Monocyte chemoattractant protein-1 expressed in neurons and astrocytes during focal ischemia in mice

Che, Xiaoming; Ye, Wen; Panga, Li; Wu, Du Chu; Yang, Guo Yuan

doi:10.1016/s0006-8993(01)02328-9

Cited by 189 publications

(135 citation statements)

References 33 publications

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“…Endangered neurons can release proinflammatory chemokines such as monocyte chemoattractant protein-1 (MCP-1/CCL2) and secondary lymphoid-tissue chemokine (SLC/CCL21). Expression of MCP-1 and SLC is increased in neurons after ischemia [29,30]. Subsequently, recruited and activated microglial cells produce inflammatory mediators, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), which contribute to delayed neuronal death [31].…”

Section: Discussionmentioning

confidence: 99%

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

et al. 2010

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Background Because of the lack of reproducible brainstem ischemia models in rodents, the temporal profile of ischemic lesions in the brainstem after transient brainstem ischemia has not been evaluated intensively. Previously, we produced a reproducible brainstem ischemia model of Mongolian gerbils. Here, we showed the temporal profile of ischemic lesions after transient brainstem ischemia. Results Brainstem ischemia was produced by occlusion of the bilateral vertebral arteries just before their entry into the transverse foramina of the cervical vertebrae of Mongolian gerbils. Animals were subjected to brainstem ischemia for 15 min, and then reperfused for 0 d (just after ischemia), 1 d, 3 d and 7 d (n = 4 in each group). Sham-operated animals (n = 4) were used as control. After deep anesthesia, the gerbils were perfused with fixative for immunohistochemical investigation. Ischemic lesions were detected by immunostaining for microtubule-associated protein 2 (MAP2). Just after 15-min brainstem ischemia, ischemic lesions were detected in the lateral vestibular nucleus and the ventral part of the spinal trigeminal nucleus, and these ischemic lesions disappeared one day after reperfusion in all animals examined. However, 3 days and 7 days after reperfusion, ischemic lesions appeared again and clusters of ionized calcium-binding adapter molecule-1(IBA-1)-positive cells were detected in the same areas in all animals. Conclusion These results suggest that delayed neuronal cell death took place in the brainstem after transient brainstem ischemia in gerbils.

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Section: Discussionmentioning

confidence: 99%

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

et al. 2010

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“…However, a significant upregulation or dysregulation of CNS expression of CCL2 occurs in a variety of acute and chronic neuroinflammatory and neurodegenerative CNS disorders, implicating a role for CCL2 in pathological conditions. For example, CCL2 levels in the CNS are elevated in brain injury (Little et al, 2006), cerebral ischemia (Che et al, 2001;Minami et al, 2006), multiple sclerosis (Mahad and Ransohoff, 2003;McManus et al, 1998), human immunodeficiency virus (HIV)-associated dementia (Cinque et al, 1998) and Alzheimer's disease (Galimberti et al, 2006). Both neurotoxic and neuroprotective roles for CCL2 have been proposed in these conditions.…”

Section: Introductionmentioning

confidence: 99%

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

Cho

Gruol

2008

Journal of Neuroimmunology

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Emerging evidence indicates that chemokines can regulate both the physiology and biochemistry of CNS neurons and glia. In the current study, Western blot analysis showed that in rat hippocampal neuronal/glial cultures the signal transduction pathway activated by CCL2, a chemokine expressed in the normal brain and at elevated levels during neuroinflammation, involves a G-protein coupled receptor, p38 MAPK as well as its immediate upstream kinase MKK3/6, and the downstream transcription factor CREB. ERK 1/2 and the transcription factors STAT1 and STAT3 do not play a prominent role. CCL2 also altered Ca 2+ influx and synaptic network activity in the hippocampal neurons. These results suggest an important role for p38 MAPK and CREB in hippocampal actions of CCL2.

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“…In experimental brain ischemia model, MCP-1 messenger RNA and MCP-1 protein in the ischemic cortex are expressed after focal brain ischemia (Che et al, 2001;Kim et al, 1995;Wang et al, 1995). Recent studies using genetic models have reported that MCP-1 deficiency attenuates infarct volume in the murine stroke model (Hughes et al, 2001), and overexpression of MCP-1 causes larger infarct volume and more chemoattraction of monocytes and macrophages into ischemic region than wild-type control (Chen et al, 2003), suggesting that elevated MCP-1 levels might lead to an increased influx of monocytes and evolution of size in brain infarction.…”

mentioning

confidence: 99%

Anti—Monocyte Chemoattractant Protein-1 Gene Therapy Protects against Focal Brain Ischemia in Hypertensive Rats

Kumai

Ooboshi

Takada

et al. 2004

J Cereb Blood Flow Metab

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Summary:Monocyte chemoattractant protein-1 (MCP-1) is expressed in the ischemic cortex after focal brain ischemia and appears to exacerbate ischemic damage. The authors examined the effect of gene transfer of dominant negative MCP-1, called 7ND, 90 minutes after induction of focal brain ischemia in hypertensive rats. Adenoviral vectors encoding mutant MCP-1 (Ad7ND; n ‫ס‬ 11), or Escherichia coli ␤-galactosidase (AdlacZ; n ‫ס‬ 17) as control were injected into the lateral ventricle of male spontaneously hypertensive rats. Both AdlacZ (n ‫ס‬ 12) and Ad7ND (n ‫ס‬ 6) administration provided transgene expression as early as 6 hours after injection and the expression further increased on day 1, followed by a sustained detection on day 5. Five days after ischemia, infarct volume (75 ± 13 mm 3 , n ‫ס‬ 5, mean ± SD) significantly reduced to 72% of control (104 ± 22 mm 3 , n ‫ס‬ 5, P < 0.05) by 7ND gene transfer. Numbers of leukocytes in the vessels (48.3 ± 32.9/cm 2 ) and macrophage/monocyte infiltration (475.2 ± 125.5 /mm 2 ) of the infarct area in the Ad7ND group were significantly less than those measured in the AdlacZ group (143.8 ± 72.1/cm 2 and 671.8 ± 125.5/mm 2 , P < 0.05, respectively). In summary, the postischemic gene transfer of dominant negative MCP-1 attenuated the infarct volume and infiltration of inflammatory cells, suggesting potential usefulness of the anti-MCP-1 gene therapy.

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Monocyte chemoattractant protein-1 expressed in neurons and astrocytes during focal ischemia in mice

Cited by 189 publications

References 33 publications

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

Anti—Monocyte Chemoattractant Protein-1 Gene Therapy Protects against Focal Brain Ischemia in Hypertensive Rats

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