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[Expression and function of Fractalkine and its receptor in 5XFAD mouse]
1Department of Ophthalmology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China.
Abstract:
Objective: To detect the expression and the function of Fractalkine(CX3CL1) and its receptor CX3CR1 in neurodegenerative changes of the retina. Methods: Twelve 5XFAD mouse and twelve wild type mouse were enrolled. Frozen sections were prepared for histopathological tests. Immunofluorescence study for Amyloid β, CX3CL1 and CX3CR1 was carried out. Co-expression study for CX3CR1/CD11b or CX3CR1/CD68 was carried out. Total protein and total mRNA from the eyes of both 5XFAD and wild type mouse were extracted. The expression of mRNA and protein of CX3CL1 and CX3CR1 in the eyes were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blots test, respectively. Results: In wild type mouse, both CX3CL1 and its receptor CX3CR1 can be detected in the retina with low expression, however there is no Amyloid β depositions in retina. In 6 months 5XFAD mouse, an obvious up-regulated Amyloid β expression can be seen in the RPE cells, and the number of both CX3CL1 and CX3CR1 positive cells has up-regulated in the ganglion cell layer of eyes accompanied with the increased expression of their mRNA and protein. The co-expression study showed that CX3CR1 co-expressed with CD11b, but not with CD68. Conclusion: Fractalkine and its receptor play a role in Amyloid β inducing degenerative retinal inflammation in 5XFAD mouse.
Insights
Fractalkine (CX3CL1) and its receptor CX3CR1 are upregulated in the retinas of 5XFAD mice, indicating a role in amyloid-beta-induced retinal inflammation.
Area of Science:
- Neuroscience
- Ophthalmology
- Immunology
Background:
- Neuroinflammation is a key feature of neurodegenerative diseases.
- Fractalkine (CX3CL1) and its receptor CX3CR1 are involved in immune cell trafficking and function.
- Amyloid-beta deposition is implicated in retinal degeneration.
Purpose of the Study:
- To investigate the expression and function of Fractalkine (CX3CL1) and CX3CR1 in the context of neurodegenerative changes in the retina.
- To determine the role of CX3CL1/CX3CR1 in amyloid-beta-induced retinal inflammation.
Main Methods:
- Utilized 5XFAD transgenic mice and wild-type littermates.
- Performed histopathological analysis, immunofluorescence staining for amyloid-beta, CX3CL1, and CX3CR1.
- Conducted co-expression studies (CX3CR1/CD11b, CX3CR1/CD68) and quantified mRNA/protein levels via RT-PCR and Western blot.
Main Results:
- Wild-type mice showed low baseline expression of CX3CL1 and CX3CR1 with no amyloid-beta deposition.
- 6-month-old 5XFAD mice exhibited upregulated amyloid-beta in RPE cells.
- Upregulated CX3CL1 and CX3CR1 expression, along with increased mRNA and protein levels, were observed in the ganglion cell layer of 5XFAD mice.
- CX3CR1 co-expressed with CD11b, a marker for microglia/macrophages.
Conclusions:
- Fractalkine and its receptor are upregulated in the retina during amyloid-beta-induced neurodegeneration.
- The CX3CL1/CX3CR1 axis plays a significant role in mediating retinal inflammation in 5XFAD mice.
- Targeting the CX3CL1/CX3CR1 pathway may offer therapeutic potential for retinal neurodegenerative diseases.
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