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Article ; Online: Glycogen synthase kinase 3 signaling in neural regeneration in vivo.

Zhang, Jing / Yang, Shu-Guang / Zhou, Feng-Quan

2023

Abstract: Glycogen synthase kinase 3 (GSK3) signaling plays important and broad roles in regulating neural development in vitro and in vivo. Here, we reviewed recent findings of GSK3-regulated axon regeneration in vivo in both the peripheral and central nervous ... ...

Abstract	Glycogen synthase kinase 3 (GSK3) signaling plays important and broad roles in regulating neural development in vitro and in vivo. Here, we reviewed recent findings of GSK3-regulated axon regeneration in vivo in both the peripheral and central nervous systems and discussed a few controversial findings in the field. Overall, current evidence indicates that GSK3β signaling serves as an important downstream mediator of the PI3K-AKT pathway to regulate axon regeneration in parallel with the mTORC1 pathway. Specifically, the mTORC1 pathway supports axon regeneration mainly through its role in regulating cap-dependent protein translation, whereas GSK3β signaling might be involved in regulating N6-methyladenosine (m6A) mRNA methylation-mediated cap-independent protein translation. In addition, GSK3 signaling also plays key roles in reshaping the neuronal transcriptomic landscape during neural regeneration. Finally, we proposed some research directions to further elucidate the molecular mechanisms underlying the regulatory function of GSK3 signaling and discover novel GSK3 signaling-related therapeutic targets. Together, we hope to provide an updated and insightful overview of how GSK3 signaling regulates neural regeneration in vivo.
Language	English
Publishing date	2023-12-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2500949-7
ISSN	1759-4685 ; 1759-4685
ISSN (online)	1759-4685
ISSN	1759-4685
DOI	10.1093/jmcb/mjad075
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Intercellular communication atlas reveals Oprm1 as a neuroprotective factor for retinal ganglion cells.

Qian, Cheng / Xin, Ying / Cheng, Qi / Wang, Hui / Zack, Donald / Blackshaw, Seth / Hattar, Samer / Feng-Quan, Zhou / Qian, Jiang

Research square

2023

Abstract: The progressive death of mature neurons often results in neurodegenerative diseases. While the previous studies have mostly focused on identifying intrinsic mechanisms controlling neuronal survival, the extracellular environment also plays a critical ... ...

Abstract	The progressive death of mature neurons often results in neurodegenerative diseases. While the previous studies have mostly focused on identifying intrinsic mechanisms controlling neuronal survival, the extracellular environment also plays a critical role in regulating cell viability. Here we explore how intercellular communication contributes to the survival of retinal ganglion cells (RGCs) following the optic nerve crush (ONC). Although the direct effect of the ONC is restricted to the RGCs, we observed transcriptomic responses in other retinal cells to the injury based on the single-cell RNA-seq, with astrocytes and Müller glia having the most interactions with RGCs. By comparing the RGC subclasses showing distinct resilience to ONC-induced cell death, we found that the high-survival RGCs tend to have more ligand-receptor interactions with other retinal cells, suggesting that these RGCs are intrinsically programmed to foster more communication with their surroundings. Furthermore, we identified top 47 interactions that are stronger in the high-survival RGCs, likely representing neuroprotective interactions. We performed functional assays on one of the receptors, μ opioid receptor (Oprm1), a receptor known to play roles in regulating pain, reward, and addictive behavior. Although Oprm1 is preferentially expressed in intrinsically photosensitive retinal ganglion cells (ipRGCs), its neuroprotective effect could be transferred to multiple RGC subclasses by specific overexpressing Oprm1 in pan-RGCs in ONC, excitotoxicity, and glaucoma models. Lastly, manipulating Oprm1 activity improved visual functions and altered pupillary light response in mice. Our study provides an atlas of cell-cell interactions in both intact and post-ONC retina and an effective strategy to predict molecular mechanisms in neuroprotection, underlying the principal role played by extracellular environment in supporting neuron survival.
Language	English
Publishing date	2023-08-17
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3193738/v1
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Article ; Online: Updates and challenges of axon regeneration in the mammalian central nervous system.

Qian, Cheng / Zhou, Feng-Quan

Journal of molecular cell biology

2020 Volume 12, Issue 10, Page(s) 798–806

Abstract: Axon regeneration in the mammalian central nervous system (CNS) has been a long-standing and highly challenging issue. Successful CNS axon regeneration will benefit many human diseases involving axonal damage, such as spinal cord injury, traumatic brain ... ...

