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Article ; Online: Emerging role of RNA m6A modification in chronic pain.

Albik, Sfian / Tao, Yuan-Xiang

2021 Volume 162, Issue 7, Page(s) 1897–1898

MeSH term(s)	Chronic Pain/genetics ; Humans ; Methylation ; Methyltransferases ; Mixed Function Oxygenases ; Proto-Oncogene Proteins ; RNA ; RNA-Binding Proteins ; Transcription Factors
Chemical Substances	Proto-Oncogene Proteins ; RNA-Binding Proteins ; Transcription Factors ; YTHDF2 protein, human ; RNA (63231-63-0) ; Mixed Function Oxygenases (EC 1.-) ; TET1 protein, human (EC 1.-) ; Methyltransferases (EC 2.1.1.-)
Language	English
Publishing date	2021-03-18
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	193153-2
ISSN	1872-6623 ; 0304-3959
ISSN (online)	1872-6623
ISSN	0304-3959
DOI	10.1097/j.pain.0000000000002219
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Zs.A 1158: Show issues

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Article ; Online: Systemic administration of NIS-lncRNA antisense oligonucleotide alleviates neuropathic pain.

Berkman, Tolga / Li, Xiang / Liang, Yingping / Korban, Anna / Bekker, Alex / Tao, Yuan-Xiang

Neuroscience letters

2023 Volume 817, Page(s) 137512

Abstract: Objective: The antisense oligonucleotide (ASO) is an FDA-approved strategy in the treatment of neurological diseases. We have shown the viability of using intrathecal ASO to suppress nerve injury-specific long noncoding RNA (NIS-lncRNA) in dorsal root ... ...

Abstract	Objective: The antisense oligonucleotide (ASO) is an FDA-approved strategy in the treatment of neurological diseases. We have shown the viability of using intrathecal ASO to suppress nerve injury-specific long noncoding RNA (NIS-lncRNA) in dorsal root ganglion (DRG), resulting in a stable and long-lasting antinociceptive effect on NP. This study examined whether systemic administration of NIS-lncRNA ASO relieved the chronic constriction injury (CCI)-induced nociceptive hypersensitivity. Methods: A single subcutaneous injection of NIS-lncRNA ASO at a dose of 1,000 µg was carried out 7 days after CCI or sham surgery in male mice. Behavioral tests were performed one day before surgery and at different days after surgery. DRG and spinal cord were finally collected for quantitative real-time RT-PCR and Western blot assays. Results: NIS-lncRNA ASO significantly alleviated CCI-induced mechanical allodynia, heat hyperalgesia, and cold hyperalgesia starting on day 14 or 21 post-ASO injection and lasting for at least 7 days on the ipsilateral side. Additionally, CCI-induced spontaneous pain and ipsilateral dorsal horn neuronal and astrocyte hyperactivation were blocked on day 28 after NIS-lncRNA ASO injection. As predicted, the CCI-induced increases in the levels of NIS-lncRNA and its downstream target C-C motif chemokine ligand 2 in the ipsilateral lumbar 3 and 4 DRGs were attenuated on day 28 following NIS-lncRNA ASO injection. Conclusion: Our findings indicate that systemic administration of NIS-lncRNA ASO also produces a stable and long-lasting antinociceptive effect on neuropathic pain. NIS-lncRNA ASO may have potential clinical application in the treatment of this disorder.
MeSH term(s)	Animals ; Male ; Mice ; Analgesics ; Chronic Pain ; Ganglia, Spinal ; Hyperalgesia/drug therapy ; Neuralgia/drug therapy ; Oligonucleotides, Antisense/pharmacology ; Oligonucleotides, Antisense/therapeutic use ; Rats, Sprague-Dawley ; RNA, Long Noncoding/genetics ; Spinal Cord Dorsal Horn ; Rats
Chemical Substances	Analgesics ; Oligonucleotides, Antisense ; RNA, Long Noncoding
Language	English
Publishing date	2023-10-06
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2023.137512
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Zs.A 1166: Show issues

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Article ; Online: NT-3 contributes to chemotherapy-induced neuropathic pain through TrkC-mediated CCL2 elevation in DRG neurons.

Sharma, Dilip / Feng, Xiaozhou / Wang, Bing / Yasin, Bushra / Bekker, Alex / Hu, Huijuan / Tao, Yuan-Xiang

EMBO reports

2024

Abstract: Cancer patients undergoing treatment with antineoplastic drugs often experience chemotherapy-induced neuropathic pain (CINP), and the therapeutic options for managing CINP are limited. Here, we show that systemic paclitaxel administration upregulates the ...

