Increased Lipocalin-2 in the retinal pigment epithelium of Cryba1 cKO mice is associated with a chronic inflammatory response

Mallika Valapala, Malia Edwards, Stacey Hose, Rhonda Grebe, Imran A. Bhutto, Marisol Cano, Thorsten Berger, Tak W. Mak, Eric Wawrousek, James T. Handa, Gerard A. Lutty, J. Samuel Zigler, Debasish Sinha

Research output: Contribution to journalArticle


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), reactive gliosis, and immune cell infiltration. LCN2 may contribute to induction of a chronic inflammatory response in this mouse model with AMD-like pathology.

Original languageEnglish (US)
Pages (from-to)1091-1094
Number of pages4
JournalAging Cell
Issue number6
StatePublished - Dec 1 2014



  • Age-related macular degeneration
  • Cryba1 cKO mice, inflammation
  • Lipocalin-2
  • Lysosomes
  • Retinal pigment epithelium

ASJC Scopus subject areas

  • Aging
  • Cell Biology

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