Abstract	Axon regeneration in the mammalian central nervous system (CNS) has been a long-standing and highly challenging issue. Successful CNS axon regeneration will benefit many human diseases involving axonal damage, such as spinal cord injury, traumatic brain injury, glaucoma, and neurodegenerative diseases. The current consensus is that the diminished intrinsic regenerative ability in mature CNS neurons and the presence of extrinsic inhibitors blocking axon regrowth are two major barriers for axon regeneration. During the past decade, studies targeting the intrinsic axon growth ability via regulation of gene transcription have produced very promising results in optic nerve and/or spinal cord regeneration. Manipulations of various signaling pathways or the nuclear transcription factors directly have been shown to sufficiently drive CNS axon regrowth. Converging evidence reveals that some pro-regenerative transcriptomic states, which are commonly accomplished by more comprehensive epigenetic regulations, exist to orchestrate the complex tasks of injury sensing and axon regeneration. Moreover, genetic reprogramming achieved via transcriptome and epigenome modifications provides novel mechanisms for enhancing axon regeneration. Recent studies also highlighted the important roles of remodeling neuronal cytoskeleton in overcoming the extrinsic inhibitory cues. However, our knowledge about the cellular and molecular mechanisms by which neurons regulate their intrinsic axon regeneration ability and response to extrinsic inhibitory cues is still fragmented. Here, we provide an update about recent research progress in axon regeneration and discuss major remaining challenges for long-distance axon regeneration and the subsequent functional recovery.
MeSH term(s)	Animals ; Axons/physiology ; Central Nervous System/physiology ; Epigenesis, Genetic ; Humans ; Mammals/physiology ; Nerve Regeneration/genetics ; Nerve Regeneration/physiology ; Recovery of Function
Language	English
Publishing date	2020-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2500949-7
ISSN	1759-4685 ; 1674-2788
ISSN (online)	1759-4685
ISSN	1674-2788
DOI	10.1093/jmcb/mjaa026
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Article: Editorial: The role of astrocyte in vascular aging.

Lin, Sen / Zhou, Feng-Quan / Cheng, Jin-Bo / Sun, Xiang-Dong / He, Gui-Qiong

Frontiers in aging neuroscience

2022 Volume 14, Page(s) 961288

Language	English
Publishing date	2022-08-03
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2022.961288
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Article ; Online: Reprogramming neurons for regeneration: The fountain of youth.

Yang, Shu-Guang / Wang, Xue-Wei / Qian, Cheng / Zhou, Feng-Quan

Progress in neurobiology

2022 Volume 214, Page(s) 102284

Abstract: Neurons in the central nervous system (CNS) are terminally differentiated cells that gradually lose their ability to support regeneration during maturation due to changes in transcriptomic and chromatin landscape. Similar transcriptomic changes also ... ...

Abstract	Neurons in the central nervous system (CNS) are terminally differentiated cells that gradually lose their ability to support regeneration during maturation due to changes in transcriptomic and chromatin landscape. Similar transcriptomic changes also occur during development when stem cells differentiate into different types of somatic cells. Importantly, differentiated cells can be reprogrammed back to induced pluripotent stems cells (iPSCs) via global epigenetic remodeling by combined overexpression of pluripotent reprogramming factors, including Oct4, Sox2, Klf4, c-Myc, Nanog, and/or Lin28. Moreover, recent findings showed that many proneural transcription factors were able to convert non-neural somatic cells into neurons bypassing the pluripotent stage via direct reprogramming. Interestingly, many of these factors have recently been identified as key regulators of CNS neural regeneration. Recent studies indicated that these factors could rejuvenate mature CNS neurons back to a younger state through cellular state reprogramming, thus favoring regeneration. Here we will review some recent findings regarding the roles of genetic cellular state reprogramming in regulation of neural regeneration and explore the potential underlying molecular mechanisms. Moreover, by using newly emerging techniques, such as multiomics sequencing with big data analysis and Crispr-based gene editing, we will discuss future research directions focusing on better revealing cellular state reprogramming-induced remodeling of chromatin landscape and potential translational application.
MeSH term(s)	Adolescent ; Cell Differentiation ; Cellular Reprogramming ; Chromatin ; Humans ; Induced Pluripotent Stem Cells/physiology ; Neurons
Chemical Substances	Chromatin
Language	English
Publishing date	2022-05-06
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2022.102284
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Article ; Online: In Situ Forming Gel Polymer Electrolyte for High Energy-Density Lithium Metal Batteries.

