[Expression and function of Fractalkine and its receptor in 5XFAD mouse].
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.
Department of Ophthalmology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China.
L Q
LQ
Chu
Y
Y
Lu
B
B
Karen
J
J
Xu
Q
Q
Liu
Quan
Q
Zhou
D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D015153:Blotting, Western; D054428:Chemokine CX3CL1 / Q000378:metabolism*; D051379:Mice; D012333:RNA, Messenger / Q000378:metabolism; D054387:Receptors, CXCR / Q000378:metabolism*; D012160:Retina / Q000378:metabolism*; D012173:Retinitis / Q000378:metabolism; D015854:Up-Regulation
D016229:Amyloid beta-Peptides; D054428:Chemokine CX3CL1; D012333:RNA, Messenger; D054387:Receptors, CXCR