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Spleen Tyrosine Kinase Mediates Microglial Activation in Mice With Diabetic Retinopathy
Diabetic retinopathy (DR) is a leading cause of blindness in developed countries, in which microglial activation is involved. However, the mechanism of microglial activation in DR remains largely unknown. We used Cx3cr1CreERT2; Sykfl/fl mice to knockout microglial spleen tyrosine kinase (Syk) in the...
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Published in: | Translational vision science & technology 2021-04, Vol.10 (4), p.20-20 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Diabetic retinopathy (DR) is a leading cause of blindness in developed countries, in which microglial activation is involved. However, the mechanism of microglial activation in DR remains largely unknown.
We used Cx3cr1CreERT2; Sykfl/fl mice to knockout microglial spleen tyrosine kinase (Syk) in the retina of mice (cKO mice) after streptozotocin injection to induce diabetes. We also isolated primary retinal microglia from wild-type and cKO mice, respectively, to explore the role of microglial Syk in DR.
The deletion of microglial Syk in the retina of mice or in the primary retinal microglia inhibited microglial activation and inflammatory response, eventually leading to the improvement of DR by regulating the expressions of interferon regulatory factor 8 (Irf8) and Pu.1 both in vivo and in vitro.
The deletion of microglial Syk in the retina effectively ameliorated microglial activation-induced DR, suggesting the potential of microglial Syk as a therapeutic target for DR.
Microglial spleen tyrosine kinase might serve as a potential therapeutic target for diabetic retinopathy. |
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ISSN: | 2164-2591 2164-2591 |
DOI: | 10.1167/tvst.10.4.20 |