Clinical value of lncRNA SOX2-OT in pulmonary arterial hypertension and its role in pulmonary artery smooth muscle cell proliferation, migration, apoptosis, and inflammatory

Jiang, Yunfei; Hei, Bingchang; Hao, Wenbo; Shu-dong, Lin; Wang, Yuanyuan; Liu, Xuzhi; Meng, Xianguo; Guan, Zhanjiang

doi:10.1016/j.hrtlng.2022.04.002

Cited by 15 publications

(14 citation statements)

References 41 publications

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“…Studies have revealed that HSPA8 [262], HSP90AA1 [259], MYH9 [339], SORT1 [335], ACTA2 [307], SOX2 [773], SMAD4 [774], GATA2 [775], CCND1 [776], SPI1 [777] and SMARCA4 [778] plays a key role in cardiovascular diseases. The altered expression of HSPA8 [174], MYH9 [209], FLNA (filamin A) [444], SOX2 [779], GATA2 [780], EP300 [781] and SMARCA4 [782] plays a key role in the progression of hypertension. HSPA8 [600], MYH9 [647], CDH1 [630], SORT1 [643], ACTA2 [626], RARA (retinoic acid receptor alpha) [656], hsa-mir-152-3p [783], SOX2 [784] and EP300 [785] are mainly associated with type 2 diabetes mellitus.…”

Section: Discussionmentioning

confidence: 99%

Screening and identification of key biomarkers in diabetic kidney disease and its complications: Evidence from bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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Diabetic patients are prone to diabetic kidney disease (DKD), which may cause cardiovascular damage, hypertension and obesity, and reduce quality of life. As a result, the life quality of patients was seriously reduced. However, the pathogenesis of diabetic kidney disease (DKD) has not been fully elucidated, and current treatments remain inadequate. Therefore, it is essential to explore the molecular mechanism of DKD and its complications. Next Generation Sequancing (GSE217709) dataset was obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were picked out by R software. Then Gene ontology (GO) and REACTOME pathway enrichment analysis were performed by g:Profiler database, protein-protein interaction (PPI) of DEGs was constructed by Human Integrated Protein-Protein Interaction rEference (HIPPIE) database . Module analysis was carried out by Cytoscape plug-in PEWCC. Subsequently, miRNA-hub gene regulatory network and TF- hub gene regulatory network were performed by miRNet database and NetworkAnalyst database. Finally, validation of hub genes was performed by receiver operating characteristic (ROC) curve analysis to predict the diagnostic effectiveness of the hub genes. In total, 958 DEGs, including 479 up regulated and 479 down regulated genes, were identified. The GO and pathway enrichment changes of DEGs were mainly enriched in biological regulation, multicellular organismal process, signaling by GPCR and extracellular matrix organization. Ten hub genes (HSPA8, HSP90AA1, HSPA5, SDCBP, HSP90B1, VCAM1, MYH9, FLNA, MDFI and PML) associated with DKD and its complications were identified. Bioinformatics analysis is a useful tool to explore the molecular mechanism and pathogenesis of DKD and its complications. The identified hub genes may participate in the onset and development of DKD and its complications and serve as therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Screening and identification of key biomarkers in diabetic kidney disease and its complications: Evidence from bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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“…Notably, miR-21 overexpression facilitated chronic hypoxia-induced PASMC proliferation and pulmonary vascular remodeling, and the possible mechanism was that miR-21 negatively regulated the E3 ubiquitin ligase WWP1 and then activated TGF-b1 signaling in mice in vivo and in vitro (110). Furthermore, Jiang, Hei, et al (111) identified that increased lncRNA SOX2-OT promoted PASMC growth and migration by negatively reducing downstream miR-455-3p expression and elevating SUMO1 levels. In contrast, miR-92b-3P suppressed the proliferation of PASMCs under hypoxic conditions and improved PAH by inhibiting USP28 expression in vitro (112).…”

