The endoplasmic reticulum stress transducer old astrocyte specifically induced substance positively regulates glial scar formation in spinal cord injury

Yoshikazu, Sumida; Kamei, Naosuke; Suga, Norifumi; Ochi, Mitsuo; Adachi, Nobuo

doi:10.1097/wnr.0000000000001128

Cited by 8 publications

(7 citation statements)

References 24 publications

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“…Most of them show a tissue-specific preferential expression, however, CREB3, CREB3L1, and CREB3L2 co-express in different cells of the CNS (Figure 2) where they participate in essential processes (Table 1 and Figure 3). For example, CREB3L1 and CREB3L2 are involved in neurite outgrowth (Macgillavry et al, 2011; Okuda et al, 2014) while CREB3 and CREB3L1 modulate (directly or indirectly) axonal growth after an injury (Ying et al, 2014; Sumida et al, 2018). CREB3 regulates pathogenic mechanisms of herpes and polio virus (Lu and Misra, 2000; Liang et al, 2006), and in non-CNS cells a CREB3-ARF4 signaling pathway mediates the susceptibility to pathogens (Reiling et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…Up-Regulation of its expression was also demonstrated in reactive astrocytes proximal to a spinal cord injury (Nikaido et al, 2002). Studies performed in CREB3L1 knock-out mice indicated that, in astrocytes, CREB3L1 promotes glial scars formation, impedes axon growth and functional recovery after spinal injury (Sumida et al, 2018). Furthermore, CREB3L1 protein expression was detected in astrocytes and in neuronal primary cultures obtained from hippocampi of mice, but its mRNA up-regulation was detected only in astrocytes after treatment with kainic acid (KA).…”

Section: Creb3 Family In the Central Nervous Systemmentioning

confidence: 99%

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CREB3 Transcription Factors: ER-Golgi Stress Transducers as Hubs for Cellular Homeostasis

Sampieri

Giusto

Álvarez

2019

Front. Cell Dev. Biol.

106

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CREB3 family of transcription factors are ER localized proteins that belong to the bZIP family. They are transported from the ER to the Golgi, cleaved by S1P and S2P proteases and the released N-terminal domains act as transcription factors. CREB3 family members regulate the expression of a large variety of genes and according to their tissue-specific expression profiles they play, among others, roles in acute phase response, lipid metabolism, development, survival, differentiation, organelle autoregulation, and protein secretion. They have been implicated in the ER and Golgi stress responses as regulators of the cell secretory capacity and cell specific cargos. In this review we provide an overview of the diverse functions of each member of the family (CREB3, CREB3L1, CREB3L2, CREB3L3, CREB3L4) with special focus on their role in the central nervous system.

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Section: Discussionmentioning

confidence: 99%

Section: Creb3 Family In the Central Nervous Systemmentioning

confidence: 99%

CREB3 Transcription Factors: ER-Golgi Stress Transducers as Hubs for Cellular Homeostasis

Sampieri

Giusto

Álvarez

2019

Front. Cell Dev. Biol.

106

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“…CREB3 factors have been characterized as regulators of genes-encoding components of the secretory pathway ( Fox et al, 2010 ; Sampieri et al, 2019 ). In addition, CREB3, CREB3L1, and CREB3L2 are expressed in different cell types of the CNS ( MacGillavry et al, 2011 ; Okuda et al, 2014 ; Ying et al, 2014 ; Sumida et al, 2018 ). We hypothesize that levels of the CREB3 family members could be modified during PC12 cell differentiation, and, therefore, mRNA levels of all were quantified by qRT-PCR assays ( Figure 2A ).…”

Section: Resultsmentioning

confidence: 99%

“…Changes in CREB3 agree with those observed in a microarray study performed on PC12 cells treated with NGF ( Dijkmans et al, 2008 ). Although it has been described that CREB3 participates in axonal regeneration ( Ying et al, 2014 , 2015 ) and that, in astrocytes, CREB3L1 impedes axon growth and functional recovery after spinal injury ( Sumida et al, 2018 ), many questions about the molecular mechanisms of CREB3 transcription factors in these neuronal processes remain unknown. In terms of the participation of CREB3 transcription factors in differentiation processes, our research group ( Garcia et al, 2017 ) has previously reported the adaptation of the Golgi complex in a CREB3L1-dependent manner in rat thyroid cells incubated with TSH (thyroid stimulating hormone).…”

Section: Discussionmentioning

confidence: 99%

CREB3L2 Modulates Nerve Growth Factor-Induced Cell Differentiation

Sampieri

Chabán

Giusto

et al. 2021

Front. Mol. Neurosci.

