Linarin Protects the Kidney against Ischemia/Reperfusion Injury &lt;i&gt;via&lt;/i&gt; the Inhibition of Bioactive ETS2/IL-12

Yang, Chengyu; Zhao, Liang; Zhou, Bin; Luan, Hong; Shen, Xizhong; Luo, Congjuan; Cao, Christine Do; Xu, Yan

doi:10.1248/bpb.b20-00508

Cited by 9 publications

(11 citation statements)

References 31 publications

(32 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mechanistically, atherogenic conditions could induce ETS2 expression in endothelial cells, and ETS2 enrichment augments the formation and destabilization of atherosclerotic lesions, while ETS2silencing shows therapeutic effects 38 . Evidently, inactivation of ETS2 enhances the anti‐inflammatory effect of linarin in kidney ischemia/reperfusion injury 39 . Activation of ETS2 promotes neutrophil migration and inflammation, but depleting ETS2 ameliorates inflammatory disease and reduces pathology in neutrophilic dermatoses 40 …”

Section: Discussionmentioning

confidence: 99%

“…38 Evidently, inactivation of ETS2 enhances the anti-inflammatory effect of linarin in kidney ischemia/reperfusion injury. 39 Activation of ETS2 promotes neutrophil migration and inflammation, but depleting ETS2 ameliorates inflammatory disease and reduces pathology in neutrophilic dermatoses. 40 In conclusion, our research highlights that the level of miR-145-5p is down-regulated and that of ETS2 is up-regulated and that the TGF-β1/Smad signaling pathway is activated in LPS-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

microRNA‐145‐5p attenuates acute lung injury via targeting ETS2

Qiao

et al. 2022

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

The protective effect of microRNA (miR)‐145‐5p in acute lung injury (ALI) has been discovered previously. Thus, in this study, we attempted to further investigate the mechanism of miR‐145‐5p in ALI through the downstream E26 transformation‐specific proto‐oncogene 2 (ETS2)/transforming growth factor β1 (TGF‐β1)/Smad pathway. A lipopolysaccharide (LPS)‐induced ALI rat model was established. The expression of miR‐145‐5p in ALI rat lung tissues was up‐regulated. Afterward, pathological damage in the lung tissue, the wet/dry (W/D) ratio, apoptosis, and serum inflammatory factor contents were observed. miR‐145‐5p, ETS2, TGF‐β1, Smad2/3, and phosphorylated Smad2/3 levels were measured in rats. miR‐145‐5p expression was down‐regulated, ETS2 expression was up‐regulated, and the TGF‐β1/Smad pathway was activated in LPS‐exposed rats. Overexpression of miR‐145‐5p inactivated the TGF‐β1/Smad pathway and attenuated ALI, as reflected by relieved pathological damage, a decreased W/D ratio, reduced apoptosis, and suppressed inflammatory response. In contrast, loss of miR‐145‐5p or elevated ETS2 levels worsened ALI and activated the TGF‐β1/Smad pathway. Moreover, elevation of ETS2 diminished miR‐145‐5p‐mediated protection against ALI. Evidently, miR‐145‐5p negatively regulates ETS2 expression and inactivates the TGF‐β1/Smad pathway to ameliorate ALI in rats.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

microRNA‐145‐5p attenuates acute lung injury via targeting ETS2

Qiao

et al. 2022

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

show abstract

“…shows therapeutic effects [38]. Evidently, inactivation of ETS2 acts bene cially to enhance the antiin ammatory effect of linarin in kidney ischemia/reperfusion injury [39]. Activation of ETS2 is able to promote neutrophil migration and in ammation, but depleting ETS2 ameliorates in ammatory disease and reduces pathology in neutrophilic dermatoses [40].…”

