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10.1038/s41419-018-0794-4 http://scihub22266oqcxt.onion/10.1038/s41419-018-0794-4 C6037763!6037763!29988039     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29988039&cmd=llinks): Failed to open stream: HTTP request failed! 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Glutathione depletion induces ferroptosis, autophagy, and premature cell senescence in retinal pigment epithelial cells |pdf=|usr=}}{{29988039}} gab.com Text Glutathione depletion induces ferroptosis, autophagy, and premature cell senescence in retinal pigment epithelial cells JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29988039 #FOAvip Glutathione (GSH) protects against oxidative damage in many tissues, including retinal pigment epithelium (RPE). Oxidative stress-mediated senescence and death of RPE and subsequent death of photoreceptors have been observed in age-related macular degeneration (AMD). Although the consequences of GSH depletion have been described previously, questions remain regarding the molecular mechanisms. We herein examined the downstream effects of GSH depletion on stress-induced premature senescence (SIPS) and cell death in human RPE cells. Briefly, cultured ARPE-19 cells were depleted of GSH using: (1) incubation in cystine (Cys2)-free culture medium; (2) treatment with buthionine sulphoximine (BSO, 1000?�M) to block de novo GSH synthesis for 24?48?h; or (3) treatment with erastin (10?�M for 12?24?h) to inhibit Cys2/glutamate antiporter (system xc?). These treatments decreased cell viability and increased both soluble and lipid reactive oxygen species (ROS) generation but did not affect mitochondrial ROS or mitochondrial mass. Western blot analysis revealed decreased expression of ferroptotic modulator glutathione peroxidase 4 (GPX4). Increased autophagy was apparent, as reflected by increased LC3 expression, autophagic vacuoles, and autophagic flux. In addition, GSH depletion induced SIPS, as evidenced by increased percentage of the senescence-associated ?-galactosidase-positive cells, increased senescence-associated heterochromatin foci (SAHF), as well as cell cycle arrest at the G1 phase. GSH depletion-dependent cell death was prevented by selective ferroptosis inhibitors (8??M Fer-1 and 600?nM Lip-1), iron chelator DFO (80??M), as well as autophagic inhibitors Baf-A1 (75?nM) and 3-MA (10?mM). Inhibiting autophagy with Baf-A1 (75?nM) or 3-MA (10?mM) promoted SIPS. In contrast, inducing autophagy with rapamycin (100?nM) attenuated SIPS. Our findings suggest that GSH depletion induces ferroptosis, autophagy, and SIPS. In addition, we found that autophagy is activated in the process of ferroptosis and reduces SIPS, suggesting an essential role of autophagy in ferroptosis and SIPS. Twit Text FOAVip Glutathione depletion induces ferroptosis, autophagy, and premature cell senescence in retinal pigment epithelial cells ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29988039 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29988039 #FOAvip English Wikipedia <ref>{{Cite pmid|29988039}}</ref> Glutathione depletion induces ferroptosis, autophagy, and premature cell senescence in retinal pigment epithelial cells #MMPMID29988039 Sun Y; Zheng Y; Wang C; Liu Y Cell Death Dis 2018[Jul]; 9 (7): � PMID29988039show ga Glutathione (GSH) protects against oxidative damage in many tissues, including retinal pigment epithelium (RPE). Oxidative stress-mediated senescence and death of RPE and subsequent death of photoreceptors have been observed in age-related macular degeneration (AMD). Although the consequences of GSH depletion have been described previously, questions remain regarding the molecular mechanisms. We herein examined the downstream effects of GSH depletion on stress-induced premature senescence (SIPS) and cell death in human RPE cells. Briefly, cultured ARPE-19 cells were depleted of GSH using: (1) incubation in cystine (Cys2)-free culture medium; (2) treatment with buthionine sulphoximine (BSO, 1000?�M) to block de novo GSH synthesis for 24?48?h; or (3) treatment with erastin (10?�M for 12?24?h) to inhibit Cys2/glutamate antiporter (system xc?). These treatments decreased cell viability and increased both soluble and lipid reactive oxygen species (ROS) generation but did not affect mitochondrial ROS or mitochondrial mass. Western blot analysis revealed decreased expression of ferroptotic modulator glutathione peroxidase 4 (GPX4). Increased autophagy was apparent, as reflected by increased LC3 expression, autophagic vacuoles, and autophagic flux. In addition, GSH depletion induced SIPS, as evidenced by increased percentage of the senescence-associated ?-galactosidase-positive cells, increased senescence-associated heterochromatin foci (SAHF), as well as cell cycle arrest at the G1 phase. GSH depletion-dependent cell death was prevented by selective ferroptosis inhibitors (8??M Fer-1 and 600?nM Lip-1), iron chelator DFO (80??M), as well as autophagic inhibitors Baf-A1 (75?nM) and 3-MA (10?mM). Inhibiting autophagy with Baf-A1 (75?nM) or 3-MA (10?mM) promoted SIPS. In contrast, inducing autophagy with rapamycin (100?nM) attenuated SIPS. Our findings suggest that GSH depletion induces ferroptosis, autophagy, and SIPS. In addition, we found that autophagy is activated in the process of ferroptosis and reduces SIPS, suggesting an essential role of autophagy in ferroptosis and SIPS. �Glutathione depletion induces ferroptosis, autophagy, and premature ce(epmc).pdf DeepDyve Pubget Overpricing