same Site As Tmentioning

confidence: 99%

Neutralizing endogenous chemokines with small molecules

Galzi

Hachet‐Haas

Bron

et al. 2010

Pharmacology & Therapeutics

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Regulation of cellular responses to external stimuli such as hormones, neurotransmitters, or cytokines is achieved through the control of all steps of the complex cascade starting with synthesis, going through maturation steps, release, distribution, degradation and/or uptake of the signalling molecule interacting with the target protein. One possible way of regulation, referred to as scavenging or neutralization of the ligand, has been increasingly studied, especially for small protein ligands. It shows innovative potential in chemical biology approaches as well as in disease treatment. Neutralization of protein ligands, as for example cytokines or chemokines can lead to the validation of signalling pathways under physiological or pathophysiological conditions, and in certain cases, to the development of therapeutic molecules now used in autoimmune diseases, chronic inflammation and cancer treatment. This review explores the field of ligand neutralization and tries to determine to what extent small chemical molecules could substitute for neutralizing antibodies in therapeutic approaches.

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“…The deletion of the CCL3/MIP-1alpha gene reduced astrocytosis and microgliosis in the hippocampus after the administration of beta-amyloid (1-40) (Passos et al 2009). Another study, however, demonstrated that CCL3/MIP-1alpha secreted by astrocytes promotes the differentiation of embryonic neuronal cells and has neuroprotective functions (Park et al 2009). These contradictory data prompted us explore the role of CCL3/MIP-1alpha in neuroinflammation in a model of LPS-induced brain injury.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of CCL3/MIP‑1alpha regulated by MAPKs and NF‑kappaB mediates microglial inflammatory response in LPS‑induced brain injury

Zhu¹,

Wei²,

Chen³

et al. 2016

Acta Neurobiologiae Experimentalis

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Growing evidence suggests that macrophage inflammatory protein (MIP)-1alpha (synonym CCL3) is upregulated in the neuroinflammatory processes initiated by some brain disorders, but its precise role and regulatory mechanism remain unclear. The present work aims to evaluate the role of CCL3/MIP-1alpha in lipopolysaccharide (LPS)-induced brain injury, and investigate whether the MAPKs and NF-kappaB regulate CCL3/MIP-1alpha expression. We firstly examined the patterns of CCL3/MIP-1alpha expression and phosphorylation of MAPKs in the brains of rats 6, 24, and 72 h after LPS administration. Additionally, LPS-treated rats were administered an anti-MIP-1alpha neutralizing antibody, and the microglial reaction and the expression of both cyclooxygenase-2 and inducible nitric oxide synthase (iNOS) were analyzed. We finally evaluated the effect of an inhibitor of P38 MAPK, an inhibitor of ERK1/2, or an inhibitor of NF-kappaB, on the levels of CCL3/MIP-1alpha protein and numbers of microglia in the brain. In the observation period, LPS induced CCL3/MIP-1alpha expression, which localized to OX-42-labeled microglia, leading to time-dependent increases in the phosphorylation of P38 MAPK and ERK1/2. The expression pattern of induced CCL3/MIP-1alpha was partly consistent with the phosphorylation of MAPKs (P38 MAPK, ERK1/2). Anti-MIP-1alpha attenuated microglial accumulation and the upregulation of cyclooxygenase-2 and iNOS. The inhibition of P38 MAPK, ERK1/2, or NF-kappaB signaling reduced the induced upregulation of CCL3/MIP-1alpha and the microglial accumulation. Our data suggest that upregulated CCL3/MIP-1alpha mediates the accumulation of microglia and the neuroinflammatory reaction, and its expression may be regulated by MAPKs and NF-kappaB in LPS-induced brain injury.

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Chemokines released from astrocytes promote chemokine receptor 5-mediated neuronal cell differentiation

Cited by 32 publications

References 37 publications

Genome-wide Expression Profiling of Human Lymphoblastoid Cell Lines Identifies CHL1 as a Putative SSRI Antidepressant Response Biomarker

Genome-wide Expression Profiling of Human Lymphoblastoid Cell Lines Identifies CHL1 as a Putative SSRI Antidepressant Response Biomarker

Neutralizing endogenous chemokines with small molecules

Upregulation of CCL3/MIP‑1alpha regulated by MAPKs and NF‑kappaB mediates microglial inflammatory response in LPS‑induced brain injury

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