Long non-coding RNA H19 contributes to spinal cord ischemia/reperfusion injury through increasing neuronal pyroptosis by miR-181a-5p/HMGB1 axis

Guo, Lili; Wang, Dan; Alexander, Hildrich Yasmal; Ren, Xiaoyan; Ma, Hong

doi:10.18632/aging.204160

Cited by 7 publications

(5 citation statements)

References 42 publications

(47 reference statements)

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“…After lysis and centrifugation, the supernatant was collected. According to the methods provided by the kit supplier (Beyotime Biotechnology, Shanghai, China), the levels of TNF-α (PT512), IL-1β (PI301), and IL-18 (PI553) were determined by enzyme-linked immunosorbent assay (ELISA) (Guo et al 2022 ).…”

Section: Methodsmentioning

confidence: 99%

AQP3-mediated activation of the AMPK/SIRT1 signaling pathway curtails gallstone formation in mice by inhibiting inflammatory injury of gallbladder mucosal epithelial cells

Wang,

Zhang,

Zhou

et al. 2023

Mol Med

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Background Inflammatory injury of gallbladder mucosal epithelial cells affects the development of cholelithiasis, and aquaporin 3 (AQP3) is an important regulator of inflammatory response. This study reports a mechanistic insight into AQP3 regulating gallstone formation in cholelithiasis based on high-throughput sequencing. Methods A mouse model of cholelithiasis was induced using a high-fat diet, and the gallbladder tissues were harvested for high-throughput sequencing to obtain differentially expressed genes. Primary mouse gallbladder mucosal epithelial cells were isolated and induced with Lipopolysaccharides (LPS) to mimic an in vitro inflammatory injury environment. Cell biological phenotypes were detected by TdT-mediated dUTP Nick-End Labeling (TUNEL) assay, flow cytometry, Cell Counting Kit-8 (CCK-8) assay, and Trypan blue staining. In addition, enzyme linked immunosorbent assay (ELISA) determined the production of inflammatory factors in mouse gallbladder mucosa. Results Whole-transcriptome sequencing data analysis identified 489 up-regulated and 1007 down-regulated mRNAs. Bioinformatics analysis revealed that AQP3 was significantly down-regulated in mice with cholelithiasis. AQP3 might also confer an important role in LPS-induced gallbladder mucosal injury. Overexpression of AQP3 activated the AMPK (adenosine monophosphate-activated protein kinase) / SIRT1 (sirtuin-1) signaling pathway to reduce LPS-induced inflammatory injury of the gallbladder mucosa epithelium, thereby ameliorating gallbladder damage and repressing gallstone formation in mice. Conclusion Data from our study highlight the inhibitory role of AQP3 in gallbladder damage and gallstone formation in mice by reducing inflammatory injury of gallbladder mucosal epithelial cells, which is achieved through activation of the AMPK/SIRT1 signaling pathway.

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Section: Methodsmentioning

confidence: 99%

AQP3-mediated activation of the AMPK/SIRT1 signaling pathway curtails gallstone formation in mice by inhibiting inflammatory injury of gallbladder mucosal epithelial cells

Wang,

Zhang,

Zhou

et al. 2023

Mol Med

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“…However, poly(dA)oligo(dT), nucleotides composed of a 2:1 mix of poly(dA) and 18-mer oligo(dT) (Masuda et al, 2018), can reverse the above effect and accelerate neuronal pyroptosis. Guo et al (2022) proposed that PC12 suffering OGD/R or SCIRI could increase the expression level of lncRNA H19 and aggravate neuronal pyroptosis. MiR-181a-5p, a negative regulator of HMGB1, was inhibited by upstream lncRNA H19.…”

Section: Neuronmentioning

confidence: 99%

“… Guo et al (2022) proposed that PC12 suffering OGD/R or SCIRI could increase the expression level of lncRNA H19 and aggravate neuronal pyroptosis. MiR-181a-5p, a negative regulator of HMGB1, was inhibited by upstream lncRNA H19.…”

