Lithium alleviated spinal cord injury (SCI)-induced apoptosis and inflammation in rats via BDNF-AS/miR-9-5p axis

Wang, Fang; Chang, Sue; Li, Jie; Wang, Dong; Li, Haopeng; He, Xijing

doi:10.1007/s00441-020-03298-3

Cited by 24 publications

(13 citation statements)

References 35 publications

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“…In Sham group, laminectomy was performed only. In SCI group, spinal cord contusion was induced by a 10-g rod falling from the height of 25 mm after laminectomy [ 21 ]. In DNase I group, rats in this group were injected with DNase I (dilate in saline; Roche; 5 mg/kg) via tail vein immediately after SCI was induced.…”

Section: Methodsmentioning

confidence: 99%

“…The score ranges from 0 to 21. In inclined plate test, the maximum angles of the inclined plate with rats staying on it for 10 seconds was recorded at 0, 1, 7, 14, 21, and 28 days after the operation, respectively [ 21 ]. Footstep analysis, immerse the hind feet of rats in ink, lay one-meter-long absorbent paper, and then make them walk along the absorbent paper freely 7 days after the operation.…”

Section: Methodsmentioning

confidence: 99%

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Macrophage Extracellular Traps Exacerbate Secondary Spinal Cord Injury by Modulating Macrophage/Microglia Polarization via LL37/P2X7R/NF-κB Signaling Pathway

Zhang

Guo

Hao

et al. 2022

Oxidative Medicine and Cellular Longevity

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Persistent inflammation in the secondary spinal cord injury (SCI) is an important reason for the failure of nerve repair, which is partly due to the continuous activation of local M1-like macrophage/microglia. It is reported that extracellular trap (ET) has been a new way of cell death, which can be released by macrophages and named macrophage extracellular trap (Met). Furthermore, it exists widely in the pathophysiological process of many diseases, but it has been rarely studied in the field of SCI. In this study, we constructed a spinal cord contusion model and assessed the function outcome of SCI rats. We used immunofluorescence, flow cytometry, and transmission electron microscope (TEM) to demonstrate the existence of Mets. Besides, some related experiments had also been employed to explore the relationship between Mets and M1 polarization of macrophage/microglia. We also performed Co-IP and Western blotting to reveal a new extracellular proinflammatory signal pathway. Finally, we made a linear regression analysis between the concentrations of specific markers of Mets in human serum and ASIA scores. Briefly, our results suggested that macrophages infiltrated in SCI area could induce macrophage/microglia to differentiate into M1-like cells by releasing Mets, which may be achieved partly through LL37-P2X37-NF-κB signal pathway. However, limiting Mets could effectively inhibit M1 polarization and promote function recovery. In addition, the concentrations of Met related proteins in human serum showed high correlation with ASIA scores and could be applied to reflect the severity of SCI. In conclusion, Mets may be a new target for SCI therapy and a promising index for SCI assessment.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Macrophage Extracellular Traps Exacerbate Secondary Spinal Cord Injury by Modulating Macrophage/Microglia Polarization via LL37/P2X7R/NF-κB Signaling Pathway

Zhang

Guo

Hao

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…LncRNA BDNF antisense (BDNF-AS) has been reported as a target of anti-inflammatory treatments. Specifically, lithium treatment decreased inflammation via decreasing BDNF-AS levels, and increasing its target miR-9-5p, in a rat model of spinal cord injury [62]. According to this putative role in facilitating inflammation, increased levels of BDNF-AS can impair cognition in neurodegenerative preclinical models.…”

Section: Long Non-coding Rnas In Alzheimer's Disease Related To Infla...mentioning

confidence: 99%

Long Non-coding RNAs, Extracellular Vesicles and Inflammation in Alzheimer’s Disease