Abstract	Cancer patients undergoing treatment with antineoplastic drugs often experience chemotherapy-induced neuropathic pain (CINP), and the therapeutic options for managing CINP are limited. Here, we show that systemic paclitaxel administration upregulates the expression of neurotrophin-3 (Nt3) mRNA and NT3 protein in the neurons of dorsal root ganglia (DRG), but not in the spinal cord. Blocking NT3 upregulation attenuates paclitaxel-induced mechanical, heat, and cold nociceptive hypersensitivities and spontaneous pain without altering acute pain and locomotor activity in male and female mice. Conversely, mimicking this increase produces enhanced responses to mechanical, heat, and cold stimuli and spontaneous pain in naive male and female mice. Mechanistically, NT3 triggers tropomyosin receptor kinase C (TrkC) activation and participates in the paclitaxel-induced increases of C-C chemokine ligand 2 (Ccl2) mRNA and CCL2 protein in the DRG. Given that CCL2 is an endogenous initiator of CINP and that Nt3 mRNA co-expresses with TrkC and Ccl2 mRNAs in DRG neurons, NT3 likely contributes to CINP through TrkC-mediated activation of the Ccl2 gene in DRG neurons. NT3 may be thus a potential target for CINP treatment.
Language	English
Publishing date	2024-04-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.1038/s44319-024-00133-6
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Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Hippocampal HDAC6 promotes POCD by regulating NLRP3-induced microglia pyroptosis via HSP90/HSP70 in aged mice.

Lin, Qi-Cheng / Wang, Jiao / Wang, Xin-Lin / Pan, Chi / Jin, Shao-Wu / Char, Steven / Tao, Yuan-Xiang / Cao, Hong / Li, Jun

Biochimica et biophysica acta. Molecular basis of disease

2024 Volume 1870, Issue 5, Page(s) 167137

Abstract: Background: Postoperative Cognitive Dysfunction (POCD) has attracted increased attention, but its precise mechanism remains to be explored. This study aimed to figure out whether HDAC6 could regulate NLRP3-induced pyroptosis by modulating the functions ... ...

Abstract	Background: Postoperative Cognitive Dysfunction (POCD) has attracted increased attention, but its precise mechanism remains to be explored. This study aimed to figure out whether HDAC6 could regulate NLRP3-induced pyroptosis by modulating the functions of HSP70 and HSP90 in microglia to participate in postoperative cognitive dysfunction in aged mice. Methods: Animal models of postoperative cognitive dysfunction in aged mice were established by splenectomy under sevoflurane anesthesia. Morris water maze was used to examine the cognitive function and motor ability. Sixteen-months-old C57BL/6 male mice were randomly divided into six groups: control group (C group), sham surgery group (SA group), splenectomy group (S group), splenectomy + HDAC6 inhibitor ACY-1215 group (ACY group), splenectomy + HDAC6 inhibitor ACY-1215 + HSP70 inhibitor Apoptozole group (AP group), splenectomy + solvent control group (SC group). The serum and hippocampus of mice were taken after mice were executed. The protein levels of HDAC6, HSP90, HSP70, NLRP3, GSDMD-N, cleaved-Caspase-1 (P20), IL-1β were detected by western blotting. Serum IL-1β, IL-6 and S100β were measured using ELISA assay, and cell localization of HDAC6 was detected by immunofluorescence. In vitro experiments, BV2 cells were used to validate whether this mechanism worked in microglia. The protein levels of HDAC6, HSP90, HSP70, NLRP3, GSDMD-N, P20, IL-1β were detected by western blotting and the content of IL-1β in the supernatant was measured using ELISA assay. The degree of acetylation of HSP90, the interaction of HSP70, HSP90 and NLRP3 were analyzed by coimmunoprecipitation assay. Results: Splenectomy under sevoflurane anesthesia in aged mice could prolong the escape latency, reduce the number of crossing platforms, increase the expression of HDAC6 and activate the NLRP3 inflammasome to induce pyroptosis in hippocampus microglia. Using ACY-1215 could reduce the activation of NLRP3 inflammasome, the pyroptosis of microglia and the degree of spatial memory impairment. Apoptozole could inhibit the binding of HSP70 to NLRP3, reduce the degradation of NLRP3 and reverse the protective effect of HDAC6 inhibitors. The results acquired in vitro experiments closely resembled those in vivo, LPS stimulation led to the pyroptosis of BV2 microglia cells and the release of IL-1β due to the activation of the NLRP3 inflammasome, ACY-1215 showed the anti-inflammatory effect and Apoptozole exerted the opposite effect. Conclusions: Our findings suggest that hippocampal HDAC6 promotes POCD by regulating NLRP3-induced microglia pyroptosis via HSP90/HSP70 in aged mice.
Language	English
Publishing date	2024-03-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2024.167137
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Article ; Online: Sensory neuron-specific long noncoding RNA in small non-peptidergic dorsal root ganglion neurons selectively impairs nerve injury-induced mechanical hypersensitivity.

