Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration
Sara Romero‐Vázquez, Alfredo Adán, Marc Figueras‐Roca, Víctor Llorenç, Mark Slevin, Gemma Vilahur, Lina Badimón, Andrew D. Dick, Blanca Molins
Abstract
and that mCRP, but not pCRP, is able to cross the RPE monolayer in ARPE-19 cells. Alternatively, mCRP can originate from the dissociation of pCRP in the surface of lipopolysaccharide-damaged RPE in both ARPE-19 and primary porcine RPE lines. In addition, we found that the proinflammatory phenotype of mCRP in the RPE depends on its topological localization. Together, our findings further support mCRP contribution to AMD progression enhancing oBRB disruption.
Topics & Concepts
Proinflammatory cytokineRetinal pigment epitheliumMacular degenerationBlood–retinal barrierRetinalPhenotypeIn vitroCell biologyDegeneration (medical)MedicineChemistryBiologyPathologyOphthalmologyImmunologyInflammationEndocrinologyBiochemistryGeneDiabetes mellitusDiabetic retinopathyRetinal Diseases and TreatmentsRetinal Imaging and AnalysisGlaucoma and retinal disorders