Up-regulated miR-106b inhibits ox-LDL-induced endothelial cell apoptosis in atherosclerosis

Zhang, Yunqing; Wang, Li; Xu, Jie; Kong, Xiaomei; Zou, Lin

doi:10.1590/1414-431x20198960

Cited by 17 publications

(5 citation statements)

References 40 publications

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“…In the established macrophage related ceRNA subnetwork, the two lncRNA AL138756.1 and LINC01094 lack sufficient investigation, while for the downregulated miRNAs, some of them have been implicated to be protective against AS. miR-106b can inhibit ox-LDL-induced endothelial cell apoptosis in AS [ 20 ]. It also inhibits the expression of PTEN in vascular ECs, which could block TNF-α-induced activation of caspase-3, thus preventing ECs apoptosis in AS [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Constructing a ceRNA-immunoregulatory network associated with the development and prognosis of human atherosclerosis through weighted gene co-expression network analysis

Liu

2021

Aging

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There is now overwhelming experimental and clinical evidence that atherosclerosis (AS) is a chronic inflammatory disease. The recent discovery of a new group of mediators known as competing endogenous RNA (ceRNA) offers a unique opportunity for investigating immunoregulation in AS. In this study, we used gene expression profiles from GEO database to construct a lncRNA-miRNA-mRNA ceRNA network during AS plaque development through weighted gene co-expression network analysis (WGCNA). GO annotation and pathway enrichment analysis suggested that the ceRNA network was mainly involved in the immune response. CIBERSORT and GSVA were used to calculate the immune cell infiltration score and identified macrophage as hub immunocyte in plaque development. A macrophage related ceRNA subnetwork was constructed through correlation analysis. Samples from Biobank of Karolinska Endarterectomy (BiKE) were used to identify prognostic factors from the subnetwork and yielded 7 hub factors that can predict ischemic events including macrophage GSVA score and expression value of AL138756.1, CTSB, MAFB, LYN, GRK3, and BID. A nomogram based on the key factors was established. GSEA identified that the PD1 signaling pathway was negatively associated with these prognostic factors which may explain the cardiovascular side effect of immune checkpoint therapy in anti-tumor treatment.

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Section: Discussionmentioning

confidence: 99%

Constructing a ceRNA-immunoregulatory network associated with the development and prognosis of human atherosclerosis through weighted gene co-expression network analysis

Liu

2021

Aging

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“…Currently, clinical treatment of AS mainly includes pharmacological therapy and revascularization therapy. Ox-LDL induces the proliferation and migration of smooth muscle cells and is considered to be a key factor in AS development [ 23 ]. Moreover, Ox-LDL is an important pathogenic factor that induces excessive oxidative stress and apoptosis in vascular endothelial cells, which ultimately promoted AS development [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

CircLZIC regulates ox-LDL-induced HUVEC cell proliferation and apoptosis via Micro-330-5p/NOTCH2 axis in atherosclerosis

Men,

Hu,

2024

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Atherosclerosis (AS) is a major chronic non-communicable disease and a primary cause of cardiovascular disease. Recent studies have shown that circRNAs are potential epigenetic factors that regulate vascular endothelial inflammatory responses and AS progression. Therefore, identification of the circRNAs that regulate ox-LDL levels is a critical step to understanding the pathology of AS. Our study is aim to investigate how circLZIC regulates atherosclerosis (AS) via the Micro-330-5p/NOTCH2 regulatory axis. The results showed that CircLZIC and NOTCH2 are highly expressed in human AS clinical samples, while Micro-330-5p is expressed locally. The CCK-8 experiment results showed that circLZIC promotes the proliferation of HUVECS cells. Flow cytometry analysis showed that circLZIC act as an inhibitor of HUVEC cell apoptosis. The expression level of Micro-330-5p can be up-regulated by transfection of small interfering RNA against circLZIC. Further, Starbase predicted that Micro-330-5p could target and regulate NOTCH2. Next, we confirmed that overexpression of Micro-330-5p could significantly reduce the expression of fluorescein using the double Luciferase reporter assay. RIP-qRT-PCR experiment showed that Micro-330-5p and NOTCH2 mRNAs are effectively enriched by ago2 protein. Further, we found that knocking down circLZIC increases the expression of Micro-330-5p and promotes cell apoptosis, while inhibiting the expression of NOTCH2 and cell activity. On the other hand, co-transfection of Micro-330-5p inhibitor decreases Micro-330-5p expression and inhibit cell apoptosis, while increasing NOTCH2 expression and cell activity. In conclusion, CircLZIC regulates HUVEC cell activity by the Micro-330-5p/NOTCH2 signaling pathway, suggesting that circLZIC plays a key role in atherosclerosis development.

