Long non‐coding <scp>RNA XIST</scp> alleviates sepsis‐induced acute kidney injury through inhibiting inflammation and cell apoptosis via regulating <scp>miR</scp>‐155‐5p/<scp>WWC1</scp> axis

Wang, Lei; Cao, Qiumei

doi:10.1002/kjm2.12442

Cited by 16 publications

(14 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among the upstream lncRNAs of hsa-let-7b-5p, only XIST has been found to be involved in sepsis regulation. Studies have shown that silencing or downregulation of XIST expression protects against sepsis-induced multiorgan dysfunction (Wang et al, 2021;Wang and Cao, 2022). Findings from those studies are consistent with our prediction that XIST−hsa-let-7b-5p−TGFBR1/DUSP1 may be a vital ceRNA regulatory network in sepsis.…”

Section: Discussionsupporting

confidence: 91%

Identification of the key ferroptosis-related genes involved in sepsis progression and experimental validation in vivo

Liu

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Background: Ferroptosis has a vital role in sepsis, but the mechanism is not known. Understanding the mechanism of ferroptosis during sepsis will aid in developing improved therapeutic strategies.Methods: We used the Gene Expression Omnibus database and FerrDb database to obtain ferroptosis-related differentially expressed genes (DEGs) between sepsis patients and healthy volunteers (HVs). Analyses of PPI networks, functional enrichment, as well as use of the MCODE algorithm were used to identify key ferroptosis-related DEGs. Expression of key ferroptosis-related DEGs was verified using: GSE57065 and GSE65682 datasets; rats in which ferroptosis was induced with erastin; sepsis-induced acute lung injury (siALI) rats. The effects of acupoint catgut embedding (ACE) on ferroptosis and expression of key ferroptosis-related DEGs in the lungs of siALI rats were also observed. A Cox proportional hazard model was used to verify the effect of key ferroptosis-related DEGs on the survival of sepsis patients. Cytoscape was used to construct ceRNA networks and gene–transcription factor networks.Results: Between sepsis patients and HVs, we identified 33 ferroptosis-related DEGs. According to analyses of PPI networks and the MCODE algorithm, we obtained four modules, of which the most significant module contained nine ferroptosis-related DEGs. Functional-enrichment analyses showed that four of the nine DEGs were enriched in the MAPK signaling pathway: MAPK14, VEGFA, TGFBR1, and DUSP1. We verified expression of these four genes in GSE57065 and GSE65682 datasets and ferroptosis rats. In addition, expression of these four genes and that of the oxidative-stress indicators GSSG and MDA was upregulated, and glutathione peroxidase-4 (GPX4) expression was downregulated, in siALI rats, but ACE reversed these changes. The Cox proportional hazard model showed that survival of sepsis patients in the high-risk group was shorter than that in the low-risk group. We found that the XIST−hsa-let-7b-5p−TGFBR1/DUSP1 ceRNA network and transcription factor E2F1 may be important regulators of these four DEGs.Conclusion: Our results suggest that MAPK14, VEGFA, TGFBR1, and DUSP1 may be key regulatory targets of ferroptosis in sepsis, and that ACE pretreatment may be antioxidant treatment for sepsis and alleviate ferroptosis. These findings provide a basis for further ferroptosis-related study in sepsis and provide new targets for its treatment.

show abstract

Section: Discussionsupporting

confidence: 91%

Identification of the key ferroptosis-related genes involved in sepsis progression and experimental validation in vivo

Liu

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…lncRNA CTBP1-AS2 targets miR-155-5p and upregulates FOXO1 to abate HG-elicited proliferation, oxidative stress, ECM accumulation, and inflammation in human glomerular mesangial cells [ 32 ]. lncRNA XIST targets miR-155-5p and upregulates WWC1 to dampen inflammatory cytokine generation and cell apoptosis, hence attenuating acute kidney injury induced by sepsis [ 33 ]. Here, we discovered that miR-155-5p’s expression was greatly uplifted in the plasma and lung tissues of the SAP-ALI rats, but SGB notably drove down its expression.…”

Section: Discussionmentioning

confidence: 99%

Stellate ganglion block relieves acute lung injury induced by severe acute pancreatitis via the miR-155-5p/SOCS5/JAK2/STAT3 axis

Wang

et al. 2022

Eur J Med Res

Self Cite

View full text Add to dashboard Cite

Acute lung injury (ALI), a prevalent complication of severe acute pancreatitis (SAP), is also a leading contributor to respiratory failure and even death of SAP patients. Here, we intended to investigate the function and mechanism of stellate ganglion block (SGB) in ameliorating SAP-induced ALI (SAP-ALI). We engineered an SAP-ALI model in rats and treated them with SGB. HE staining and the dry and wet method were implemented to evaluate pathological alterations in the tissues and pulmonary edema. The rats serum changes of the profiles of TNF-α, IL-6, IL-1β, and IL-10 were examined. The profiles of miR-155-5p and SOCS5/JAK2/STAT3 were detected. Functional assays were performed for confirming the role of miR-155-5p in modulating the SOCS5/JAK2/STAT3 pathway in pulmonary epithelial cells. Our findings revealed that SGB vigorously alleviated SAP rat lung tissue damage and lung edema and lessened the generation of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β. SGB enhanced SOCS5 expression, hampered miR-155-5p, and suppressed JAK2/STAT3 pathway activation. As evidenced by mechanism studies, miR-155-5p targeted the 3′UTR of SOCS5 and repressed its expression, hence resulting in JAK2/STAT3 pathway activation. During animal trials, we discovered that SGB ameliorated SAP-ALI, boosted SOCS5 expression, and mitigated the levels of pro-inflammatory factors and miR-155-5p in the plasma. In vitro, miR-155-5p overexpression substantially facilitated pulmonary epithelial cell apoptosis, inflammation, and JAK2/STAT3 pathway activation and restrained SOCS5 expression. All in all, our work hinted that SGB could modulate the miR-155-5p/SOCS5/JAK2/STAT3 axis to alleviate SAP-ALI.

show abstract

“…The impact of Xist expression on inflammation appears to be context dependent and has not yet been investigated in the context of NSCs. Some studies have found that it promotes inflammation ( Chen et al., 2021 ; Yan et al., 2022a ) and others that it reduces inflammation ( Shenoda et al., 2021 ; Wang and Cao, 2022 ). Therefore the apparently contradictory patterns of expression observed in Sox2ot and Xist may be due to multiple regulatory mechanisms acting in parallel.…”

Section: Discussionmentioning

confidence: 99%

What has single-cell transcriptomics taught us about long non-coding RNAs in the ventricular-subventricular zone?

Becker¹,

Sun²,

Alammari³

et al. 2023

Stem Cell Reports

View full text Add to dashboard Cite

Long non‐coding RNA XIST alleviates sepsis‐induced acute kidney injury through inhibiting inflammation and cell apoptosis via regulating miR‐155‐5p/WWC1 axis

Cited by 16 publications

References 33 publications

Identification of the key ferroptosis-related genes involved in sepsis progression and experimental validation in vivo

Identification of the key ferroptosis-related genes involved in sepsis progression and experimental validation in vivo

Stellate ganglion block relieves acute lung injury induced by severe acute pancreatitis via the miR-155-5p/SOCS5/JAK2/STAT3 axis

What has single-cell transcriptomics taught us about long non-coding RNAs in the ventricular-subventricular zone?

Contact Info

Product

Resources

About