LncRNA XIST serves as a diagnostic biomarker in gestational diabetes mellitus and its regulatory effect on trophoblast cell via miR-497-5p/FOXO1 axis

Li, Yanchuan; Yuan, Xiaohui; Shi, Ziyun; Wang, Haili; Ren, Duomei; Ya, Zhang; Fan, Yangyang; Liu, Yanfeng; Cui, Zhangxia

doi:10.21037/cdt-21-110

Cited by 16 publications

(13 citation statements)

References 36 publications

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“…Our research exhibited that the lncRNA XIST was expressed in abundance in the plasma of DVT patients compared with the plasma of normal people. There were similar reports in other cardiovascular diseases related to DVT [9][10][11]. In addition, we found that lncRNA XIST knockdown could increase cell viability and reduce apoptosis and ameliorate the change of TF level in HUVECs induced by IL-1β.…”

Section: Discussionsupporting

confidence: 87%

Knockdown of lncRNA XIST Ameliorates IL-1β-Induced Apoptosis of HUVECs and Change of Tissue Factor Level via miR-103a-3p/HMGB1 Axis in Deep Venous Thrombosis by Regulating the ROS/NF-κB Signaling Pathway

Cao

Zhou

Wang

et al. 2022

Cardiovascular Therapeutics

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Background. The effect of lncRNA X inactive-specific transcript (XIST) inducing cardiovascular diseases on deep vein thrombosis (DVT) and its mechanism has not been reported. In this study, we uncovered the mystery that lncRNA XIST causes DVT with HUVEC dysfunction. Method. The expression levels of lncRNA XIST and miR-103a-3p were detected by qRT-PCR, and HMGB1 expression was determined by qRT-PCR and western blot. The correlations among the expression levels of lncRNA XIST, miR-103a-3p, and HMGB1 were determined by Spearman’s rank-order correlation test. XIST siRNA (si-XIST) was transfected into HUVECs to knock down the intrinsic expression of lncRNA XIST. The influences of si-XIST on interleukin-1 beta- (IL-1β-) treated HUVEC viability and apoptosis and the level of tissue factor (TF) were detected by MTT, flow cytometry, and ELISA kit, respectively. The relationships between lncRNA XIST, miR-103a-3p, and HMGB1 were predicted by the Encyclopedia of RNA Interactomes (ENCORI) database and verified by dual luciferase reporter assay. The effects of lncRNA XIST and miR-103a-3p on HMGB1 expression were detected by qRT-PCR, western blot, and immunofluorescence analysis. The levels of ROS/NF-κB pathway-related proteins were detected to study the regulatory mechanism of lncRNA XIST/miR-103a-3p/HMGB1 on IL-1β-treated HUVECs apoptosis and change of TF level. Results. The upregulated expression levels of lncRNA XIST and HMGB1 and downregulated level of miR-103a-3p were found in the plasma of DVT patients and IL-1β-treated HUVECs. Si-XIST promoted cell viability and inhibited HUVEC apoptosis and ameliorated the change of TF level triggered by IL-1β. lncRNA XIST sponged miR-103a-3p and miR-103a-3p targeted HMGB1. Si-XIST inhibited the ROS/NF-κB pathway to suppress HUVEC apoptosis and ameliorate the change of TF level induced by IL-1β via the miR-103a-3p/HMGB1 axis. Conclusion. lncRNA XIST sponged miR-103a-3p improving HMGB1 expression to exacerbate DVT by activating the ROS/NF-κB signaling pathway. Our findings indicated that lncRNA XIST can be used as a potential therapeutic target in DVT.

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Section: Discussionsupporting

confidence: 87%

Knockdown of lncRNA XIST Ameliorates IL-1β-Induced Apoptosis of HUVECs and Change of Tissue Factor Level via miR-103a-3p/HMGB1 Axis in Deep Venous Thrombosis by Regulating the ROS/NF-κB Signaling Pathway

Cao

Zhou

Wang

et al. 2022

Cardiovascular Therapeutics

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“…The protein PSMB8 was observed in the proteosome that is responsible for ATP-dependent protein degradation, which is a direct reason for developing T2D [ 60 ]. Patients with T2D had a higher level of XIST expression than those without diabetes [ 61 ]. Type 2 diabetes risk is substantially increased by DUSP8 expression in individuals [ 62 ].…”