Wang, Bing / Liang, Yingping / Bekker, Alex / Hu, Huijuan / Tao, Yuan-Xiang

Life sciences

2023 Volume 332, Page(s) 122120

Abstract: Aims: Nerve injury-induced mechanical hypersensitivity is one of major clinical symptoms in neuropathic pain patients. Understanding molecular mechanisms underlying this symptom is crucial for developing effective therapies. The present study was to ... ...

Abstract	Aims: Nerve injury-induced mechanical hypersensitivity is one of major clinical symptoms in neuropathic pain patients. Understanding molecular mechanisms underlying this symptom is crucial for developing effective therapies. The present study was to investigate whether sensory neuron-specific long noncoding RNA (SS-lncRNA) predominantly expressed in small non-peptidergic dorsal root ganglion (DRG) neurons repaired nerve injury-induced mechanical hypersensitivity. Materials and methods: SS-lncRNA downregulation in the mas-related G protein-coupled receptor member D (Mrgprd)-expressed DRG neurons was rescued and mimicked by crossbreeding Mrgprd Key findings: Rescuing SS-lncRNA downregulation in the Mrgprd-expressed DRG neurons significantly reversed the spinal nerve ligation (SNL)-induced reduction of the calcium-activated potassium channel subfamily N member 1 (KCNN1) in these DRG neurons and alleviated the SNL-induced mechanical hypersensitivity, without affecting the SNL-induced heat and cold nociceptive hypersensitivities, on the ipsilateral side. Conversely, mimicking SS-lncRNA downregulation in the Mrgprd-expressed DRG neurons reduced basal KCNN1 expression in these DRG neurons and produced the enhanced response to mechanical stimulation, but not thermal and cold stimuli, on bilateral sides. Mechanistically, SS-lncRNA downregulation caused a reduction in its binding to lysine-specific demethylase 6B (KDM6B) and consequent recruitment of less KDM6B to Kcnn1 promoter and an increase of H3K27me3 enrichment in this promoter in injured DRG. Significance: Our findings suggest that SS-lncRNA downregulation in small non-peptidergic sensory neurons is required specifically for nerve injury-induced mechanical hypersensitivity likely through silencing KCNN1 expression caused by KDM6B-gated increase of H3K27me3 enrichment in Kcnn1 promoter in these neurons.
MeSH term(s)	Rats ; Humans ; Mice ; Animals ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Rats, Sprague-Dawley ; Ganglia, Spinal/metabolism ; Histones/metabolism ; Sensory Receptor Cells/metabolism ; Hyperalgesia/genetics ; Hyperalgesia/metabolism ; Jumonji Domain-Containing Histone Demethylases/metabolism
Chemical Substances	RNA, Long Noncoding ; Histones ; KDM6B protein, human (EC 1.14.11.-) ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-)
Language	English
Publishing date	2023-09-21
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2023.122120
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Article ; Online: Expression of acetyl-histone H3 and acetyl-histone H4 in dorsal root ganglion and spinal dorsal horn in rat chronic pain models.

Liang, Lingli / Tao, Yuan-Xiang

Life sciences

2018 Volume 211, Page(s) 182–188

Abstract: Aims: Histone acetylation and deacetylation are two histone posttranslational modifications that are usually controlled by histone acetyltransferases (HATs) and histone deacetylases (HDACs). Although HATs or HDACs Inhibitors could relieve pain ... ...

