scholarly journals Myricetin Ameliorates Ox-LDL-induced HUVECs Apoptosis and Inflammation via lncRNA GAS5 Upregulating the Expression of miR-29a-3p

2020 ◽  
Author(s):  
Yunpeng Bai ◽  
Qingliang Chen ◽  
Nan Jiang ◽  
zhigang guo
Keyword(s):  
Western Blot ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cell Counting ◽  
Protective Effects ◽  
Cell Dysfunction ◽  
Rna Immunoprecipitation ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation ◽  
Relationship Of

Abstract BackgroundOxidized low-density lipoprotein (ox-LDL)-induced an endothelial cell dysfunction is a significant event in the progression of atherosclerosis[1]. Even myricetin (Myr) has been exhibited strong antioxidant potency, the effect on atherosclerosis is still elusive. MethodsHUVECs were subjected to ox-LDL, before which cells were preconditioned with Myr. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to assess the impacts of ox-LDL and Myr on HUVECs. The expression of EndMT markers was determined by Western blot analysis and immunocytochemistry. In addition, the relationship of GAS5 and miR-29a-3p was evaluated by RNA Fluorescent in Situ Hybridization (FISH) and RNA immunoprecipitation (RIP) assay. ResultsMyr preconditioning prevented ox-LDL-induced apoptosis, inflammatory response, and EndMT. GAS5 was upregulated in response to ox-LDL while it was down-regulated by Myr preconditioning. GAS5 over-expression attenuates Myr protective effects against ox-LDL–mediated HUVEC injury. Besides, miR-29a-3p is a target of GAS5 and down-regulated miR-29a-3p could further resuced the effects of GAS5 in ox-LDL–mediated HUVEC. Furthermore, Myr inactivated the TLR4/NF-κB signaling pathway in ox-LDL-treated HUVEC by down-regulating GAS5 or upregulating miR-26a-5p. ConclusionMyr possessed an anti-inflammatory and anti-EndMT function against ox-LDL-induced HUVEC injury by regulating the GAS5/miR-29a-3p, indicating that Myr may have an important therapeutic function for atherosclerosis.

scholarly journals Myricetin ameliorates ox-LDL-induced HUVECs apoptosis and inflammation via lncRNA GAS5 upregulating the expression of miR-29a-3p

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yunpeng Bai ◽  
Xiankun Liu ◽  
Qingliang Chen ◽  
Tongyun Chen ◽  
Nan Jiang ◽  
...  
Keyword(s):  
Western Blot ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cell Counting ◽  
Protective Effects ◽  
Cell Dysfunction ◽  
Rna Immunoprecipitation ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation ◽  
Relationship Of

AbstractOxidized low-density lipoprotein (ox-LDL)-induced endothelial cell dysfunction is a significant event in the progression of atherosclerosis. Even Myricetin (Myr) has been exhibited strong antioxidant potency, the effect on atherosclerosis is still elusive. HUVECs were subjected to ox-LDL, before which cells were preconditioned with Myr. Cell Counting Kit-8 assay, flow cytometry, quantitative real-time polymerase chain reaction and Western blot were carried out to assess the impacts of ox-LDL and Myr on HUVECs. The expression of EndMT markers was determined by Western blot analysis and immunocytochemistry. In addition, the relationship of GAS5 and miR-29a-3p was evaluated by RNA Fluorescent in Situ Hybridization and RNA immunoprecipitation assay. Myr preconditioning prevented ox-LDL-induced apoptosis, inflammatory response, and EndMT. GAS5 was upregulated in response to ox-LDL while it was down-regulated by Myr preconditioning. GAS5 over-expression attenuates Myr protective effects against ox-LDL–mediated HUVEC injury. Besides, miR-29a-3p is a target of GAS5 and down-regulated miR-29a-3p could further reduce the effects of GAS5 in ox-LDL–mediated HUVEC. Furthermore, Myr inactivated the TLR4/NF-κB signalling pathway in ox-LDL-treated HUVEC by down-regulating GAS5 or upregulating miR-26a-5p. Myr possessed an anti-inflammatory and anti-EndMT function against ox-LDL-induced HUVEC injury by regulating the GAS5/miR-29a-3p, indicating that Myr may have an important therapeutic function for atherosclerosis.

