miR-1227-3p participates in the development of fetal growth restriction via regulating trophoblast cell proliferation and apoptosis

Cui, Jiawen; Kang, Xinyi; Shan, Yanxing; Zhang, Mingjin; Gao, Ying; Wu, Wei; Chen, Liping

doi:10.1038/s41598-022-10127-w

Cited by 5 publications

(4 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It disrupts the receptor-ligand relationship, thereby inhibiting TLR9 activation [ 24 ]. HTR-8/SVneo cells are a heterogeneous population of trophoblast and mesenchymal cells characterized by rapid cell division, migration and invasion [ 34 , 35 ], and are commonly used to study the pathological mechanism of major obstetric syndromes involving FGR [ 36 , 37 ]. Therefore, we utilized ODN1668 and HCQ to treat HTR-8/SVneo cells to investigate the role of TLR9 in trophoblast proliferation and migration.…”

Section: Resultsmentioning

confidence: 99%

The Gut Microbiota of Pregnant Rats Alleviates Fetal Growth Restriction by Inhibiting the TLR9/MyD88 Pathway

Tang

et al. 2023

J. Microbiol. Biotechnol.

View full text Add to dashboard Cite

Fetal growth restriction (FGR) is a prevalent obstetric condition. This study aimed to investigate the role of Toll-like receptor 9 (TLR9) in regulating the inflammatory response and gut microbiota structure in FGR. An FGR animal model was established in rats, and ODN1668 and hydroxychloroquine (HCQ) were administered. Changes in gut microbiota structure were assessed using 16S rRNA sequencing, and fecal microbiota transplantation (FMT) was conducted. HTR-8/Svneo cells were treated with ODN1668 and HCQ to evaluate cell growth. Histopathological analysis was performed, and relative factor levels were measured. The results showed that FGR rats exhibited elevated levels of TLR9 and myeloid differentiating primary response gene 88 (MyD88). In vitro experiments demonstrated that TLR9 inhibited trophoblast cell proliferation and invasion. TLR9 upregulated lipopolysaccharide (LPS), LPS-binding protein (LBP), interleukin (IL)-1β and tumor necrosis factor (TNF)-α while downregulating IL-10. TLR9 activated the TARF3-TBK1-IRF3 signaling pathway. In vivo experiments showed HCQ reduced inflammation in FGR rats, and the relative cytokine expression followed a similar trend to that observed in vitro. TLR9 stimulated neutrophil activation. HCQ in FGR rats resulted in changes in the abundance of Eubacterium_coprostanoligenes _group at the family level and the abundance of Eubacterium_coprostanoligenes _group and Bacteroides at the genus level. TLR9 and associated inflammatory factors were correlated with Bacteroides , Prevotella , Streptococcus , and Prevotellaceae_Ga6A1 _group. FMT from FGR rats interfered with the therapeutic effects of HCQ. In conclusion, our findings suggest that TLR9 regulates the inflammatory response and gut microbiota structure in FGR, providing new insights into the pathogenesis of FGR and suggesting potential therapeutic interventions.

show abstract

Section: Resultsmentioning

confidence: 99%

The Gut Microbiota of Pregnant Rats Alleviates Fetal Growth Restriction by Inhibiting the TLR9/MyD88 Pathway

Tang

et al. 2023

J. Microbiol. Biotechnol.

View full text Add to dashboard Cite

show abstract

“…Moreover, seven genes in HIF-1 signaling pathways were screened out with LASSO to construct the logistic regression model including MKNK1, ARNT, FLT1, SERPINE1, ENO3, LDHA, BCL2. MKNK1 was found significantly increased in FGR-affected placenta [ 31 ], while its function in preeclampsia remained to be investigated. Previous study has reported that HIF-1 Beta, encoded by ARNT, is associated with placental morphogenesis, angiogenesis, and cell differentiation [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Diagnostic signature composed of seven genes in HIF-1 signaling pathway for preeclampsia