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“…Meanwhile, the growth factors and cytokines secreted by infiltrating white cells also affect the proliferation of smooth muscle cells (30). Ox-LDL is a carrier of oxygen-free radicals, which can produce toxic effects on vascular cells, promote their apoptosis and cause vascular endothelial damage (31). In the present study, the results of flow cytometry showed that the apoptotic rate of the ox-LDL group was significantly increased compared with the control group and S/V pretreatment could significantly reduce the apoptotic rate.…”

Section: Discussionmentioning

confidence: 99%

Sacubitril/valsartan inhibits ox‑LDL‑induced MALAT1 expression, inflammation and apoptosis by suppressing the TLR4/NF‑κB signaling pathway in HUVECs

et al. 2021

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The therapeutic effect of sacubitril/valsartan (S/V) on heart failure has been confirmed, while its role in atherosclerosis remains largely unexplored. The present study aimed to investigate the effects of S/V on the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), inflammation and apoptosis in human umbilical vein endothelial cells (HUVECs) induced by oxidized low-density lipoprotein (ox-LDL) and to elucidate its possible mechanism. Cell Counting Kit-8 assay was used to detect cell viability. Reverse transcription-quantitative PCR was performed to detect the MALAT1 expression. ELISA was performed to detect the levels of IL-1β, IL-6 and TNF-α. Flow cytometry was conducted to detect the apoptotic rate of cells. A nitric oxide (NO) detection kit was used to determine the concentration of NO. Western blotting analysis was performed to determine the levels of intercellular cell adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, endothelin-1, caspase-3, Bax, Bcl-2, Toll-like receptor 4 (TLR4), p65 and p-p65. Compared with the ox-LDL group, S/V treatment significantly increased the cell viability, NO concentration and Bcl-2 expression, decreased the levels of IL-1β, IL-6 and TNF-α and reduced the expressions of MALAT1, ICAM-1, VCAM-1, cleaved-caspase-3, Bax, TLR4 and p-p65. Overall, the findings suggested that S/V could downregulate the expression of MALAT1, inhibit inflammation and apoptosis and improve endothelial function in ox-LDL-induced HUVECs via inactivating the TLR4/NF-κB signaling pathway. Therefore, S/V might be utilized as a promising therapeutic strategy for the prevention and treatment of atherosclerosis.

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Up-regulated miR-106b inhibits ox-LDL-induced endothelial cell apoptosis in atherosclerosis

Cited by 17 publications

References 40 publications

Constructing a ceRNA-immunoregulatory network associated with the development and prognosis of human atherosclerosis through weighted gene co-expression network analysis

Constructing a ceRNA-immunoregulatory network associated with the development and prognosis of human atherosclerosis through weighted gene co-expression network analysis

CircLZIC regulates ox-LDL-induced HUVEC cell proliferation and apoptosis via Micro-330-5p/NOTCH2 axis in atherosclerosis

Sacubitril/valsartan inhibits ox‑LDL‑induced MALAT1 expression, inflammation and apoptosis by suppressing the TLR4/NF‑κB signaling pathway in HUVECs

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