Open AccessLong non‐coding RNA MALAT 1 regulates retinal neurodegeneration through CREB signaling
Author(s) -
Yao Jin,
Wang XiaoQun,
Li YuJie,
Shan Kun,
Yang Hong,
Wang YangNingZhi,
Yao MuDi,
Liu Chang,
Li XiuMiao,
Shen Yi,
Liu JingYu,
Cheng Hong,
Yuan Jun,
Zhang YangYang,
Jiang Qin,
Yan Biao
Publication year - 2016
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.15252/emmm.201505725
Subject(s) - malat1 , creb , neurodegeneration , biology , microbiology and biotechnology , neuroscience , signal transduction , long non coding rna , medicine , transcription factor , rna , genetics , pathology , disease , gene
The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNA s (lnc RNA s) are important players in many biological processes and human disorders. We previously identified a role of MALAT 1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT 1 in retinal neurodegeneration. We show that MALAT 1 expression is significantly up‐regulated in the retinas, Müller cells, and primary retinal ganglion cells ( RGC s) upon stress. MALAT 1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro . MALAT 1‐ CREB binding maintains CREB phosphorylation by inhibiting PP 2A‐mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT 1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT 1 might regulate the development of retinal neurodegeneration through CREB signaling.