Mice deficient in fractalkine are less susceptible to cerebral ischemia-reperfusion injury
Abstract
Fractalkine (FKN), also known as neurotactin, is a CX(3)C chemokine that exists in both secreted and neuronal membrane-bound forms and is upregulated during brain inflammation. There is accumulating evidence that FKN induces chemotaxis by binding to its receptor CX(3)CR1 on leukocytes and microglia. We generated FKN-deficient mice to study the role of FKN in postischemic brain injury. After transient focal cerebral ischemia, FKN-deficient mice had a 28% reduction in infarction size and lower mortality rate, when compared to wild-type littermates. The findings of this study indicate a possible role for FKN in augmenting postischemic injury and mortality after transient focal cerebral ischemia.
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CX3CR1 deficiency ameliorates pathology in murine stroke models.
“In contrast , CX3CR1 deficiency ameliorates pathology in murine stroke models.”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [20]
The effect of CX3CR1 deficiency appears to depend on the nature of the CNS insult.
“Indeed, the effect of CX3CR1 deficiency appears to depend on the nature of the CNS insult as recent studies demonstrated that Cx3cr1 knockout mice exhibit smaller infarcts after transient middle cerebral artery occlusion.19,20”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [20]
Cx3cr1 knockout mice exhibit smaller infarcts after transient middle cerebral artery occlusion.
“Indeed, the effect of CX3CR1 deficiency appears to depend on the nature of the CNS insult as recent studies demonstrated that Cx3cr1 knockout mice exhibit smaller infarcts after transient middle cerebral artery occlusion.19,20”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [20]
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- Authors
- Soriano, S. G., Amaravadi, L. S., Wang, Y. F., Zhou, H., Yu, G. X., Tonra, J. R., Fairchild-Huntress, V., Fang, Q., Dunmore, J. H., Huszar, D., & Pan, Y.
- Affiliations
- Boston Children's Hospital (US)
- Takeda Oncology (United States) (US)
- Corresponding author
- Soriano, Sulpicio G.
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2002-04
- Volume
- 125
- Issue
- 1-2
- Pages
- 59-65
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W2077196241
- Cited by
- 222
- References
- 20
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 5 · 2023: 7 · 2022: 4 · 2021: 6 · 2020: 6 · 2019: 8 · 2018: 4 · 2017: 8 · 2016: 11 · 2015: 15 · 2014: 15 · 2013: 13 · 2012: 10
- FWCI
- 5.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Keywords
- fractalkine, CX3C chemokines, CX3CR1, transient focal cerebral ischemia, ischemia-reperfusion injury, infarct size, neuroprotection, chemokine receptors, neuroinflammation, microglia
- MeSH terms
- Animals, Ischemic Attack, Transient, Disease Susceptibility, Membrane Proteins, Mice, Inbred BALB C, RNA, Messenger, Reperfusion Injury, Gene Expression, Mice, Knockout, Infarction, Middle Cerebral Artery, Chemokines, CX3C, Mice, Chemokine CX3CL1
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