Abstract	Aims: Histone acetylation and deacetylation are two histone posttranslational modifications that are usually controlled by histone acetyltransferases (HATs) and histone deacetylases (HDACs). Although HATs or HDACs Inhibitors could relieve pain hypersensitivities in chronic pain animal models, it is not clear on the expression of global histone acetylation in the dorsal root ganglion (DRG) or spinal dorsal horn in chronic pain conditions. Main methods: A spinal nerve ligation (SNL)-induced neuropathic pain model and a complete Freund's adjuvant (CFA)-induced inflammatory pain model in rats were used to examine the expression of total acetyl-histone H3 (AcH3) and total acetyl-histone H4 (AcH4) by immunofluorescence or western blot. Key findings: AcH3 and AcH4 not only localized in neuronal nuclei, but also in nuclei of glial cells in the DRG. Unilateral SNL induced the increase of AcH3 and AcH4 expression in the injured lumbar 5 (L5) DRG, but not in the uninjured L5 DRG or the spinal dorsal horn, while unilateral intraplantar injection of CFA increased AcH3 and AcH4 expression in the ipsilateral L4/5 spinal dorsal horn, but not in the L4/5 DRG. Significance: These results provide morphological evidence for global histone acetylation expression in the DRG and spinal cord and indicate the differential expression in the DRG and spinal dorsal horn in different chronic pain models. More precise epigenetic mechanisms of histone acetylation on the target genes need to be revealed.
MeSH term(s)	Acetylation ; Animals ; Chronic Pain/metabolism ; Chronic Pain/pathology ; Disease Models, Animal ; Ganglia, Spinal/metabolism ; Histones/metabolism ; Male ; Neuralgia/metabolism ; Neuralgia/pathology ; Neurogenic Inflammation/metabolism ; Neurogenic Inflammation/pathology ; Pain Measurement ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Dorsal Horn/metabolism
Chemical Substances	Histones
Language	English
Publishing date	2018-09-17
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2018.09.029
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Article ; Online: C/EBPβ Participates in Nerve Trauma-Induced TLR7 Upregulation in Primary Sensory Neurons.

He, Long / Cao, Jing / Jiang, Bao-Chun / Yang, Jian-Jun / Tao, Yuan-Xiang / Ai, Yanqiu

Molecular neurobiology

2022 Volume 59, Issue 4, Page(s) 2629–2641

Abstract: Nerve trauma-induced toll-like receptor 7 (TLR7) expression level increases in primary sensory neurons in injured dorsal root ganglion (DRG) avails to neuropathic pain, but the reason is still unknown. In the current study, we showed that unilateral ... ...

Abstract	Nerve trauma-induced toll-like receptor 7 (TLR7) expression level increases in primary sensory neurons in injured dorsal root ganglion (DRG) avails to neuropathic pain, but the reason is still unknown. In the current study, we showed that unilateral lumbar 4 (L4) spinal nerve ligation (SNL) upregulated CCAAT/enhancer-binding protein-β (C/EBPβ) expression in ipsilateral L4 DRG. Preventing this elevation attenuated the SNL-induced upregulation of TLR7 in the ipsilateral L4 DRG and inhibited cold/thermal hyperalgesia and mechanical allodynia. In injected DRG, mimicking nerve trauma-induced C/EBPβ upregulation increased TLR7 levels, augmented responses to cold/thermal/mechanical stimuli, and caused ipsilateral spontaneous pain with no SNL. Mechanistically, SNL upregulated binding of increased C/EBPβ to Tlr7 promoter in ipsilateral L4 DRG. Accorded that C/EBPβ could trigger the activation of Tlr7 promoter and co-expressed with Tlr7 mRNA in individual DRG neurons, our findings strongly suggest the role of C/EBPβ in nerve trauma-mediated TLR7 upregulation in injured primary sensory neurons.
MeSH term(s)	Animals ; CCAAT-Enhancer-Binding Protein-beta/metabolism ; Ganglia, Spinal/metabolism ; Hyperalgesia/metabolism ; Rats ; Rats, Sprague-Dawley ; Sensory Receptor Cells/metabolism ; Toll-Like Receptor 7/genetics ; Toll-Like Receptor 7/metabolism ; Trauma, Nervous System/metabolism ; Up-Regulation
Chemical Substances	CCAAT-Enhancer-Binding Protein-beta ; TLR7 protein, rat ; Toll-Like Receptor 7
Language	English
Publishing date	2022-02-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-022-02763-0
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Zs.A 2411: Show issues

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Article ; Online: Corrigendum to "Antidepressant-like effects of helicid on a chronic unpredictable mild stress-induced depression rat model: Inhibiting the IKK/IκBα/NF-κB pathway through NCALD to reduce inflammation" [Int. Immunopharmacol. 93 (2021) 107165].

Zhang, Yuan-Xiang / Zhang, Xiao-Tong / Li, Hong-Jin / Zhou, Tao-Feng / Zhou, An-Cheng / Zhong, Zheng-Ling / Liu, Yan-Hao / Yuan, Li-Li / Zhu, Hao-Yu / Luan, Di / Tong, Jiu-Cui

International immunopharmacology

2023 Volume 121, Page(s) 110611

Language	English
Publishing date	2023-07-17
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2023.110611
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Article ; Online: Contribution of activating lateral hypothalamus-lateral habenula circuit to nerve trauma-induced neuropathic pain in mice.