Xue, Jin-Xin / Liu, Feng-Quan / Xiang, Tian-Qi / Jia, Si-Xin / Zhou, Jian-Jun / Li, Lin

Small (Weinheim an der Bergstrasse, Germany)

2023 Volume 20, Issue 4, Page(s) e2307553

Abstract: In situ forming gel polymer electrolyte (GPE) is one of the most feasible ways to improve the safety and cycle performances of lithium metal batteries with high energy density. However, most of the in situ formed GPEs are not compatible with high-voltage ...

Abstract	In situ forming gel polymer electrolyte (GPE) is one of the most feasible ways to improve the safety and cycle performances of lithium metal batteries with high energy density. However, most of the in situ formed GPEs are not compatible with high-voltage cathode materials. Here, this work provides a novel strategy to in situ form GPE based on the mechanism of Ritter reaction. The Ritter reaction in liquid electrolyte has the advantage of appropriate reaction temperature and no additional additives. The polymer chains are cross-linked by amide groups with the formation of GPE with superior electrochemical properties. The GPE has high ionic conductivity (1.84 mS cm
Language	English
Publishing date	2023-09-15
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2168935-0
ISSN	1613-6829 ; 1613-6810
ISSN (online)	1613-6829
ISSN	1613-6810
DOI	10.1002/smll.202307553
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Article ; Online: Inflammatory Factor IL1α Induces Aberrant Astrocyte Proliferation in Spinal Cord Injury Through the Grin2c/Ca

Xia, Yu / Ding, Lu / Zhang, Changlin / Xu, Qi / Shi, Ming / Gao, Tianshun / Zhou, Feng-Quan / Deng, David Y B

Neuroscience bulletin

2023 Volume 40, Issue 4, Page(s) 421–438

Abstract: Spinal cord injury (SCI) is one of the most devastating traumas, and the aberrant proliferation of astrocytes usually causes neurological deficits. However, the mechanism underlying astrocyte over-proliferation after SCI is unclear. Grin2c (glutamate ... ...

Abstract	Spinal cord injury (SCI) is one of the most devastating traumas, and the aberrant proliferation of astrocytes usually causes neurological deficits. However, the mechanism underlying astrocyte over-proliferation after SCI is unclear. Grin2c (glutamate ionotropic receptor type 2c) plays an essential role in cell proliferation. Our bioinformatic analysis indicated that Grin2c and Ca
MeSH term(s)	Astrocytes/metabolism ; Cell Proliferation ; Interleukin-1alpha/metabolism ; Spinal Cord/pathology ; Spinal Cord Injuries
Chemical Substances	Interleukin-1alpha
Language	English
Publishing date	2023-10-21
Publishing country	Singapore
Document type	Journal Article
ZDB-ID	2419741-5
ISSN	1995-8218 ; 1673-7067
ISSN (online)	1995-8218
ISSN	1673-7067
DOI	10.1007/s12264-023-01128-4
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Article ; Online: In vivo glial trans-differentiation for neuronal replacement and functional recovery in central nervous system.

Qian, Cheng / Dong, Bryan / Wang, Xu-Yang / Zhou, Feng-Quan

The FEBS journal

2021 Volume 288, Issue 16, Page(s) 4773–4785

Abstract: The adult mammalian central nervous system (CNS) is deficient in intrinsic machineries to replace neurons lost in injuries or progressive degeneration. Various types of these neurons constitute neural circuitries wired to support vital sensory, motor, ... ...

Abstract	The adult mammalian central nervous system (CNS) is deficient in intrinsic machineries to replace neurons lost in injuries or progressive degeneration. Various types of these neurons constitute neural circuitries wired to support vital sensory, motor, and cognitive functions. Based on the pioneer studies in cell lineage conversion, one promising strategy is to convert in vivo glial cells into neural progenitors or directly into neurons that can be eventually rewired for functional recovery. We first briefly summarize the well-studied regeneration-capable CNS in the zebrafish, focusing on their postinjury spontaneous reprogramming of the retinal Müller glia (MG). We then compare the signaling transductions, and transcriptional and epigenetic regulations in the zebrafish MGs with their mammalian counterparts, which perpetuate certain barriers against proliferation and neurogenesis and thus fail in MG-to-progenitor conversion. Next, we discuss emerging evidence from mouse studies, in which the in vivo glia-to-neuron conversion could be achieved with sequential or one-step genetic manipulations, such as the conversions from retinal MGs to interneurons, photoreceptors, or retinal ganglion cells (RGCs), as well as the conversions from midbrain astrocytes to dopaminergic or GABAergic neurons. Some of these in vivo studies showed considerable coverage of subtypes in the newly induced neurons and partial reestablishment in neural circuits and functions. Importantly, we would like to point out some crucial technical concerns that need to be addressed to convincingly show successful glia-to-neuron conversion. Finally, we present challenges and future directions in the field for better neural function recovery.
MeSH term(s)	Animals ; Cell Differentiation ; Central Nervous System/metabolism ; Humans ; Nerve Regeneration ; Neuroglia/metabolism ; Recovery of Function
Language	English
Publishing date	2021-01-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15681
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Article ; Online: UCHL1 facilitates protein aggregates clearance to enhance neural stem cell activation in spinal cord injury.

