Do retinal pigment epithelial cells use a MerTK-dependent mechanism to limit the phagocytic particle binding activity of αvβ5 integrin?
Expressing β5-GFP is sufficient to reverse phagocytic deficiencies of RPE cells derived from β5(-/-)  mice, indicating that these cells do not irreversibly lose other components of the phagocytic machinery. RPE cells expressing the engulfment receptor MerTK control POS binding by limiting activity of endogenous αvβ5 and αvβ5-GFP integrins, although they reside at the apical, phagocytic surface. In contrast, RPE cells permanently or transiently losing MerTK expression lack this regulatory mechanism and bind excess POS via surface αvβ5 receptors. Taken together, these data reveal a novel feedback mechanism that restricts binding of POS to surface αvβ5 integrin receptors in RPE cells.
Adherence to medication can improve healthcare outcomes but is associated with higher total healthcare expenses, especially during the years immediately following the onset of diabetes. Long-term follow-up is needed for further investigation.