Upregulation of JHDM1D-AS1 alleviates neuroinflammation and neuronal injury via targeting miR-101-3p-DUSP1 in spinal cord after brachial plexus injury

Liu, Luping; Zhang, Jie; Bo, Ping; Li, Weiqiang; Wang, Yingsong

doi:10.1016/j.intimp.2020.106962

Cited by 26 publications

(23 citation statements)

References 34 publications

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“…A substantial proportion of altered lncRNAs belonged to the antisense RNA family ( Figure 1B ). Among these antisense RNAs, we identified the previously described JHDM1D-AS1 ( Kondo et al., 2017 ; Yao et al., 2019 ; Shi et al., 2019 ; Liu et al., 2020 ), which is physically located on chromosome 7 (140,177,261–140,179,640 bp). Expression patterns of JHDM1D-AS1 antisense RNA were also significantly higher in whole-blood transcriptomes obtained from publicly available data of all-cause patients with sepsis (n = 156) relative to healthy donors (n = 82) ( Supplementary Figure 1B ) ( Scicluna et al., 2020 ).…”

Section: Resultsmentioning

confidence: 99%

“…A recent study provided evidence for a role of JHDM1D-AS1 in rat microglia cells during neuronal injury ( Liu et al., 2020 ). Interestingly, JHDM1D-AS1 expression was downregulated in microglial cells upon LPS-induced TLR4 activation, whereas overexpression of JHDM1D-AS1 suppressed inflammatory responses, potentially by targeting NF-ĸB-activation through the miR-101-3p/DUSP1 pathway.…”

Section: Discussionmentioning

confidence: 99%

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The Long Non-Coding Antisense RNA JHDM1D-AS1 Regulates Inflammatory Responses in Human Monocytes

Malmström

Khan

Veer

et al. 2022

Front. Cell. Infect. Microbiol.

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Monocytes are key players in innate immunity, with their ability to regulate inflammatory responses and combat invading pathogens. There is a growing body of evidence indicating that long non-coding RNA (lncRNA) participate in various cellular biological processes, including the innate immune response. The immunoregulatory properties of numerous lncRNAs discovered in monocytes remain largely unexplored. Here, by RNA sequencing, we identified a lncRNA JHDM1D-AS1, which was upregulated in blood monocytes obtained from patients with sepsis relative to healthy controls. JHDM1D-AS1 expression was induced in primary human monocytes exposed to Toll-like receptor ligands, such as lipopolysaccharide (LPS), or bacteria. The inducibility of JHDM1D-AS1 expression in monocytes depended, at least in part, on nuclear factor–κB activation. JHDM1D-AS1 knockdown experiments in human monocyte-derived macrophages revealed significantly enhanced expression of inflammatory mediators, before and after exposure to LPS, relative to control cells. Specifically, genes involved in inflammatory responses were upregulated (e.g., CXCL2, CXCL8, IL1RN, TREM1, TNF, and IL6), whereas genes involved in anti-inflammatory pathways were downregulated (e.g., SOCS1 and IL10RA). JHDM1D-AS1 overexpression in a pro-monocytic cell line revealed diminished pro-inflammatory responses subsequent to LPS challenge. Collectively, these findings identify JHDM1D-AS1 as a potential anti-inflammatory mediator induced in response to inflammatory stimuli.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Long Non-Coding Antisense RNA JHDM1D-AS1 Regulates Inflammatory Responses in Human Monocytes

Malmström

Khan

Veer

et al. 2022

Front. Cell. Infect. Microbiol.

