Quietness Circ 0000962 promoted nerve cell inflammation through PIK3CA/Akt/NF-κB signaling by miR-302b-3p in spinal cord injury

He, Rui; Tang, Guo-Lin; Niu, Lei; Ge, Chang; Zhang, Xiaoqi; Ji, Xiaofeng; Huang, Fang; Luo, Zaili; Chen, Min; Shang, Xifu

doi:10.21037/apm.2020.02.13

Cited by 18 publications

(12 citation statements)

References 21 publications

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“… 27 Circ_0000962 was found to have a neuroprotective effect by activating PI3K/Akt and blocking of NF‐κB via miR‐302b‐3p to suppress inflammatory response in vitro cell model of SCI. 28 Additionally, Sun et al showed that circTYW1 contributed to functional recovery in rats after SCI and suppressed apoptosis in the lesion site as well as oxygen‐glucose deprivation (OGD)‐induced PC12 cells by activating ERK1/2 signaling through miR‐380/FGF9 axis. 29 Therefore, circRNAs are also have roles in function recovery after SCI.…”

Section: Discussionmentioning

confidence: 99%

CircSmox knockdown alleviates PC12 cell apoptosis and inflammation in spinal cord injury by miR‐340‐5p/Smurf1 axis

Han

Mou

Jing

et al. 2023

Immunity Inflam & Disease

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Background Spinal cord injury (SCI) is a traumatic central nervous system disorder that leads to irreversible neurological dysfunction. Emerging evidence has shown that differentially expressed circular RNAs (circRNAs) after SCI is closely associated with the pathophysiological process. Herein, the potential function of circRNA spermine oxidase (circSmox) in functional recovery after SCI was investigated. Methods Differentiated PC12 cells stimulated with lipopolysaccharide (LPS) were employed as an in vitro model for neurotoxicity research. Levels of genes and proteins were detected by quantitative real‐time PCR and Western blot analysis. Cell viability and apoptosis were determined by CCK‐8 assay and flow cytometry. Western blot analysis was used to detect the protein level of apoptosis‐related markers. The levels of interleukin (IL)‐1β, IL‐6, IL‐8, and tumor necrosis factor (TNF)‐α. Dual‐luciferase reporter, RIP, and pull‐down assays were used to confirm the target relationship between miR‐340‐5p and circSmox or Smurf1 (SMAD Specific E3 Ubiquitin Protein Ligase 1). Results LPS elevated the levels of circSmox and Smurf1, but decreased the levels of miR‐340‐5p in PC12 cells in a dose‐dependent manner. Functionally, circSmox silencing alleviated LPS‐induced apoptosis and inflammation in PC12 cells in vitro. Mechanistically, circSmox directly sponged miR‐340‐5p, which targeted Smurf1. Rescue experiments showed that miR‐340‐5p inhibition attenuated the neuroprotective effect of circSmox siRNA in PC12 cells. Moreover, miR‐340‐5p suppressed LPS‐triggered neurotoxicity in PC12 cells, which was reversed by Smurf1 overexpression. Conclusion CircSmox enhances LPS‐induced apoptosis and inflammation via miR‐340‐5p/Smurf1 axis, providing an exciting view of the potential involvement of circSmox in SCI pathogenesis.

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Section: Discussionmentioning

confidence: 99%

CircSmox knockdown alleviates PC12 cell apoptosis and inflammation in spinal cord injury by miR‐340‐5p/Smurf1 axis

Han

Mou

Jing

et al. 2023

Immunity Inflam & Disease

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“…For example, GRB1 relieved SCI via altering miR-130b-5p/TLR4/NF-κB pathway [ 23 ]. circ_0000962 inhibited the inflammation in the SCI cell model via activating PI3K/Akt and inactivating NF-κB by sponging miR-302b-3p [ 7 ]. Thus, we explored the impact of LPS-induced XIST in the NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA XIST knockdown relieves the injury of microglia cells after spinal cord injury by sponging miR-219-5p