scholarly journals Notoginsenoside R1 Protects HUVEC Against Oxidized Low Density Lipoprotein (Ox-LDL)-Induced Atherogenic Response via Down-Regulating miR-132

2018 ◽  
Vol 51 (4) ◽  
pp. 1739-1750 ◽  
Author(s):  
Changgeng Fu ◽  
Dexin Yin ◽  
Haiying Nie ◽  
Dajun Sun
Keyword(s):  
Western Blot ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Matrix Gla Protein ◽  
Cell Counting ◽  
Intercellular Adhesion Molecule ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Qrt Pcr ◽  
Induced Apoptosis

Background/Aims: Radix notoginseng is a well-known traditional Chinese herbal medicine, has extensively pharmacological activities in cardiovascular system. Notoginsenoside R1 (NGR1) is one main active ingredient of Radix notoginseng. The purpose of this study was to evaluate the functional effects of NGR1 on atherosclerosis (AS). Methods: Human umbilical vascular endothelial cells (HUVECs) were subjected to oxidized low density lipoprotein (ox-LDL), before which cells were preconditioned with NGR1. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, Transwell assay, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to assess the impacts of ox-LDL and NGR1 on HUVECs. Besides, the expression of microRNA-132 (miR-132), and the regulatory role of miR-132 in Matrix Gla Protein (MGP) expression were measured by qRT-PCR and Western blot. Results: NGR1 pre-conditioning prevented ox-LDL-induced apoptosis, migration and overproduction of Monocyte Chemoattractant Protein 1 (MCP-1) and Intercellular Adhesion Molecule 1 (ICAM-1). miR-132 was up-regulated in response to ox-LDL while was down-regulated by NGR1 pre-conditioning. The protective actions of NGR1 in ox-LDL-treated HUVECs were enhanced by miR-132 inhibitor, while were attenuated by miR-132 mimic. Besides, the up-regulated miR-132 could further decrease the expression of MGP, which acted as an anti-migratory and anti-adhesive factor. Furthermore, ox-LDL-induced the activation of c-Jun N-terminal Kinase (JNK) and Nuclear Factor Kappa B (NF-κB) pathways were partially attenuated by NGR1, and were fully eliminated by NGR1 treatment together with MGP overexpression. Conclusion: NGR1 prevents ox-LDL-induced apoptosis, migration and adhesion-related molecule release in HUVECs possibly via down-regulating miR-132, and subsequent up-regulating MGP.

LncRNA OIP5-AS1 accelerates ox-LDL-treated HUVECs injury by NF-κB pathway via miR-30c-5p

2021 ◽  
pp. 1-12
Author(s):  
Lei Zhang ◽  
Qiulai Li ◽  
Yanxia Chen ◽  
Qiao Zhu
Keyword(s):  
Oxidative Stress ◽  
Vascular Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Vital Role ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Sod Activity ◽  
Interacting Protein ◽  
Rna Immunoprecipitation

BACKGROUND: Oxidized low-density lipoprotein (ox-LDL) could induce endothelial injury and played a vital role in the progression and development of atherosclerosis. This study aimed to investigate the role of Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) in ox-LDL-induced human umbilical vascular endothelial cells (HUVECs) injury and the potential mechanisms. METHODS: Cell proliferation and apoptosis were evaluated by Cell Counting Kit-8 (CCK-8) assay and flow cytometry assay, respectively. The levels of lactate dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were detected by corresponding detection kits, respectively. Quantitative real-time PCR (qRT-PCR) was conducted to measure the expression of OIP5-AS1 or microRNA-30c-5p (miR-30c-5p) in HUVECs. Binding between OIP5-AS1 and miR-30c-5p was predicted through bioinformatics analysis and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Western blot was used to analyze p-IκB, IκB, p-p65 and p65 levels. RESULTS: In HUVECs, exposure to ox-LDL led to a decrease in cell viability and an increase in LDH release and apoptosis with concomitant enhancement of oxidative stress, as evidenced by increased ROS and MDA generation, as well as decreased SOD activity and NO levels, while OIP5-AS1 knockdown or miR-30c-5p upregulation could rescue these effects above. Mechanically, OIP5-AS1 functioned as a sponge of miR-30c-5p. OIP5-AS1-induced injury and apoptosis, oxidative stress and activation of NF-κB pathway were reversed by miR-30c-5p in ox-LDL-treated HUVECs. CONCLUSION: OIP5-AS1 contributed to ox-LDL-treated HUVECs injury by activation of NF-κB pathway via miR-30c-5p.

