Long non‐coding RNA MALAT1 regulates retinal neurodegeneration through CREB signaling
The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. Howe...
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Published in | EMBO molecular medicine Vol. 8; no. 4; pp. 346 - 362 |
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Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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London
Nature Publishing Group UK
01.04.2016
EMBO Press John Wiley and Sons Inc Springer Nature |
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Abstract | The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT1 in retinal neurodegeneration. We show that MALAT1 expression is significantly up‐regulated in the retinas, Müller cells, and primary retinal ganglion cells (RGCs) upon stress. MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival
in vivo
and
in vitro
. MALAT1‐CREB binding maintains CREB phosphorylation by inhibiting PP2A‐mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT1 might regulate the development of retinal neurodegeneration through CREB signaling.
Synopsis
Long non‐coding RNA MALAT1 knockdown decreases retinal reactive gliosis, Müller cell activation, and RGC survival via interactions with CREB signaling.
MALAT1 expression is up‐regulated in retinas, Müller cells, and primary retinal ganglion cells (RGCs) under stress.
MALAT1 knockdown decreases reactive gliosis, Müller cell activation, and RGC survival
in vivo
and
in vitro
.
MALAT1 interacts with the CREB signaling pathway to regulate Müller cell and RGC function.
MALAT1 dysregulation is implicated in several human neurological diseases.
Graphical Abstract
Long non‐coding RNA MALAT1 knockdown decreases retinal reactive gliosis, Müller cell activation, and RGC survival via interactions with CREB signaling. |
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AbstractList | The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT1 in retinal neurodegeneration. We show that MALAT1 expression is significantly up‐regulated in the retinas, Müller cells, and primary retinal ganglion cells (RGCs) upon stress. MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival
in vivo
and
in vitro
. MALAT1‐CREB binding maintains CREB phosphorylation by inhibiting PP2A‐mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT1 might regulate the development of retinal neurodegeneration through CREB signaling.
Synopsis
Long non‐coding RNA MALAT1 knockdown decreases retinal reactive gliosis, Müller cell activation, and RGC survival via interactions with CREB signaling.
MALAT1 expression is up‐regulated in retinas, Müller cells, and primary retinal ganglion cells (RGCs) under stress.
MALAT1 knockdown decreases reactive gliosis, Müller cell activation, and RGC survival
in vivo
and
in vitro
.
MALAT1 interacts with the CREB signaling pathway to regulate Müller cell and RGC function.
MALAT1 dysregulation is implicated in several human neurological diseases.
Graphical Abstract
Long non‐coding RNA MALAT1 knockdown decreases retinal reactive gliosis, Müller cell activation, and RGC survival via interactions with CREB signaling. Abstract The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT1 in retinal neurodegeneration. We show that MALAT1 expression is significantly up‐regulated in the retinas, Müller cells, and primary retinal ganglion cells (RGCs) upon stress. MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro. MALAT1‐CREB binding maintains CREB phosphorylation by inhibiting PP2A‐mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT1 might regulate the development of retinal neurodegeneration through CREB signaling. The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non-coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT1 in retinal neurodegeneration. We show that MALAT1 expression is significantly up-regulated in the retinas, Müller cells, and primary retinal ganglion cells (RGCs) upon stress. MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro MALAT1-CREB binding maintains CREB phosphorylation by inhibiting PP2A-mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT1 might regulate the development of retinal neurodegeneration through CREB signaling. The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT1 in retinal neurodegeneration. We show that MALAT1 expression is significantly up‐regulated in the retinas, Müller cells, and primary retinal ganglion cells (RGCs) upon stress. MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro. MALAT1‐CREB binding maintains CREB phosphorylation by inhibiting PP2A‐mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT1 might regulate the development of retinal neurodegeneration through CREB signaling. The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non-coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT1 