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Z. Sun; Antigen Presenting Function Renders Microglia a Neuroprotective Role in Co-Cultured Rat Retinal Tissues. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5095.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the expression of major histocompatibility complexII (MHC-II) and co-stimulatory molecue B7.1/CD80 on retinalmicroglia after T cell factor interleukin-4 (IL-4) or advancedglycation end products (AGEs) stimulation. To further discussthe relationship between changes in microglial antigen presentingfunction and apoptotic cells in cultured rat retinal tissues.
Retinal microglia harvested from mixed culture system were seededin Petri dishes in certain densities for different procedures.Culture medium of various IL-4 or AGEs levels were added intothe dishes as treating sample, with pure medium as controls.A portion of treated microglial cells were collected for MHC-IIand CD80 detection, while the others were washed and culturedin medium, subsequently co-cultured with rat retinas for another24 hours, followed by TUNEL analysis on the retinas.
Compared with controls, IL-4 elevated the expression of bothMHC-II and CD80, while AGEs supressed both. Western blottingdemonstrated the increase of MHC-II protein expression in microglialcells treated with IL-4, contrast to the AGEs group. However,the expression of CD80 protein in the IL-4 group, which markedlydecreased in the AGEs group, did not change markedly comparedto the controls. IL-4 treated microglia induced less apoptoticcells in co-cultured retinas than AGEs counterpats.
Microglial behaviors depend on local microencironment. Appropriateregulation by IL-4 increase the antigen presenting functionof microglia, which is furtherly induced to be protective. Onthe other hand, AGEs renders microlgia destructive featuresby inhibiting its antigen presenting function.
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