Apelin Promotes Endothelial Progenitor Cell Angiogenesis in Rheumatoid Arthritis Disease via the miR-525-5p/Angiopoietin-1 Pathway

Chang, Ting‐Kuo; Zhong, You-Han; Liu, Shan‐Chi; Huang, Chien-Chung; Tsai, Cheng-Han; Lee, Hsiang-Ping; Wang, Shih‐Wei; Hsu, Chin‐Jung; Tang, Chih‐Hsin

doi:10.3389/fimmu.2021.737990

Cited by 14 publications

(7 citation statements)

References 53 publications

(78 reference statements)

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“…In addition, miR‐525‐5 could regulate epithelial‐mesenchymal transition and cell proliferation in glioma by targeting Stat‐1 44 . Recently, miR‐525‐5p has been shown to be involved in EPCs angiogenesis in rheumatoid arthritis disease 45 . Our findings suggest that LINC00659 could participate in the regulation of proliferation and apoptosis of endothelial cells (HUVECs) through regulating miR‐525‐5p/Bax axis.…”

Section: Discussionmentioning

confidence: 66%

“… 44 Recently, miR‐525‐5p has been shown to be involved in EPCs angiogenesis in rheumatoid arthritis disease. 45 Our findings suggest that LINC00659 could participate in the regulation of proliferation and apoptosis of endothelial cells (HUVECs) through regulating miR‐525‐5p/Bax axis. However, it should be mentioned that although HUVECs are venous cell lines, they are not from deep veins (such as human saphenous vein endothelial cells).…”

Section: Discussionmentioning

confidence: 77%

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By modulating miR‐525‐5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis

Zhu

Chen

2023

Immunity Inflam & Disease

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Background Deep vein thrombosis (DVT) is a vascular disease that has no effective treatment at present. Endothelial cells play a crucial role in the processes vasoconstriction, platelet activation, and blood coagulation and are an integral part of the vascular response to injury resulting in thrombus formation. Objective The aim of this study was to investigate the roles and mechanisms of long noncoding RNA LINC00659 (LINC00659) in endothelial cells. Methods The functions of LINC00659 and miR‐525‐5p on endothelial cells were explored by cell transfection assays, and the expression levels of LINC00659, miR‐525‐5p, and Bax in human umbilical vein endothelial cells (HUVECs) were assessed with reverse transcriptase‐quantitative polymerase chain reaction (RT‐qPCR). Binding sites of LINC00659 and miR‐525‐5p were subsequently analyzed with bioinformatics software, and validated with dual‐luciferase reporter gene assay. Effects of LINC00659 and miR‐525‐5p on proliferation and apoptosis of HUVECs were detected with MTT (3‐(45)‐dimethylthiahiazo (‐z‐y1)‐35‐di‐phenytetrazoliumromide) assay and flow cytometry. RT‐qPCR and western blot analysis were used to evaluate the mRNA and protein levels of apoptosis‐related markers Bcl‐2 and Bax in HUVECs. Results LINC00659 directly targeted and negatively regulated miR‐525‐5p, and Bax was a target of miR‐525‐5p. Upregulation of LINC00659 could inhibit proliferation and promote apoptosis of HUVECs, while the silencing of LINC00659 could increase the viability of HUVECs and inhibit apoptosis via upregulating miR‐525‐5p. Further mechanistic studies revealed miR‐525‐5p could negatively regulate Bax in HUVECs, and increased the viability of HUVECs and inhibited apoptosis by downregulating Bax expression. Conclusion LINC00659 played an important role in DVT by regulating the apoptosis of vascular endothelial cells through regulating miR‐525‐5p/Bax axis.

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 77%

By modulating miR‐525‐5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis

Zhu

Chen

2023

Immunity Inflam & Disease

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“…Further biological function analysis revealed that among these 7 signal transduction pathways enriched by network pharmacology analysis, excluding the apelin signaling pathway mainly act in physiological processes such as adipogenesis, 30 angiogenesis, 31 cardiovascular functions, 32 calcium signaling pathway related to environmental information processing and energy supply and demand, 33 chemokine signaling pathway regulates immune cell trafficking, 34 TGF-β signaling pathway, AMPK signaling pathway, 35 Wnt signaling pathway 36 and p53 signaling pathway 37 is fibrosis closely related. The top 20 degree targets in PPI analysis were filtered and constructed a target-pathway network to elaborate the key signal pathway the Sch A affected in the treatment of PF among these four fibrosis-related pathways ( Figure 7D ), enriched KEGG pathway analysis of top 20 degree core targets and 4 pathways are visualized in Figure 7E , and TGF-β signaling pathway (3 targets) was the pathway with highest top 20 core targets, compared with AMPK signaling pathway (2 targets), Wnt signaling pathway (2 targets), p53 signaling pathway (1 target).…”