Yang

Ding

et al. 2023

BMC Pregnancy Childbirth

View full text Add to dashboard Cite

Purpose In this study, we explored the relationship of genes in HIF-1 signaling pathway with preeclampsia and establish a logistic regression model for diagnose preeclampsia using bioinformatics analysis. Method Two microarray datasets GSE75010 and GSE35574 were downloaded from the Gene Expression Omnibus database, which was using for differential expression analysis. DEGs were performed the Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and Gene set enrichment analysis (GSEA). Then we performed unsupervised consensus clustering analysis using genes in HIF-1 signaling pathway, and clinical features and immune cell infiltration were compared between these clusters, as well as the least absolute shrinkage and selection operator (LASSO) method to screened out key genes to constructed logistic regression model, and receiver operating characteristic (ROC) curve was plotted to evaluate the accuracy of the model. Results 57 DEGs were identified, of which GO, KEGG and analysis GSEA showed DEGs were mostly involved in HIF-1 signaling pathway. Two subtypes were identified of preeclampsia and 7 genes in HIF1-signaling pathway were screened out to establish the logistic regression model for discrimination preeclampsia from controls, of which the AUC are 0.923 and 0.845 in training and validation datasets respectively. Conclusion Seven genes (including MKNK1, ARNT, FLT1, SERPINE1, ENO3, LDHA, BCL2) were screen out to build potential diagnostic model of preeclampsia.

show abstract

“…MicroRNAs (miRNAs) are noncoding small RNAs that regulate gene expression at the posttranscriptional level. Bioinformatics analysis showed that MEK1 was a possible target gene of miR520a-5p, but no relevant reports regarding the regulation of MEK1 by miRNAs were found in the previous literature [17][18][19][20]. In this study, the expression levels of miR520a-5p in serum of FGR group and normal birth weight control group were analyzed, and the correlation between miR520a-5p and FGR was discussed, so as to elucidate the related role of miR520a-5p in the pathogenesis of FGR, which is bene cial to provide molecular basis for the early diagnosis of FGR.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of MEK1-MAPK Pathway-based MiR520a-5p in Fetal Growth Restriction

Jha

2023

Preprint

View full text Add to dashboard Cite

this research was developed to investigate the expression level of miR520a-5p in serum of fetal growth restriction (FGR) and the role of its target genes, mitogen-activated protein kinase (MAPK) and mitogen-activated protein kinase 1 (MEK1), in the pathogenesis of FGR. Thirty cases in the FGR group and 30 cases in the normal birth weight group (control group) were selected. MiR520a-5p expression and its target genes MEK1 and MAPK mRNA in the two groups were detected by RT‒PCR. The protein levels of the target genes MEK1 and MAPK of miR520a-5p were determined by Western blotting. The Spearman grade correlation was used to analyze the correlation between the expression levels of miR520a-5p and MEK1 in serum of FGR group and the correlation between MEK1 and MAPK expression. Compared with the control group, the expression of miR520a-5p in the FGR group was significantly increased (P < 0.05). MEK1 and MAPK mRNA levels of miR520a-5p target genes in the FGR group were drastically reduced (P < 0.05), while their protein levels were decreased (P < 0.05). Spearman rank correlation analysis suggested a negative correlation between miR-520a-5p and MEK1 (r = − 0.667; P < 0.05) and a positive correlation between MEK1 and MAPK (r = 0.46; P < 0.05). MEK1 and MAPK mRNA expressions in fetal growth and development were detected, and the decreased expression of MEK1 and MAPK mRNA was correlated with the pathogenesis of FGR. MiR520a-5p may participate in the pathogenesis of FGR through the MIRR520A-5P-MEK1-MAPK signaling pathway.

show abstract

miR-1227-3p participates in the development of fetal growth restriction via regulating trophoblast cell proliferation and apoptosis

Cited by 5 publications

References 37 publications

The Gut Microbiota of Pregnant Rats Alleviates Fetal Growth Restriction by Inhibiting the TLR9/MyD88 Pathway

The Gut Microbiota of Pregnant Rats Alleviates Fetal Growth Restriction by Inhibiting the TLR9/MyD88 Pathway

Diagnostic signature composed of seven genes in HIF-1 signaling pathway for preeclampsia

Mechanism of MEK1-MAPK Pathway-based MiR520a-5p in Fetal Growth Restriction

Contact Info

Product

Resources

About