Section: Pyroptosis Of Different Cell Types Following Spinal Cord Injurymentioning

confidence: 99%

“…MiR-181a-5p, a negative regulator of HMGB1, was inhibited by upstream lncRNA H19. LncRNA H19 silence or knockdown alleviated SCIRI induced neuronal pyroptosis by downregulating HMGB1 ( Guo et al, 2022 ). Exosomes (EXOs) are important messengers for intercellular communication in various biological processes.…”

Section: Pyroptosis Of Different Cell Types Following Spinal Cord Injurymentioning

confidence: 99%

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Pyroptosis in spinal cord injury

Yin

Gong²,

Wan³

et al. 2022

Front. Cell. Neurosci.

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Spinal cord injury (SCI) often brings devastating consequences to patients and their families. Pathophysiologically, the primary insult causes irreversible damage to neurons and glial cells and initiates the secondary damage cascade, further leading to inflammation, ischemia, and cells death. In SCI, the release of various inflammatory mediators aggravates nerve injury. Pyroptosis is a new pro-inflammatory pattern of regulated cell death (RCD), mainly mediated by caspase-1 or caspase-11/4/5. Gasdermins family are pore-forming proteins known as the executor of pyroptosis and the gasdermin D (GSDMD) is best characterized. Pyroptosis occurs in multiple central nervous system (CNS) cell types, especially plays a vital role in the development of SCI. We review here the evidence for pyroptosis in SCI, and focus on the pyroptosis of different cells and the crosstalk between them. In addition, we discuss the interaction between pyroptosis and other forms of RCD in SCI. We also summarize the therapeutic strategies for pyroptosis inhibition, so as to provide novel ideas for improving outcomes following SCI.

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“…[ 6 ] Moreover, NLRP3‐dependent neuronal pyroptosis occurs in SCIR. [ 7 ] Taken together, PANoptosis may be the main cause of the mass neural death in SCIR.…”

Section: Introductionmentioning

confidence: 99%

Melatonin Exerts an Anti‐Panoptoic Role in Spinal Cord Ischemia‐Reperfusion Injured Rats

Xie,

Wu,

Shi

et al. 2023

Advanced Biology

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Paraplegia is a serious consequence of spinal cord ischemia‐reperfusion (SCIR) injury, which leads to neuron death and permanent loss of motor function. However, there is no effective treatment for SCIR. Melatonin exerts a neuroprotective effect in neurodegenerative diseases. However, whether pyroptosis, apoptosis, and necroptosis (PANoptosis) is the primary cause of the massive neural death in SCIR is unknown, and if melatonin exhibits anti‐PANoptotic effect in rescuing the disastrous damage is to be decided. This study indicates that melatonin confers neuroprotection in SCIR, attenuating the loss of Nissl body and improving Basso, Beattie & Bresnahan locomotor rating scale scores. Specifically, the apoptotic hallmarks in neurons are increased in SCIR injured spinal cord compared to the sham group. The upregulated trend is reversed by melatonin while the effect of melatonin is abolished by the administration of luzindole, a selective melatonin receptor antagonist. Moreover, similar patterns are found in the necroptotic markers in neurons, the pyroptotic indicators, and the interleukin‐1β staining in microglia. In conclusion, PANoptosis may underlie the mass neural death and paraplegia in SCIR, and melatonin confers neuroprotection to the spinal cord via inhibiting PANoptosis.

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Long non-coding RNA H19 contributes to spinal cord ischemia/reperfusion injury through increasing neuronal pyroptosis by miR-181a-5p/HMGB1 axis

Cited by 7 publications

References 42 publications

AQP3-mediated activation of the AMPK/SIRT1 signaling pathway curtails gallstone formation in mice by inhibiting inflammatory injury of gallbladder mucosal epithelial cells

AQP3-mediated activation of the AMPK/SIRT1 signaling pathway curtails gallstone formation in mice by inhibiting inflammatory injury of gallbladder mucosal epithelial cells

Pyroptosis in spinal cord injury

Melatonin Exerts an Anti‐Panoptoic Role in Spinal Cord Ischemia‐Reperfusion Injured Rats

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