Premium
LIF‐dependent JAK3 activation is not essential for retinal degeneration
Author(s) -
Lange Christina,
Thiersch Markus,
Samardzija Marijana,
Bürgi Sandra,
Joly Sandrine,
Grimm Christian
Publication year - 2010
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.06686.x
Subject(s) - janus kinase , leukemia inhibitory factor , stat protein , retinal degeneration , retinal , janus kinase 3 , microbiology and biotechnology , jak stat signaling pathway , retina , biology , signal transduction , activator (genetics) , photoreceptor cell , neuroscience , stat3 , immune system , immunology , gene , genetics , cytokine , t cell , biochemistry , interleukin 6 , tyrosine kinase , antigen presenting cell
J. Neurochem. (2010) 113 , 1210–1220. Abstract Retinal degeneration causes the induction of a leukemia inhibitory factor (LIF)‐controlled survival pathway which includes Janus kinase/signal transducer and activator of transcription signaling. Lack of LIF prevents activation of this signaling cascade and accelerates disease progression leading to a fast loss of photoreceptor cells. In this study, we show that expression of Janus kinase 3 ( Jak 3), but not of the other members of the family of Janus kinases, is induced in four different models of retinal degeneration and that LIF is essential and sufficient to activate Jak 3 gene expression. We also show that the induction of Jak 3 and Lif may not depend directly on cell death but rather on the retinal stress during photoreceptor degeneration. However, despite its dependence on LIF, JAK3 is not essential for LIF‐mediated photoreceptor protection or gene expression. Also, absence of JAK3 in knockout mice did not affect immune‐related responses in the degenerating retina. JAK3 may therefore play a different, yet unknown, role in the retinal response to photoreceptor injury.