Section: Discussionmentioning

confidence: 99%

microRNA-145-5p attenuates acute lung injury via targeting ETS2

et al. 2021

Preprint

View full text Add to dashboard Cite

Objective Previously, the protective effect of microRNA (miR)-145-5p has been discovered in acute lung injury (ALI). Thus, this study attempts to further discuss the mechanism of miR-145-5p in ALI through the downstream E26 transformation-specific proto-oncogene 2 (ETS2)/transforming growth factor β1 (TGF-β1)/Smad pathway. Methods A lipopolysaccharide (LPS)-induced rat ALI model was established. Recombinant adenovirus miR-145-5p and/or ETS2 overexpression plasmid was administrated into rats. Afterwards, pathological damage in the lung tissue, wet/dry (W/D) ratio, apoptosis and contents of serum inflammatory factors were observed. miR-145-5p, ETS2, TGF-β1, Smad2/3, phosphorylated Smad2/3 levels were measured in rats. Results miR-145-5p was down-regulated, ETS2 was up-regulated and TGF-β1/Smad pathway was activated in LPS-suffered rats. Overexpression of miR-145-5p inactivated the TGF-β1/Smad pathway and attenuated ALI, as reflected by relived pathological damage, and decreased W/D ratio, apoptosis and inflammatory response. Oppositely, loss of miR-145-5p or enhancement of ETS2 worsened ALI and activated the TGF-β1/Smad pathway. Moreover, elevation of ETS2 decreased miR-145-5p-mediated protection against ALI. Conclusion Evidently, miR-145-5p negatively regulates ETS2 expression and inactivates TGF-β1/Smad pathway to ameliorate ALI in rats.

show abstract

“…CXCL10 [76], SIGLEC1 [77] and IL1R2 [78] have been suggested to be associated with neurological diseases. CXCL9 [79], SIGLEC1 [80], IL1R2 [81], KLF15 [82] and CD207 [83] [146], STAT4 [147], CXCL8 [148], KLF2 [149], ADM (adrenomedullin) [150], EGR1 [151], TRIB1 [152], SOD2 [153], OXSR1 [154], IL6R [155], CD44 [156], LRG1 [157], PFKFB2 [158], PACSIN2 [159], MYH9 [160], DOT1L [161], CXCL16 [162], PTEN (phosphatase and tensin homolog) [163], FOXO3 [164], DDIT4 [165], PINK1 [166], IQGAP1 [167], ADIPOR1 [168], MTMR3 [169], USF2 [170], SGK1 [171], GSTO2 [172], ETS2 [173], TKT (transketolase) [174], CMIP (c-Maf inducing protein) [175], THBD (granzyme A) [464], IFNG (interferon gamma) [465], IFIH1 [466], STAT1 [467], CCR5 [468], ADCY5 [469], MT2A [470], DPP4 [471], FASLG (Fas ligand)…”

Section: Discussionmentioning

confidence: 99%

Screening key genes and signaling pathways in COVID-19 infection and its associated complications by integrated bioinformatics analysis

Vastrad¹,

Vastrad²

2021

Preprint

View full text Add to dashboard Cite

Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2)/ coronavirus disease 2019 (COVID-19) infection is the leading cause of respiratory tract infection associated mortality worldwide. The aim of the current investigation was to identify the differentially expressed genes (DEGs) and enriched pathways in COVID-19 infection and its associated complications by bioinformatics analysis, and to provide potential targets for diagnosis and treatment. Valid next-generation sequencing (NGS) data of 93 COVID 19 samples and 100 non COVID 19 samples (GSE156063) were obtained from the Gene Expression Omnibus database. Gene ontology (GO) and REACTOME pathway enrichment analysis was conducted to identify the biological role of DEGs. In addition, a protein-protein interaction network, modules, miRNA-hub gene regulatory network, TF-hub gene regulatory network and receiver operating characteristic curve (ROC) analysis were used to identify the key genes. A total of 738 DEGs were identified, including 415 up regulated genes and 323 down regulated genes. Most of the DEGs were significantly enriched in immune system process, cell communication, immune system and signaling by NTRK1 (TRKA). Through PPI, modules, miRNA-hub gene regulatory network, TF-hub gene regulatory network analysis, ESR1, UBD, FYN, STAT1, ISG15, EGR1, ARRB2, UBE2D1, PRKDC and FOS were selected as hub genes, which were expressed in COVID-19 samples relative to those in non COVID-19 samples, respectively. Among them, ESR1, UBD, FYN, STAT1, ISG15, EGR1, ARRB2, UBE2D1, PRKDC and FOS were suggested to be diagonstic factors for COVID-19. The findings from this bioinformatics analysis study identified molecular mechanisms and the key hub genes that might contribute to COVID-19 infection and its associated complications.

show abstract

Linarin Protects the Kidney against Ischemia/Reperfusion Injury <i>via</i> the Inhibition of Bioactive ETS2/IL-12

Cited by 9 publications

References 31 publications

microRNA‐145‐5p attenuates acute lung injury via targeting ETS2

microRNA‐145‐5p attenuates acute lung injury via targeting ETS2

microRNA-145-5p attenuates acute lung injury via targeting ETS2

Screening key genes and signaling pathways in COVID-19 infection and its associated complications by integrated bioinformatics analysis

Contact Info

Product

Resources

About