Ding, Lu / Chu, Weiwei / Xia, Yu / Shi, Ming / Li, Tian / Zhou, Feng-Quan / Deng, David Y B

Cell death & disease

2023 Volume 14, Issue 7, Page(s) 479

Abstract: Activation of endogenous neural stem cells (NSCs) is greatly significant for the adult neurogenesis; however, it is extremely limited in the spinal cord after injury. Recent evidence suggests that accumulation of protein aggregates impairs the ability of ...

Abstract	Activation of endogenous neural stem cells (NSCs) is greatly significant for the adult neurogenesis; however, it is extremely limited in the spinal cord after injury. Recent evidence suggests that accumulation of protein aggregates impairs the ability of quiescent NSCs to activate. Ubiquitin c-terminal hydrolase l-1 (UCHL1), an important deubiquitinating enzyme, plays critical roles in protein aggregations clearance, but its effects on NSC activation remains unknown. Here, we show that UCHL1 promotes NSC activation by clearing protein aggregates through ubiquitin-proteasome approach. Upregulation of UCHL1 facilitated the proliferation of spinal cord NSCs after spinal cord injury (SCI). Based on protein microarray analysis of SCI cerebrospinal fluid, it is further revealed that C3
MeSH term(s)	Humans ; Protein Aggregates ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/metabolism ; Cell Differentiation/physiology ; Proteasome Endopeptidase Complex/metabolism ; Neural Stem Cells/metabolism ; Spinal Cord Injuries/metabolism ; Spinal Cord/metabolism
Chemical Substances	Protein Aggregates ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; UCHL1 protein, human
Language	English
Publishing date	2023-07-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-06003-8
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Article ; Online: Intercellular communication atlas reveals Oprm1 as a neuroprotective factor for retinal ganglion cells.

Qian, Cheng / Xin, Ying / Qi, Cheng / Wang, Hui / Dong, Bryan C / Zack, Donald J / Blackshaw, Seth / Hattar, Samer / Zhou, Feng-Quan / Qian, Jiang

Nature communications

2024 Volume 15, Issue 1, Page(s) 2206

Abstract: Previous studies of neuronal survival have primarily focused on identifying intrinsic mechanisms controlling the process. This study explored how intercellular communication contributes to retinal ganglion cell (RGC) survival following optic nerve crush ... ...

Abstract	Previous studies of neuronal survival have primarily focused on identifying intrinsic mechanisms controlling the process. This study explored how intercellular communication contributes to retinal ganglion cell (RGC) survival following optic nerve crush based on single-cell RNA-seq analysis. We observed transcriptomic changes in retinal cells in response to the injury, with astrocytes and Müller glia having the most interactions with RGCs. By comparing RGC subclasses characterized by distinct resilience to cell death, we found that the high-survival RGCs tend to have more ligand-receptor interactions with neighboring cells. We identified 47 interactions stronger in high-survival RGCs, likely mediating neuroprotective effects. We validated one identified target, the μ-opioid receptor (Oprm1), to be neuroprotective in three retinal injury models. Although the endogenous Oprm1 is preferentially expressed in intrinsically photosensitive RGCs, its neuroprotective effect can be transferred to other subclasses by pan-RGC overexpression of Oprm1. Lastly, manipulating the Oprm1 activity improved visual functions in mice.
MeSH term(s)	Animals ; Mice ; Cell Communication ; Cell Death ; Cell Survival ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/metabolism ; Optic Nerve/metabolism ; Optic Nerve Injuries/metabolism ; Retinal Ganglion Cells/physiology
Chemical Substances	Neuroprotective Agents ; OPRM1 protein, human
Language	English
Publishing date	2024-03-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-46428-z
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