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“…Factors participating in the network of motor cortical remodelling after BPRA display dynamic changes. Major microRNAs (miRNAs/miRs) distributed in the motor cortex, such as miR-101-3p, miR-132, miR-134, miR-137-3p and miR-485, play vital roles in regulating neural plasticity and transhemispheric functional reorganization dendrite morphology, spontaneous synaptic responses and transmitter release after cervical spinal nerve root transfer following BPA injury [61,81,86]. Functional MRI studies revealed that the levels of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, tumour necrosis factor α (TNF-α), are important mediators in the neural plasticity and transhemispheric functional reorganization [33,36,57,98].…”

Section: Brain Changesmentioning

confidence: 99%

“…In addition, targeting miRNAs to indirectly regulate genes involved in inflammation initiated by injury and downstream signalling pathways contributing to tMN death may be a new route to prevent MN degeneration [82]. The lncRNA JHDM1D-AS1 was shown to exert antiinflammatory and neuroprotective effects via regulating the miR-101-3p/dual-specificity phosphatase 1 (DUSP1) axis in rats following BPRA [61]. Consequently, targeting the differentially expressed lncRNAs and miRNAs induced by BPA injury may uncover novel diagnostic and therapeutic options.…”

Section: Non-coding Rnasmentioning

confidence: 99%

Therapeutic strategies for brachial plexus injury

Hong¹,

Chen²,

Wu³

et al. 2021

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Brachial plexus avulsion (BPA), a severe acute peripheral nerve injury in adults, results in total loss of the motor function in the upper limb. Although immediate re-implantation surgery is widely performed to repair this lesion, the motor function cannot be fully restored. The main cause is that the growth velocity of axon is extremely slow in order to re-innervate the target muscles before atrophy develops. Therefore, the survival of spinal motoneurons (MNs) is considered to be a prerequisite for the recovery of motor function. The introduction of survival-proactive agents with anti-oxidative stress and anti-inflammation properties has emerged as a new approach to the motor function recovery following BPA. In the current review, we summarized the treatments of BPA in both mouse and rat models following re-implantation surgery. Furthermore, the pain treatment options following BPA were discussed.

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“… 92 In addition, up-regulation of JHDM1D-AS1 can reduce the inflammation and neuronal damage of the spinal cord after brachial plexus injury by targeting miR-101-3p-DUSP. 93 In the rat model of cancer pain, the expression of lncRNA-NONRATT021203.2 was increased, which can participate in the production of pain by targeting CXCL9 (C-X-C motif chemokine ligand 9). 94 Postherpetic neuralgia (PHN) is also a considerable neuropathic pain.…”

Section: Introductionmentioning

confidence: 99%

Differential Expression of Long Non-Coding RNAs and Their Role in Rodent Neuropathic Pain Models

Xu¹,

Dong²,

Zhao³

et al. 2021

JPR

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Neuropathic pain, which is accompanied by an unpleasant sensation, affects the patient’s quality of life severely. Considering the complexity of the neuropathic pain, there are huge unmet medical needs for it while current effective therapeutics remain far from satisfactory. Accordingly, exploration of mechanisms of neuropathic pain could provide new therapeutic insights. While numerous researches have pointed out the contribution of sensory neuron-immune cell interactions, other mechanisms of action, such as long non-coding RNAs (lncRNAs), also could contribute to the neuropathic pain observed in vivo. LncRNAs have more than 200 nucleotides and were originally considered as transcriptional byproducts. However, recent studies have suggested that lncRNAs played a significant role in gene regulation and disease pathogenesis. A substantial number of long non-coding RNAs were expressed differentially in neuropathic pain models. Besides, therapies targeting specific lncRNAs can significantly ameliorate the development of neuropathic pain, which reveals the contribution of lncRNAs in the generation and maintenance of neuropathic pain and provides a new therapeutic strategy. The primary purpose of this review is to introduce recent studies of lncRNAs on different neuropathic pain models.

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Upregulation of JHDM1D-AS1 alleviates neuroinflammation and neuronal injury via targeting miR-101-3p-DUSP1 in spinal cord after brachial plexus injury

Cited by 26 publications

References 34 publications

The Long Non-Coding Antisense RNA JHDM1D-AS1 Regulates Inflammatory Responses in Human Monocytes

The Long Non-Coding Antisense RNA JHDM1D-AS1 Regulates Inflammatory Responses in Human Monocytes

Therapeutic strategies for brachial plexus injury

Differential Expression of Long Non-Coding RNAs and Their Role in Rodent Neuropathic Pain Models

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