Gu, Han-Wen / Zhang, Guang-Fen / Liu, Pan-Miao / Pan, Wei-Tong / Tao, Yuan-Xiang / Zhou, Zhi-Qiang / Yang, Jian-Jun

Neurobiology of disease

2023 Volume 182, Page(s) 106155

Abstract: Neuropathic pain, a severe clinical symptom, significantly affects the quality of life in the patients. The molecular mechanisms underlying neuropathic pain have been the focus of research in recent decades; however, the neuronal circuit-mediated ... ...

Abstract	Neuropathic pain, a severe clinical symptom, significantly affects the quality of life in the patients. The molecular mechanisms underlying neuropathic pain have been the focus of research in recent decades; however, the neuronal circuit-mediated mechanisms associated with this disorder remain poorly understood. Here, we report that a projection from the lateral hypothalamus (LH) glutamatergic neurons to the lateral habenula (LHb), an excitatory LH-LHb neuronal circuit, participates in nerve injury-induced nociceptive hypersensitivity. LH glutamatergic neurons are activated and display enhanced responses to normally non-noxious stimuli following chronic constriction injury. Chemogenetic inhibition of LH glutamatergic neurons or excitatory LH-LHb circuit blocked CCI-induced nociceptive hypersensitivity. Activation of the LH-LHb circuit led to augmented responses to mechanical and thermal stimuli in mice without nerve injury. These findings suggest that LH neurons and their triggered LH-LHb circuit participate in central mechanisms underlying neuropathic pain and may be targets for the treatment of this disorder.
MeSH term(s)	Mice ; Animals ; Hypothalamic Area, Lateral ; Habenula ; Quality of Life ; Hypothalamus/physiology ; Neuralgia/etiology
Language	English
Publishing date	2023-05-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2023.106155
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Zs.A 4444: Show issues

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Article ; Online: Schwann cell-derived extracellular vesicles promote memory impairment associated with chronic neuropathic pain.

Tang, Yidan / Wu, Jiahui / Liu, Changliang / Gan, Lu / Chen, Hai / Sun, Ya-Lan / Liu, Jin / Tao, Yuan-Xiang / Zhu, Tao / Chen, Chan

Journal of neuroinflammation

2024 Volume 21, Issue 1, Page(s) 99

Abstract: Background: The pathogenesis of memory impairment, a common complication of chronic neuropathic pain (CNP), has not been fully elucidated. Schwann cell (SC)-derived extracellular vesicles (EVs) contribute to remote organ injury. Here, we showed that SC- ... ...

Abstract	Background: The pathogenesis of memory impairment, a common complication of chronic neuropathic pain (CNP), has not been fully elucidated. Schwann cell (SC)-derived extracellular vesicles (EVs) contribute to remote organ injury. Here, we showed that SC-EVs may mediate pathological communication between SCs and hippocampal neurons in the context of CNP. Methods: We used an adeno-associated virus harboring the SC-specific promoter Mpz and expressing the CD63-GFP gene to track SC-EVs transport. microRNA (miRNA) expression profiles of EVs and gain-of-function and loss-of-function regulatory experiments revealed that miR-142-5p was the main cargo of SC-EVs. Next, luciferase reporter gene and phenotyping experiments confirmed the direct targets of miR-142-5p. Results: The contents and granule sizes of plasma EVs were significantly greater in rats with chronic sciatic nerve constriction injury (CCI)than in sham rats. Administration of the EV biogenesis inhibitor GW4869 ameliorated memory impairment in CCI rats and reversed CCI-associated dendritic spine damage. Notably, during CCI stress, SC-EVs could be transferred into the brain through the circulation and accumulate in the hippocampal CA1-CA3 regions. miR-142-5p was the main cargo wrapped in SC-EVs and mediated the development of CCI-associated memory impairment. Furthermore, α-actinin-4 (ACTN4), ELAV-like protein 4 (ELAVL4) and ubiquitin-specific peptidase 9 X-linked (USP9X) were demonstrated to be important downstream target genes for miR-142-5p-mediated regulation of dendritic spine damage in hippocampal neurons from CCI rats. Conclusion: Together, these findings suggest that SCs-EVs and/or their cargo miR-142-5p may be potential therapeutic targets for memory impairment associated with CNP.
MeSH term(s)	Rats ; Animals ; MicroRNAs/metabolism ; Neuralgia/metabolism ; Neurons/metabolism ; Schwann Cells/metabolism ; Extracellular Vesicles/metabolism
Chemical Substances	MicroRNAs
Language	English
Publishing date	2024-04-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-024-03081-z
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