{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Valapala M"],"funding":["NEI NIH HHS","Research to Prevent Blindness","National Institutes of Health"],"pagination":["1091-4"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4244249"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(6)"],"pubmed_abstract":["Although chronic inflammation is believed to contribute to the pathology of age-related macular degeneration (AMD), knowledge regarding the events that elicit the change from para-inflammation to chronic inflammation in the pathogenesis of AMD is lacking. We propose here that lipocalin-2 (LCN2), a mammalian innate immunity protein that is trafficked to the lysosomes, may contribute to this process. It accumulates significantly with age in retinal pigment epithelial (RPE) cells of Cryba1 conditional knockout (cKO) mice, but not in control mice. We have recently shown that these mice, which lack βA3/A1-crystallin specifically in RPE, have defective lysosomal clearance. The age-related increase in LCN2 in the cKO mice is accompanied by increases in chemokine (C-C motif) ligand 2 (CCL2), react"],"journal":["Aging cell"],"pubmed_title":["Increased Lipocalin-2 in the retinal pigment epithelium of Cryba1 cKO mice is associated with a chronic inflammatory response."],"pmcid":["PMC4244249"],"funding_grant_id":["R01 EY019904","EY019037-S","EY14005","R01 EY014005","EY019904","P30 EY001765","R01 EY019037","R01 EY016151"],"pubmed_authors":["Mak TW","Hose S","Sinha D","Samuel Zigler J","Bhutto IA","Handa JT","Edwards M","Valapala M","Grebe R","Cano M","Wawrousek E","Lutty GA","Berger T"],"additional_accession":[]},"is_claimable":false,"name":"Increased Lipocalin-2 in the retinal pigment epithelium of Cryba1 cKO mice is associated with a chronic inflammatory response.","description":"Although chronic inflammation is believed to contribute to the pathology of age-related macular degeneration (AMD), knowledge regarding the events that elicit the change from para-inflammation to chronic inflammation in the pathogenesis of AMD is lacking. We propose here that lipocalin-2 (LCN2), a mammalian innate immunity protein that is trafficked to the lysosomes, may contribute to this process. It accumulates significantly with age in retinal pigment epithelial (RPE) cells of Cryba1 conditional knockout (cKO) mice, but not in control mice. We have recently shown that these mice, which lack βA3/A1-crystallin specifically in RPE, have defective lysosomal clearance. The age-related increase in LCN2 in the cKO mice is accompanied by increases in chemokine (C-C motif) ligand 2 (CCL2), react","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Dec","modification":"2025-04-19T07:52:07.608Z","creation":"2019-03-27T01:40:13Z"},"accession":"S-EPMC4244249","cross_references":{"pubmed":["25257511"],"doi":["10.1111/acel.12274"]}}