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Nerve growth factor (NGF) stimulates numerous cellular physiological processes, including growth, differentiation, and survival, and maintains the phenotype of several neuronal types. Most of these NGF-induced processes require adaptation of the secretory pathway since they involve extensive remodeling of membranes and protein redistribution along newly formed neuritic processes. CREB3 transcription factors have emerged as signaling hubs for the regulation of numerous genes involved in the secretory pathway and Golgi homeostasis, integrating stimuli from multiple sources to control secretion, posttranslational modifications and trafficking of proteins. Although recent studies have focused on their role in the central nervous system, little is known about their participation in cell differentiation. Therefore, we aimed to analyze the expression and signaling mechanism of CREB3 transcription factor family members, using the NGF-induced PC12 cell differentiation model. Results show that NGF treatment causes Golgi enlargement and a parallel increased expression of proteins and mRNAs encoding for proteins required for membrane transport (transport factors). Additionally, a significant increase in CREB3L2 protein and mRNA levels is detected in response to NGF. Both MAPK and cAMP signaling pathways are required for this response. Interestingly, CREB3L2 overexpression hampers the NGF-induced neurite outgrowth while its inhibition enhances the morphological changes driven by NGF. In agreement, CREB3L2 overexpressing cells display higher immunofluorescence intensity of Rab5 GTPase (a negative regulator of PC12 differentiation) than control cells. Also, Rab5 immunofluorescence levels decrease in CREB3L2-depleted cells. Taken together, our findings imply that CREB3L2 is an important downstream effector of NGF-activated pathways, leading to neuronal differentiation.

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“…OASIS is upregulated in reactive astrocytes after neuronal degeneration induced by kainic acid [ 26 ]. OASIS expression increases in reactive astrocytes after spinal cord injury, inhibiting neural regrowth, while knockdown promotes regrowth [ 27 , 28 ]. Developmental effects in Oasis-null mice include larger numbers of neural precursor cells (NPCs) and fewer GFAP-expressing astrocytes [ 26 ].…”

Section: Four Arg-tfs and Their Homologsmentioning

confidence: 99%

Regulation of Social Stress and Neural Degeneration by Activity-Regulated Genes and Epigenetic Mechanisms in Dopaminergic Neurons

Kent

Agrawal

2020

Mol Neurobiol

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Transcriptional and epigenetic regulation of both dopaminergic neurons and their accompanying glial cells is of great interest in the search for therapies for neurodegenerative disorders such as Parkinson’s disease (PD). In this review, we collate transcriptional and epigenetic changes identified in adult Drosophila melanogaster dopaminergic neurons in response to either prolonged social deprivation or social enrichment, and compare them with changes identified in mammalian dopaminergic neurons during normal development, stress, injury, and neurodegeneration. Surprisingly, a small set of activity-regulated genes (ARG) encoding transcription factors, and a specific pattern of epigenetic marks on gene promoters, are conserved in dopaminergic neurons over the long evolutionary period between mammals and insects. In addition to their classical function as immediate early genes to mark acute neuronal activity, these ARG transcription factors are repurposed in both insects and mammals to respond to chronic perturbations such as social enrichment, social stress, nerve injury, and neurodegeneration. We suggest that these ARG transcription factors and epigenetic marks may represent important targets for future therapeutic intervention strategies in various neurodegenerative disorders including PD.

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The endoplasmic reticulum stress transducer old astrocyte specifically induced substance positively regulates glial scar formation in spinal cord injury

Abstract: Supplemental Digital Content is available in the text.

Cited by 8 publications

References 24 publications

CREB3 Transcription Factors: ER-Golgi Stress Transducers as Hubs for Cellular Homeostasis

CREB3 Transcription Factors: ER-Golgi Stress Transducers as Hubs for Cellular Homeostasis

CREB3L2 Modulates Nerve Growth Factor-Induced Cell Differentiation

Regulation of Social Stress and Neural Degeneration by Activity-Regulated Genes and Epigenetic Mechanisms in Dopaminergic Neurons

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