Open AccessThe activation of the atypical PKC zeta in light‐induced retinal degeneration and its involvement in L‐ DN ase II control
Author(s) -
Jaadane Imene,
Chahory Sabine,
Leprêtre Chloé,
Omri Boubaker,
Jonet Laurent,
BeharCohen Francine,
Crisanti Patricia,
Torriglia Alicia
Publication year - 2015
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/jcmm.12539
Subject(s) - protein kinase c , retinal degeneration , apoptosis , microbiology and biotechnology , retinal , caspase , biology , programmed cell death , protein kinase a , photoreceptor cell , kinase , chemistry , biochemistry
Light‐induced retinal degeneration is characterized by photoreceptor cell death. Many studies showed that photoreceptor demise is caspase‐independent. In our laboratory we showed that leucocyte elastase inhibitor/ LEI ‐derived DN ase II ( LEI /L‐ DN ase II), a caspase‐independent apoptotic pathway, is responsible for photoreceptor death. In this work, we investigated the activation of a pro‐survival kinase, the protein kinase C ( PKC ) zeta. We show that light exposure induced PKC zeta activation. PKC zeta interacts with LEI /L‐ DN ase II and controls its DN ase activity by impairing its nuclear translocation. These results highlight the role of PKC zeta in retinal physiology and show that this kinase can control caspase‐independent pathways.