RNA-binding protein signaling in adult neurogenesis

Chan, Jim Yee Him; Sánchez-Vidaña, Dalinda Isabel; Anoopkumar‐Dukie, Shailendra; Li, Yue; Wui-Man, Lau Benson

doi:10.3389/fcell.2022.982549

Cited by 14 publications

(13 citation statements)

References 118 publications

(293 reference statements)

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“…Previous studies have shown that Fxr2 is involved in numerous neurological diseases [ 47 – 49 ]. Fxr2 participates in regulating gene expression changes and post-transcriptional processes, playing an essential role in neurogenesis and the regulation of adult neural stem cell self-renewal and maintenance [ 50 , 51 ]. Through actinomycin D and RIP experiments, we confirmed that Fxr2 could bind to Atf3 and reduce Atf3 mRNA stability.…”

Section: Discussionmentioning

confidence: 99%

Anti-ferroptosis exosomes engineered for targeting M2 microglia to improve neurological function in ischemic stroke

Wang,

Liu,

et al. 2024

J Nanobiotechnol

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Background Stroke is a devastating disease affecting populations worldwide and is the primary cause of long-term disability. The inflammatory storm plays a crucial role in the progression of stroke. In the acute phase of ischemic stroke, there is a transient increase in anti-inflammatory M2 microglia followed by a rapid decline. Due to the abundant phospholipid in brain tissue, lipid peroxidation is a notable characteristic of ischemia/reperfusion (I/R), constituting a structural foundation for ferroptosis in M2 microglia. Slowing down the decrease in M2 microglia numbers and controlling the inflammatory microenvironment holds significant potential for enhancing stroke recovery. Results We found that the ferroptosis inhibitor can modulate inflammatory response in MCAO mice, characterizing that the level of M2 microglia-related cytokines was increased. We then confirmed that different subtypes of microglia exhibit distinct sensitivities to I/R-induced ferroptosis. Adipose-derived stem cells derived exosome (ADSC-Exo) effectively decreased the susceptibility of M2 microglia to ferroptosis via Fxr2/Atf3/Slc7a11, suppressing the inflammatory microenvironment and promoting neuronal survival. Furthermore, through plasmid engineering, a more efficient M2 microglia-targeted exosome, termed M2pep-ADSC-Exo, was developed. In vivo and in vitro experiments demonstrated that M2pep-ADSC-Exo exhibits significant targeting specificity for M2 microglia, further inhibiting M2 microglia ferroptosis and improving neurological function in ischemic stroke mice. Conclusion Collectively, we illustrated a novel potential therapeutic mechanism that Fxr2 in ADSC-Exo could alleviate the M2 microglia ferroptosis via regulating Atf3/Slc7all expression, hence inhibiting the inflammatory microenvironment, improving neurofunction recovery in cerebral I/R injury. We obtained a novel exosome, M2pep-ADSC-Exo, through engineered modification, which exhibits improved targeting capabilities toward M2 microglia. This provides a new avenue for the treatment of stroke. Graphical Abstract

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Section: Discussionmentioning

confidence: 99%

Anti-ferroptosis exosomes engineered for targeting M2 microglia to improve neurological function in ischemic stroke

Wang,

Liu,

et al. 2024

J Nanobiotechnol

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“…When examined further, DEX is often involved in signaling pathways that are activated under oxidative stress and triggered by various stressors [ 127 ]. Additionally, what is worth mentioning are microRNAs (miRNAs), which play an important role in post-transcriptional gene regulation [ 128 ]. Many known miRNAs exist in the brain, some of them exclusively in neuronal tissue [ 129 ], and in DEX-affected miRNAs with demonstrated neuroprotection [ 130 , 131 ].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Dexmedetomidine against Hyperoxia-Damaged Cerebellar Neurodevelopment in the Juvenile Rat

et al. 2023

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Impaired cerebellar development of premature infants and the associated impairment of cerebellar functions in cognitive development could be crucial factors for neurodevelopmental disorders. Anesthetic- and hyperoxia-induced neurotoxicity of the immature brain can lead to learning and behavioral disorders. Dexmedetomidine (DEX), which is associated with neuroprotective properties, is increasingly being studied for off-label use in the NICU. For this purpose, six-day-old Wistar rats (P6) were exposed to hyperoxia (80% O2) or normoxia (21% O2) for 24 h after DEX (5 µg/kg, i.p.) or vehicle (0.9% NaCl) application. An initial detection in the immature rat cerebellum was performed after the termination of hyperoxia at P7 and then after recovery in room air at P9, P11, and P14. Hyperoxia reduced the proportion of Calb1+-Purkinje cells and affected the dendrite length at P7 and/or P9/P11. Proliferating Pax6+-granule progenitors remained reduced after hyperoxia and until P14. The expression of neurotrophins and neuronal transcription factors/markers of proliferation, migration, and survival were also reduced by oxidative stress in different manners. DEX demonstrated protective effects on hyperoxia-injured Purkinje cells, and DEX without hyperoxia modulated neuronal transcription in the short term without any effects at the cellular level. DEX protects hyperoxia-damaged Purkinje cells and appears to differentially affect cerebral granular cell neurogenesis following oxidative stress.

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“…As during development, both RBPs [ 7 , 112 ] and ncRNAs [ 53 , 54 , 55 , 56 , 113 , 114 , 115 , 116 ] are responsible for all the different steps of these regulatory events. Among these latter molecules, some small nucleolar RNAs (snoRNAs) also seem to play a role in learning and memory [ 117 ].…”

Section: Post-transcriptional Regulation and Synaptic Plasticity In T...mentioning

confidence: 99%

Role of Post-Transcriptional Regulation in Learning and Memory in Mammals

Di Liegro,

Schiera,

Schirò

et al. 2024

Genes

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After many decades, during which most molecular studies on the regulation of gene expression focused on transcriptional events, it was realized that post-transcriptional control was equally important in order to determine where and when specific proteins were to be synthesized. Translational regulation is of the most importance in the brain, where all the steps of mRNA maturation, transport to different regions of the cells and actual expression, in response to specific signals, constitute the molecular basis for neuronal plasticity and, as a consequence, for structural stabilization/modification of synapses; notably, these latter events are fundamental for the highest brain functions, such as learning and memory, and are characterized by long-term potentiation (LTP) of specific synapses. Here, we will discuss the molecular bases of these fundamental events by considering both the role of RNA-binding proteins (RBPs) and the effects of non-coding RNAs involved in controlling splicing, editing, stability and translation of mRNAs. Importantly, it has also been found that dysregulation of mRNA metabolism/localization is involved in many pathological conditions, arising either during brain development or in the adult nervous system.

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RNA-binding protein signaling in adult neurogenesis

Cited by 14 publications

References 118 publications

Anti-ferroptosis exosomes engineered for targeting M2 microglia to improve neurological function in ischemic stroke

Anti-ferroptosis exosomes engineered for targeting M2 microglia to improve neurological function in ischemic stroke

Protective Effect of Dexmedetomidine against Hyperoxia-Damaged Cerebellar Neurodevelopment in the Juvenile Rat

Role of Post-Transcriptional Regulation in Learning and Memory in Mammals

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