Section: Resultsmentioning

confidence: 99%

Statistical Bioinformatics to Uncover the Underlying Biological Mechanisms That Linked Smoking with Type 2 Diabetes Patients Using Transcritpomic and GWAS Analysis

et al. 2022

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Type 2 diabetes (T2D) is a chronic metabolic disease defined by insulin insensitivity corresponding to impaired insulin sensitivity, decreased insulin production, and eventually failure of beta cells in the pancreas. There is a 30–40 percent higher risk of developing T2D in active smokers. Moreover, T2D patients with active smoking may gradually develop many complications. However, there is still no significant research conducted to solve the issue. Hence, we have proposed a highthroughput network-based quantitative pipeline employing statistical methods. Transcriptomic and GWAS data were analysed and obtained from type 2 diabetes patients and active smokers. Differentially Expressed Genes (DEGs) resulted by comparing T2D patients’ and smokers’ tissue samples to those of healthy controls of gene expression transcriptomic datasets. We have found 55 dysregulated genes shared in people with type 2 diabetes and those who smoked, 27 of which were upregulated and 28 of which were downregulated. These identified DEGs were functionally annotated to reveal the involvement of cell-associated molecular pathways and GO terms. Moreover, protein–protein interaction analysis was conducted to discover hub proteins in the pathways. We have also identified transcriptional and post-transcriptional regulators associated with T2D and smoking. Moreover, we have analysed GWAS data and found 57 common biomarker genes between T2D and smokers. Then, Transcriptomic and GWAS analyses are compared for more robust outcomes and identified 1 significant common gene, 19 shared significant pathways and 12 shared significant GOs. Finally, we have discovered protein–drug interactions for our identified biomarkers.

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“…Further research has shown that diabetes is partly attributed to cell damage, namely, apoptosis of the islet β cells. The inflammatory and anti-inflammatory factors released by islet cells include IL-1 and IL-10, and the imbalance of these inflammatory and anti-inflammatory factors secreted may cause islet β-cell damage and lead to its death ( Li et al, 2021c ; Li et al, 2021a ; Tanwar et al, 2021 ). Functionally, insulin promotes glucose uptake and glycogen synthesis, and the glycogen synthesis is a further factor affecting the absorption and metabolism of blood sugar, which increases insulin sensitivity.…”

Section: Discussionmentioning

confidence: 99%

The regulatory effect and molecular mechanism of lncRNA Gm10451 on islet cell dysfunction in children with diabetes

Wang

Zhang²,

Kang³

et al. 2022

Front. Genet.

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The dysfunction of islet β-cells is one of the causes of diabetes, and lncRNA Gm10451 is also a participant in the occurrence and the development of various diseases. This study was carried out to reveal the correlation within β-cells and Gm10451. Our study was started with the cellular cultivation of MIN6 cells in vitro, where this islet β-cell line was randomly divided into the groups of control, hyperglycemia, Gm10451 siRNA tansfection, and Gm10451 tansfection. Of all these treatments, cells in the groups of Gm10451 siRNA tansfection and Gm10451 tansfection were given with lentiviral transfection under hyperglycemia condition. Further explorations were established using PCR assay and MTT method to evaluate Gm10451 expression and estimate cellular proliferation. It ended up with the enzyme-linked immunosorbent assay (ELISA) to assess Caspase 3 activity, superoxide dismutase (SOD) activity, and reactive oxygen species (ROS) content and the secretion of IL-10 and IL-1. It was found that Gm10451 expression in MIN6 cells under hyperglycemia cultivation was notably higher than the control group; likewise, a transfection with the lentivirus of Gm10451 also resulted in the upregulation of Gm10451 expression, succeeded with inhibiting cellular proliferation, enhancing Caspase 3 activity, and decreasing SOD activity. In the lentivirus transfection groups, transfection of Gm10451 elevated the ROS content and promoted IL-1 expression, and it also decreased both IL-10 expression and insulin secretion, leading to a consequence of statistically significant difference in contrast to the high-glucose group; on the contrary, transfection of Gm10451 siRNA in a high-glucose environment downregulated the expression of Gm10451 and inversed those change before, whose results were statistically significant when compared with the high-glucose group. Hyperglycemia promotes the expression of Gm10451. Targeting inhibition toward Gm10451 alleviates cellular apoptosis and the oxidative stress of islet cells, promoting proliferation and insulin secretion of islet cells.

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LncRNA XIST serves as a diagnostic biomarker in gestational diabetes mellitus and its regulatory effect on trophoblast cell via miR-497-5p/FOXO1 axis

Cited by 16 publications

References 36 publications

Knockdown of lncRNA XIST Ameliorates IL-1β-Induced Apoptosis of HUVECs and Change of Tissue Factor Level via miR-103a-3p/HMGB1 Axis in Deep Venous Thrombosis by Regulating the ROS/NF-κB Signaling Pathway

Knockdown of lncRNA XIST Ameliorates IL-1β-Induced Apoptosis of HUVECs and Change of Tissue Factor Level via miR-103a-3p/HMGB1 Axis in Deep Venous Thrombosis by Regulating the ROS/NF-κB Signaling Pathway

Statistical Bioinformatics to Uncover the Underlying Biological Mechanisms That Linked Smoking with Type 2 Diabetes Patients Using Transcritpomic and GWAS Analysis

The regulatory effect and molecular mechanism of lncRNA Gm10451 on islet cell dysfunction in children with diabetes

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