
Characterization of stress response in human retinal epithelial cells
Author(s) -
Giansanti Vincenzo,
Villalpando Rodriguez Gloria E.,
Savoldelli Michelle,
Gioia Roberta,
Forlino Antonella,
Mazzini Giuliano,
Pennati Marzia,
Zaffaroni Nadia,
Scovassi Anna Ivana,
Torriglia Alicia
Publication year - 2013
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2012.01652.x
Subject(s) - autophagy , retinal pigment epithelium , programmed cell death , retinal , microbiology and biotechnology , apoptosis , atg5 , biology , pathogenesis , chemistry , immunology , biochemistry
The pathogenesis of age‐related macular degeneration ( AMD ) involves demise of the retinal pigment epithelium and death of photoreceptors. In this article, we investigated the response of human adult retinal pigmented epithelial ( ARPE ‐19) cells to 5‐( N , N ‐hexamethylene)amiloride ( HMA ), an inhibitor of Na + /H + exchangers. We observed that ARPE ‐19 cells treated with HMA are unable to activate ‘classical’ apoptosis but they succeed to activate autophagy. In the first 2 hrs of HMA exposure, autophagy is efficient in protecting cells from death. Thereafter, autophagy is impaired, as indicated by p62 accumulation, and this protective mechanism becomes the executioner of cell death. This switch in autophagy property as a function of time for a single stimulus is here shown for the first time. The activation of autophagy was observed, at a lesser extent, with etoposide, suggesting that this event might be a general response of ARPE cells to stress and the most important pathway involved in cell resistance to adverse conditions and toxic stimuli.