Section: Resultsmentioning

confidence: 99%

The Therapeutic Mechanism of Schisandrol A and Its Metabolites on Pulmonary Fibrosis Based on Plasma Metabonomics and Network Analysis

Qiaolongbatu¹,

Zhao²,

Huang³

et al. 2023

DDDT

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Background: Schisandrol A (Sch A) is the main active ingredient of Schisandra chinensis (Turcz.) Baill. Our previous study showed that Sch A has anti-pulmonary fibrosis (PF) activity, but its metabolic-related mechanisms of action are not clear. Methods: Here, we explored the therapeutic mechanisms of Sch A on PF by ultra-high performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) metabolomics approach and network analysis. The metabolites of Sch A in mice (bleomycin + Sch A high-dose group) plasma were identified based on ultra-high performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS). Results: 32 metabolites were detected reversed to normal level after treating bleomycin (BLM)-induced PF mice with Sch A. The 32 biomarkers were enriched in energy metabolism and several amino acid metabolisms, which was the first report on the therapeutic effects of Sch A on PF through rescuing the disordered energy metabolism. The UPLC-Q-TOF/MS analysis identified 17 possible metabolites (including isomers) of Sch A in mice plasma. Network analysis revealed that Sch A and 17 metabolites were related to 269 genes, and 1109 disease genes were related to PF. The construction of the Sch A/metabolites-target-PF network identified a total of 79 intersection genes and the TGF-β signaling pathway was determined to be the main signaling pathway related to the treatment of PF by Sch A. The integrated approach involving metabolomics and network analysis revealed that the TGF-β1-ID3-creatine pathway, TGF-β1-VIM-carnosine pathway were two of the possible pathways Sch A regulated to modulate metabolic disorders, especially energy metabolism, and the metabolite of Sch A M5 was identified as a most likely active metabolite. Conclusion:The results suggested the feasibility of combining metabolomics and network analysis to reflect the effects of Sch A on the biological network and the metabolic state of PF and to evaluate the drug efficacy of Sch A and its related mechanisms.

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“…These and other results suggest hsa-miR-204 probably acts as a key molecule in the development of AS in RA and deserves further study. In addition, hsa-miR-377, hsa-miR-493, and hsa-miR-525-5p have been reported in either RA or AS ( 68 - 73 ), and whether these miRNAs take part in the other disease is also worthy of further investigation.…”

Section: Discussionmentioning

confidence: 99%

Exploration of the shared gene signatures and molecular mechanisms between atherosclerosis and rheumatoid arthritis via multi-microarray data analyses

You¹,

Zhao²,

Gou³

et al. 2022

Ann Transl Med

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Background: Accumulating evidence indicates the inflammatory state of rheumatoid arthritis (RA) predisposes to the acceleration of atherosclerosis (AS). Nevertheless, the potential mechanisms of accelerating AS in RA have not been fully elucidated. Our current study was to probe the problem via multimicroarray data analyses. Methods:The transcriptional profiling of synovial tissues from RA (GSE55235 and GSE55457) and that of atherosclerotic plaques from AS (GSE28829 and GSE41571) were downloaded from the Gene Expression Omnibus database. Bioinformatics analyses procedures included identifying common differentially expressed genes (DEGs), constructing protein-protein interaction network, key modules analysis and identifying hub genes, validating hub genes by using external datasets (GSE77298 and GSE163154), Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, constructing TF-miRNA coregulatory network and exploiting candidate drugs targeting hub genes.Results: A total of 67 common DEGs were identified for downstream analyses. GO and KEGG analyses of these genes expounded a critical role of inflammatory mediators and reactions in the comorbidities. Sixteen hub genes were identified, and their functional analyses further highlighted a complicated inflammatory micro-environment and signaling pathways involving RA and AS. Six transcription factors (TFs) and four miRNAs interacted with hub genes, and the candidate drugs targeting them were simvastatin, 5-azacytidine, bisindolylmaleimide, retinoic acid, and verteporfin, etc.Conclusions: Our comprehensive bioinformatics analyses provided a novel view regarding the potential pathogenesis of AS in RA. Furthermore, exploitation of candidate drugs might hold great promise in the future fight against the comorbidities.

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Apelin Promotes Endothelial Progenitor Cell Angiogenesis in Rheumatoid Arthritis Disease via the miR-525-5p/Angiopoietin-1 Pathway

Cited by 14 publications

References 53 publications

By modulating miR‐525‐5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis

By modulating miR‐525‐5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis

The Therapeutic Mechanism of Schisandrol A and Its Metabolites on Pulmonary Fibrosis Based on Plasma Metabonomics and Network Analysis

Exploration of the shared gene signatures and molecular mechanisms between atherosclerosis and rheumatoid arthritis via multi-microarray data analyses

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