Evento

Targeting phospholipase D pharmacologicallly prevents phagocytic function loss of retinal pigment epithelium cells exposed to high glucose levels

Tenconi, Paula Estefania Icon; Bermudez, Vicente Icon; Echevarria, Maria Sol Icon; Asatryan, Aram ; Calandria, Jorgelina ; Giusto, Norma Maria Icon; Bazan, Nicolas G. ; Mateos, Melina Valeria Icon

Otros responsables

Fecha

2022

Editorial

Fundación Revista Medicina

Revista

Título del libro

Nombre del evento

Reunión Conjunta SAIC SAI & FAIC SAFIS 2022; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología; Reunión Anual 2022 de la Sociedad Argentina de Fisiología

Fecha del evento

2022-11-16

Institución organizadora

Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología

ISSN

0025-7680

eISSN

1669-9106

ISBN

Idioma

Inglés

Tipo del evento

Reunión

Clasificación temática

Resumen

Objective: Inflammation and oxidative stress are a key factor in retinal and ocular diseases. We previously described the participation of classical phospholipase D isoforms (PLD1 and PLD2) in the inflammatory response of human retinal pigment epithelium (RPE) cells exposed to high glucose concentrations (HG). The aim of this work was to study the role of the PLD pathway in RPE phagocytic function. Materials and Methods: Two human RPE cell lines were used, ARPE-19 and ABC cells. ARPE-19 cells were exposed to HG (33 mM) or to normal glucose concentration (NG, 5.5 mM, control condition) for 24, 48 or 72 h and then non-specific phagocytosis was measured using pHrodo™ green bioparticles®. Also, photoreceptor outer segments (POS) phagocytosis was measured. To inhibit PLD1 and PLD2 cells were treated with 0.5 or 5 μM pharmacological PLD1 (VU0359595 or PLD1i) or PLD2 (VU0285655-1 or PLD2i) selective inhibitors. Also, PLD1 and PLD2 siRNA were used. Cell viability was measured by flow cytometry using propidium iodide (PI). Results: HG exposure for 48 and 72 h reduced phagocytic function of ARPE-19 cells. The loss of function induced by HG was prevented when cells were treated with 5 μM PLD1i or PLD2i. Furthermore, PLD1i and PLD2i did not affect RPE phagocytic function under physiological conditions and were able to prevent the increase in reactive oxygen species (ROS) induced by HG in RPE cells. In addition, RNAseq analyses showed for the first time PLD1 and PLD2 expression in hRPE49 and ABC cells, a novel human RPE cell line. Under physiological conditions, PLD1i and PLD2i did not affect ABC cells viability and partial silencing of both PLDs did not affect ABC cells POS phagocytosis. Conclusion: Our findings demonstrate that PLD1i and PLD2i prevent the loss of phagocytic function of RPE cells exposed to HG, without affecting RPE function or viability under non-inflammatory conditions, pointing to their potential use as therapeutic agents for retinal inflammatory diseases.

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