Section: Crosstalk Between Ubiquitin Ligases and Ncrnas Drives In Hyp...mentioning

confidence: 99%

“…Accumulating evidence has illustrated that several miRNAs and lncRNAs are associated with the progression of PAH through the involvement of ubiquitination. Three ncRNAs, miR-27b-3p, miR-21 and lncRNA SOX2-OT, promoted the proliferation of pulmonary artery smooth muscle cells (PASMCs) via downregulation of FBXW7 and WWP1 and upregulation of SUMO1 ( 109 – 111 ). The researchers revealed that overexpression of miR-27b-3p could significantly elevate GLI1 expression through inhibition of ubiquitin ligase FBXW7 expression and accelerating KLF5 accumulation by attenuating its ubiquitination degradation in rats in vivo ( 109 ).…”

Section: Crosstalk Between Ubiquitin Ligases and Ncrnas Drives In Hyp...mentioning

confidence: 99%

“…Furthermore, Jiang, Hei, et al. ( 111 ) identified that increased lncRNA SOX2-OT promoted PASMC growth and migration by negatively reducing downstream miR-455-3p expression and elevating SUMO1 levels. In contrast, miR-92b-3P suppressed the proliferation of PASMCs under hypoxic conditions and improved PAH by inhibiting USP28 expression in vitro ( 112 ).…”

Section: Crosstalk Between Ubiquitin Ligases and Ncrnas Drives In Hyp...mentioning

confidence: 99%

“…For the treatment of vascular diseases, silencing of ncRNAs provides potential therapeutic strategies by inducing ubiquitination degradation (miR-29a, miR-181b, lncRNA-Fendrr, lncRNA MIAT, lncRNA SNHG, miR-21, miR-424(322)) or inhibiting the deubiquitinating enzyme BRCC3/SUMO1 (lncRNA NEAT1, lncRNA SOX2-OT) ( 73 , 82 , 93 , 96 , 98 , 100 , 110 , 111 , 116 ). First, knocking down lncRNA NEAT1 can exert anti-inflammatory effects and protect endothelial cells by regulating the miR−204/BRCC3 axis ( 73 ).…”

Section: Prognostic and Therapeutic Targetsmentioning

confidence: 99%

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Crosstalk between ubiquitin ligases and ncRNAs drives cardiovascular disease progression

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Cardiovascular diseases (CVDs) are multifactorial chronic diseases and have the highest rates of morbidity and mortality worldwide. The ubiquitin–proteasome system (UPS) plays a crucial role in posttranslational modification and quality control of proteins, maintaining intracellular homeostasis via degradation of misfolded, short-lived, or nonfunctional regulatory proteins. Noncoding RNAs (ncRNAs, such as microRNAs, long noncoding RNAs, circular RNAs and small interfering RNAs) serve as epigenetic factors and directly or indirectly participate in various physiological and pathological processes. NcRNAs that regulate ubiquitination or are regulated by the UPS are involved in the execution of target protein stability. The cross-linked relationship between the UPS, ncRNAs and CVDs has drawn researchers’ attention. Herein, we provide an update on recent developments and perspectives on how the crosstalk of the UPS and ncRNAs affects the pathological mechanisms of CVDs, particularly myocardial ischemia/reperfusion injury, myocardial infarction, cardiomyopathy, heart failure, atherosclerosis, hypertension, and ischemic stroke. In addition, we further envision that RNA interference or ncRNA mimics or inhibitors targeting the UPS can potentially be used as therapeutic tools and strategies.

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The emerging role of long non-coding RNA SOX2-OT in cancers and non-malignant diseases

Yang,

Tan,

Chen

et al. 2024

J Physiol Biochem

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Clinical value of lncRNA SOX2-OT in pulmonary arterial hypertension and its role in pulmonary artery smooth muscle cell proliferation, migration, apoptosis, and inflammatory

Cited by 15 publications

References 41 publications

Screening and identification of key biomarkers in diabetic kidney disease and its complications: Evidence from bioinformatics and next generation sequencing data analysis

Screening and identification of key biomarkers in diabetic kidney disease and its complications: Evidence from bioinformatics and next generation sequencing data analysis

Crosstalk between ubiquitin ligases and ncRNAs drives cardiovascular disease progression

The emerging role of long non-coding RNA SOX2-OT in cancers and non-malignant diseases

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