in retinal neurodegeneration. We show that MALAT1 expression is significantly up-regulated in the retinas, Müller cells, and primary retinal ganglion cells (RGCs) upon stress. MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro MALAT1-CREB binding maintains CREB phosphorylation by inhibiting PP2A-mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT1 might regulate the development of retinal neurodegeneration through CREB signaling.The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non-coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT1 in retinal neurodegeneration. We show that MALAT1 expression is significantly up-regulated in the retinas, Müller cells, and primary retinal ganglion cells (RGCs) upon stress. MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro MALAT1-CREB binding maintains CREB phosphorylation by inhibiting PP2A-mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT1 might regulate the development of retinal neurodegeneration through CREB signaling. The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNAs (lncRNAs) are important players in many biological processes and human disorders. We previously identified a role of MALAT1 in microvascular dysfunction. However, its role in neurodegeneration is still unknown. Here, we used the eye as the model to investigate the role of MALAT1 in retinal neurodegeneration. We show that MALAT1 expression is significantly up‐regulated in the retinas, Müller cells, and primary retinal ganglion cells (RGCs) upon stress. MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro. MALAT1‐CREB binding maintains CREB phosphorylation by inhibiting PP2A‐mediated dephosphorylation, which leads to continuous CREB signaling activation. Clinical and animal experimentation suggests that MALAT1 dysfunction is implicated in neurodegenerative processes and several human disorders. Collectively, this study reveals that MALAT1 might regulate the development of retinal neurodegeneration through CREB signaling. Synopsis Long non‐coding RNA MALAT1 knockdown decreases retinal reactive gliosis, Müller cell activation, and RGC survival via interactions with CREB signaling. MALAT1 expression is up‐regulated in retinas, Müller cells, and primary retinal ganglion cells (RGCs) under stress. MALAT1 knockdown decreases reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro. MALAT1 interacts with the CREB signaling pathway to regulate Müller cell and RGC function. MALAT1 dysregulation is implicated in several human neurological diseases. Long non‐coding RNA MALAT1 knockdown decreases retinal reactive gliosis, Müller cell activation, and RGC survival via interactions with CREB signaling. 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. |
Author | Yang, Hong Yao, Mu‐Di Cheng, Hong Wang, Xiao‐Qun Shen, Yi Yuan, Jun Wang, Yang‐Ning‐Zhi Li, Xiu‐Miao Jiang, Qin Yan, Biao Zhang, Yang‐Yang Shan, Kun Liu, Jing‐Yu Li, Yu‐Jie Yao, Jin Liu, Chang |
AuthorAffiliation | 1 Eye Hospital Nanjing Medical University Nanjing China 3 Department of Neurology Jiangsu Province Hospital Nanjing China 4 Department of Neurology Jiangsu Chinese Medicine Hospital Nanjing China 2 The Fourth School of Clinical Medicine Nanjing Medical University Nanjing China 5 Department of Cardiac Surgery The first School of Clinical Medicine Nanjing Medical University Nanjing China |
AuthorAffiliation_xml | – name: 4 Department of Neurology Jiangsu Chinese Medicine Hospital Nanjing China – name: 5 Department of Cardiac Surgery The first School of Clinical Medicine Nanjing Medical University Nanjing China – name: 2 The Fourth School of Clinical Medicine Nanjing Medical University Nanjing China – name: 1 Eye Hospital Nanjing Medical University Nanjing China – name: 3 Department of Neurology Jiangsu Province Hospital Nanjing China |
Author_xml | – sequence: 1 givenname: Jin surname: Yao fullname: Yao, Jin organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University – sequence: 2 givenname: Xiao‐Qun surname: Wang fullname: Wang, Xiao‐Qun organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University – sequence: 3 givenname: Yu‐Jie surname: Li fullname: Li, Yu‐Jie organization: Eye Hospital, Nanjing Medical University – sequence: 4 givenname: Kun surname: Shan fullname: Shan, Kun organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University – sequence: 5 givenname: Hong surname: Yang fullname: Yang, Hong organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University – sequence: 6 givenname: Yang‐Ning‐Zhi surname: Wang fullname: Wang, Yang‐Ning‐Zhi organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University – sequence: 7 givenname: Mu‐Di surname: Yao fullname: Yao, Mu‐Di organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University – sequence: 8 givenname: Chang surname: Liu fullname: Liu, Chang organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University – sequence: 9 givenname: Xiu‐Miao surname: Li fullname: Li, Xiu‐Miao organization: Eye Hospital, Nanjing Medical University – sequence: 10 givenname: Yi surname: Shen fullname: Shen, Yi organization: Eye Hospital, Nanjing Medical University – sequence: 11 givenname: Jing‐Yu surname: Liu fullname: Liu, Jing‐Yu organization: Eye Hospital, Nanjing Medical University – sequence: 12 givenname: Hong surname: Cheng fullname: Cheng, Hong organization: Department of Neurology, Jiangsu Province Hospital – sequence: 13 givenname: Jun surname: Yuan fullname: Yuan, Jun organization: Department of Neurology, Jiangsu Chinese Medicine Hospital – sequence: 14 givenname: Yang‐Yang surname: Zhang fullname: Zhang, Yang‐Yang organization: Department of Cardiac Surgery, The first School of Clinical Medicine, Nanjing Medical University – sequence: 15 givenname: Qin surname: Jiang fullname: Jiang, Qin email: jqin710@vip.sina.com organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University – sequence: 16 givenname: Biao surname: Yan fullname: Yan, Biao email: yanbiao1982@hotmail.com organization: Eye Hospital, Nanjing Medical University, The Fourth School of Clinical Medicine, Nanjing Medical University |
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Keywords | reactive gliosis CREB signaling retinal neurodegeneration long non‐coding RNA |
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year: 1992 end-page: 113 article-title: Transcriptional attenuation following cAMP induction requires PP‐1‐mediated dephosphorylation of CREB publication-title: Cell – volume: 1070 start-page: 507 year: 2006 end-page: 511 article-title: Involvement of ERK and CREB signaling pathways in the protective effect of PACAP in monosodium glutamate‐induced retinal lesion publication-title: Ann NY Acad Sci – volume: 6 start-page: 734 year: 2007 end-page: 746 article-title: Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS‐ADRDA criteria publication-title: Lancet Neurol – volume: 50 start-page: 427 year: 2005 end-page: 434 article-title: Astrocyte activation and reactive gliosis publication-title: Glia – volume: 12 start-page: 861 year: 2011 end-page: 874 article-title: Non‐coding RNAs in human disease publication-title: Nat Rev Genet – volume: 15 start-page: 431 year: 2014 end-page: 442 article-title: Müller glial cell reprogramming and retina regeneration publication-title: Nat Rev Neurosci – volume: 14 start-page: 445 year: 1994 end-page: 451 article-title: Retinal pathologic changes in multiple sclerosis publication-title: Retina – volume: 9 start-page: 44 year: 2013 end-page: 53 article-title: The retina as a window to the brain‐from eye research to CNS disorders publication-title: Nat Rev Neurol |
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Snippet | The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNAs (lncRNAs) are... The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non-coding RNAs (lncRNAs) are... The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNA s (lnc RNA s) are... Abstract The nervous and vascular systems, although functionally different, share many common regulators of function maintenance. Long non‐coding RNAs... |
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SourceType | Open Website Open Access Repository Aggregation Database Index Database Publisher |
StartPage | 346 |
SubjectTerms | Alzheimer's disease Animals Brain research Cell activation Cell survival CREB signaling Cyclic AMP response element-binding protein Cyclic AMP Response Element-Binding Protein - metabolism Dephosphorylation Diabetes EMBO27 Experiments Gene expression Gliosis Grants Humans Hypoxia long non‐coding RNA Metastasis Mice Microvasculature Nervous system Neurodegeneration Neurodegenerative Diseases - pathology Non-coding RNA Phosphorylation Protein Binding Protein Processing, Post-Translational Rats, Sprague-Dawley reactive gliosis Research Article Retina Retina - pathology Retinal ganglion cells retinal neurodegeneration Ribonucleic acid RNA RNA, Long Noncoding - metabolism Signal Transduction Stress response Variance analysis Vascular system |
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Title | Long non‐coding RNA MALAT1 regulates retinal neurodegeneration through CREB signaling |
URI | https://link.springer.com/article/10.15252/emmm.201505725 https://onlinelibrary.wiley.com/doi/abs/10.15252%2Femmm.201505725 https://www.ncbi.nlm.nih.gov/pubmed/26964565 https://www.proquest.com/docview/2289934350 https://www.proquest.com/docview/1787088499 https://pubmed.ncbi.nlm.nih.gov/PMC4818754 https://doaj.org/article/189f6b42b87742b8b1f86dd42cf61a70 |
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