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 inEMBO molecular medicine Vol. 8; no. 4; pp. 346 - 362
Main Authors Yao, Jin, Wang, Xiao‐Qun, Li, Yu‐Jie, Shan, Kun, Yang, Hong, Wang, Yang‐Ning‐Zhi, Yao, Mu‐Di, Liu, Chang, Li, Xiu‐Miao, Shen, Yi, Liu, Jing‐Yu, Cheng, Hong, Yuan, Jun, Zhang, Yang‐Yang, Jiang, Qin, Yan, Biao
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.04.2016
EMBO Press
John Wiley and Sons Inc
Springer Nature
Subjects
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
reactive gliosis
CREB signaling
retinal neurodegeneration
long non‐coding RNA
Online AccessGet full text

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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.
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
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Keywords reactive gliosis
CREB signaling
retinal neurodegeneration
long non‐coding RNA
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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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springer
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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
Volume 8
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