Zhong

Bao

et al. 2021

Open Medicine

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Long noncoding RNAs have been demonstrated to play crucial roles in the pathogenesis of spinal cord injury (SCI). In this study, we aimed to explore the roles and underlying mechanisms of lncRNA X-inactive specific transcript (XIST) in SCI progression. SCI mice model was constructed and evaluated by the Basso–Beattie–Bresnahan method. The SCI cell model was constructed by treating BV2 cells with lipopolysaccharide (LPS). The levels of XIST and miR-219-5p were determined by the reverse transcription quantitative polymerase chain reaction. The concentrations of inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Protein levels were measured via western blot assay. Cell viability and apoptosis were evaluated by cell counting kit-8 assay and flow cytometry analysis, respectively. The relationship between XIST and miR-219-5p was analyzed by online tool starBase, dual-luciferase reporter assay, and RNA immunoprecipitation assay. As a result, the XIST level was enhanced and the miR-219-5p level was declined in the SCI mice model. XIST was also upregulated in LPS-induced BV2 cells. LPS treatment restrained BV2 cell viability and accelerated apoptosis and inflammatory response. XIST knockdown effectively weakened LPS-induced BV2 cell injury. miR-219-5p was identified as a target of XIST. Moreover, inhibition of miR-219-5p restored the impacts of XIST knockdown on cell viability, apoptosis, and inflammation in LPS-treated BV2 cells. In addition, LPS-induced XIST promoted the activation of the nuclear factor-κB (NF-κB) pathway by sponging miR-219-5p. In conclusion, XIST silencing promoted microglial cell viability and repressed apoptosis and inflammation by sponging miR-219-5p, thus promoting the recovery of SCI.

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“…Li et al ( 2020 ) reported that the down-regulated Circ0001723 related to miR-380-3p-HIF-1α induces pro-inflammatory effects 1 day after experimental SCI in rats, via NF-κB signaling pathway suppression, including the expression of NLPR3 inflammasome and caspase-1 proteins. In vitro SCI studies in rats have shown that the upregulation of Circ0000962 decreased inflammation, via down-regulation of miR-302b-3p and subsequent modulation of PI3K/Akt and NF-κB signaling pathways (He et al, 2020 ). The high expression of circRNA-2960 was able to promote the secondary injury by sponging the miR-124, exacerbating the inflammatory response and inducing apoptosis (Chen et al, 2021 ).…”

Section: Circrnas In Sci Neuroinflammationmentioning

confidence: 99%

Circular RNAs: The Novel Actors in Pathophysiology of Spinal Cord Injury

Sámano

Mladinić

Mazzone

2021

Front. Integr. Neurosci.

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Spinal Cord Injury (SCI) can elicit a progressive loss of nerve cells promoting disability, morbidity, and even mortality. Despite different triggering mechanisms, a cascade of molecular events involving complex gene alterations and activation of the neuroimmune system influence either cell damage or repair. Effective therapies to avoid secondary mechanisms underlying SCI are still lacking. The recent progression in circular RNAs (circRNAs) research has drawn increasing attention and opened a new insight on SCI pathology. circRNAs differ from traditional linear RNAs and have emerged as the active elements to regulate gene expression as well as to facilitate the immune response involved in pathophysiology-related conditions. In this review, we focus on the impact and possible close relationship of circRNAs with pathophysiological mechanisms following SCI, where circRNAs could be the key transcriptional regulatory molecules to define neuronal death or survival. Advances in circRNAs research provide new insight on potential biomarkers and effective therapeutic targets for SCI patients.

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Quietness Circ 0000962 promoted nerve cell inflammation through PIK3CA/Akt/NF-κB signaling by miR-302b-3p in spinal cord injury

Cited by 18 publications

References 21 publications

CircSmox knockdown alleviates PC12 cell apoptosis and inflammation in spinal cord injury by miR‐340‐5p/Smurf1 axis

CircSmox knockdown alleviates PC12 cell apoptosis and inflammation in spinal cord injury by miR‐340‐5p/Smurf1 axis

Long noncoding RNA XIST knockdown relieves the injury of microglia cells after spinal cord injury by sponging miR-219-5p

Circular RNAs: The Novel Actors in Pathophysiology of Spinal Cord Injury

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