Canseco-Rodriguez¹,

Masola²,

Aliperti³

et al. 2022

Preprint

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Alzheimer´s Disease (AD) has currently no effective treatment; however, preventive measures can significantly delay the progress/onset of the disease. Thus, accurate and early prediction of risk is an important strategy to alleviate the AD burden. Neuroinflammation is a major factor prompting the onset of the disease. Inflammation exerts its toxic effect via multiple mechanisms. Amongst others, it is affecting gene expression via modulation of non-coding RNAs (ncRNAs), such as miRNAs. Recent evidence supports that inflammation can also affect long non-coding RNAs (lncRNAs) expression. While the association between miRNAs and inflammation in AD has been extensively studied, the role of lncRNAs in neurodegenerative diseases has been less explored. In this review, we focus on lncRNAs and inflammation in the context of AD. Furthermore, since plasma-isolated extracellular vesicles (EVs) are increasingly recognized as an effective monitoring strategy of brain pathologies, we have focused on the studies reporting dysregulated lncRNAs in EVs isolated from AD patients and controls. The revised literature shows a positive association between pro-inflammatory lncRNAs and AD. However, the reports evaluating lncRNAs alterations in EVs isolated from plasma of patients and controls, although still limited confirm the value of specific lncRNAs associated with AD as reliable biomarkers. This is an emerging field that will open new avenues to improve risk prediction, patients’ stratification and may lead to the discovery of potential novel therapeutic targets for AD

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“…LncRNA Brain-derived Neurotrophic Factor Antisense (BDNF-AS) has been reported as a target of anti-inflammatory treatments. Specifically, lithium treatment decreased inflammation via decreasing BDNF-AS levels and increasing its target miR-9-5p in a rat model of spinal cord injury (SCI), and it reduced the inflammatory effect caused by H 2 O 2 in SH-SY5Y cells [ 61 ]. According to this putative role in facilitating inflammation, increased levels of BDNF-AS can impair cognition in neurodegenerative preclinical models.…”

Section: Long Non-coding Rnas In Alzheimer’s Disease Related To Infla...mentioning

confidence: 99%

Long Non-Coding RNAs, Extracellular Vesicles and Inflammation in Alzheimer’s Disease

Canseco-Rodriguez

Masola

Aliperti

et al. 2022

IJMS

View full text Add to dashboard Cite

Alzheimer’s Disease (AD) has currently no effective treatment; however, preventive measures have the potential to reduce AD risk. Thus, accurate and early prediction of risk is an important strategy to alleviate the AD burden. Neuroinflammation is a major factor prompting the onset of the disease. Inflammation exerts its toxic effect via multiple mechanisms. Amongst others, it is affecting gene expression via modulation of non-coding RNAs (ncRNAs), such as miRNAs. Recent evidence supports that inflammation can also affect long non-coding RNA (lncRNA) expression. While the association between miRNAs and inflammation in AD has been studied, the role of lncRNAs in neurodegenerative diseases has been less explored. In this review, we focus on lncRNAs and inflammation in the context of AD. Furthermore, since plasma-isolated extracellular vesicles (EVs) are increasingly recognized as an effective monitoring strategy for brain pathologies, we have focused on the studies reporting dysregulated lncRNAs in EVs isolated from AD patients and controls. The revised literature shows a positive association between pro-inflammatory lncRNAs and AD. However, the reports evaluating lncRNA alterations in EVs isolated from the plasma of patients and controls, although still limited, confirm the value of specific lncRNAs associated with AD as reliable biomarkers. This is an emerging field that will open new avenues to improve risk prediction and patient stratification, and may lead to the discovery of potential novel therapeutic targets for AD.

show abstract

Lithium alleviated spinal cord injury (SCI)-induced apoptosis and inflammation in rats via BDNF-AS/miR-9-5p axis

Cited by 24 publications

References 35 publications

Macrophage Extracellular Traps Exacerbate Secondary Spinal Cord Injury by Modulating Macrophage/Microglia Polarization via LL37/P2X7R/NF-κB Signaling Pathway

Macrophage Extracellular Traps Exacerbate Secondary Spinal Cord Injury by Modulating Macrophage/Microglia Polarization via LL37/P2X7R/NF-κB Signaling Pathway

Long Non-coding RNAs, Extracellular Vesicles and Inflammation in Alzheimer’s Disease

Long Non-Coding RNAs, Extracellular Vesicles and Inflammation in Alzheimer’s Disease

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