The role of TLR4/NF-κB signaling pathway in activated microglia of rats with chronic high intraocular pressure and vitro scratch injury-induced microglia
Autor: | Yini Zhao, Qian Sha, Dong Chang, Yi Tao, Hongjun Wang, Xuefei Wang, Mingzhe Li, Hui Liu, Xiamu Xiya, Xiang-yuan Song |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Male Retinal Ganglion Cells genetic structures Immunology Cautery Proinflammatory cytokine Cell Line Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine medicine Immunology and Allergy Animals Humans Pharmacology Retina Innate immune system Microglia Cell Death business.industry Interleukin-6 Tumor Necrosis Factor-alpha NF-kappa B Glaucoma Optic Nerve eye diseases Rats Toll-Like Receptor 4 Disease Models Animal 030104 developmental biology medicine.anatomical_structure Retinal ganglion cell 030220 oncology & carcinogenesis TLR4 Optic nerve Cancer research Ocular Hypertension sense organs Signal transduction Neurogenic Inflammation business Signal Transduction |
Zdroj: | International immunopharmacology. 83 |
ISSN: | 1878-1705 |
Popis: | Glaucoma is a kind of blind-causing disease with structural damages of optic nerve and defection of visual field. It is believed that the death of retinal ganglion cell (RGC) is a consequential event of over-reactive immune orchestral cells such as microglia. Previous evidences in animal and clinical studies show the innate immunity plays a pivotal role in neuro-inflammation of glaucoma. Toll-like receptor 4 (TLR4) is expressed on microglia and mediates many neuroinflammatory diseases. We aimed to explore the impacts of high intraocular pressure (IOP) on rat microglia in retina and the regulation of TLR4/NF-κB signaling pathway in scratched microglia cells. In our study, we successfully established chronic high IOP rat model by episcleral vein cauterization (EVC) which behaved like the chronic glaucoma. Besides, we set up an in vitro scratch-induced injury model in rat microglia cells. We found the level of activated microglia cells were significantly increased in the retina of chronic high IOP groups. Moreover, the inhibition of TLR4/NF-κB signaling pathway suppressed the expression of TLR4 protein and mRNA levels of P50, IL-6 and TNF-α. Our original study provided a theoretical basis on targeting TLR4/NF-κB to suppress pro-inflammatory factors releasing in activated microglia and it might be a good treatment target to prevent glaucoma from progressing. |
Databáze: | OpenAIRE |
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