Long non-coding RNA GAS5 knockdown facilitates proliferation and impedes apoptosis by regulating miR-128-3p/FBLN2 axis in ox-LDL-induced THP-1 cells

2020 ◽  
pp. 1-12
Author(s):  
Zijian Shen ◽  
Haigang Li
Keyword(s):  
Cell Proliferation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Rna Immunoprecipitation ◽  
Non Coding Rnas ◽  
Induced Apoptosis ◽  
Long Non Coding Rna

BACKGROUND: Long non-coding RNAs (lncRNAs) are found to involve in modulating the development of atherosclerosis (AS). But the molecular mechanism of lncRNA growth-arrest specific transcript 5 (GAS5) in AS is not fully understood. METHODS: QRT-PCR was performed to measure the abundances of GAS5, miR-128-3p and fibulin 2 (FBLN2). Oxidized low-density lipoprotein (ox-LDL)-treated THP-1 cells were employed as cell models of AS. The cell proliferation and apoptosis were analyzed using CCK-8 and Flow cytometry assays, respectively. Levels of all protein were examined by western blot. The interaction among GAS5, miR-128-3p and FBLN2 was confirmed via dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. RESULTS: GAS5 was elevated and miR-128-3p was decreased in the serum of patients with AS and ox-LDL-stimulated THP-1 cells. Ox-LDL stimulation inhibited proliferation and induced apoptosis of THP-1 cells. Meanwhile, GAS5 directly targeted miR-128-3p and inversely modulated its expression. Importantly, GAS5 depletion facilitated cell proliferation and impaired apoptosis in ox-LDL-induced THP-1 cells. Additionally, GAS5 augmented FBLN2 expression through sponging miR-128-3p, and miR-128-3p facilitated proliferation and retarded apoptosis of ox-LDL-induced THP-1 cells by targeting FBLN2. CONCLUSION: GAS5 knockdown promoted the growth of ox-LDL-induced THP-1 cells through down-modulating FBLN2 and increasing miR-128-3p, suggesting the potential value of GAS5 for treatment of AS.

scholarly journals Platelet-rich plasma protects HUVECs against oX-LDL-induced injury

Open Medicine ◽  
2018 ◽  
Vol 13 (1) ◽  
pp. 41-52 ◽  
Author(s):  
Yang Wang ◽  
Jinsong Wang ◽  
Yonghui Li ◽  
Shenming Wang ◽  
Xiaonan Zhu
Keyword(s):  
Caspase 3 ◽  
Platelet Rich Plasma ◽  
Umbilical Vein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Annexin V ◽  
Tube Formation ◽  
Cell Counting ◽  
Linear Pattern ◽  
Induced Apoptosis

AbstractPlatelet-rich plasma (PRP) contains a variety of cytokines, some of which ameliorate oX-LDL (oxidized low-density lipoprotein)-induced endothelial cell (EC) injury. Therefore, we hypothesized that PRP might alleviate oX-LDL-induced injury.MethodologyHuman umbilical vein endothelial cells (HUVECs) were divided into four groups: a PPP (platelet-poor plasma) group, an oX-LDL group, an oX-LDL+PRP group and a PRP group. CCK-8 (Cell Counting Kit) assay, Annexin V-FITC/7-AAD and Hochest 33342 staining were performed to assess cell proliferation and apoptosis. Tube formation and cell migration assays were performed to evaluate HUVEC-mediated vasculogenesis and migration. Expression levels of Bcl-2, Bax, caspase-3, cleaved caspase-3, PI3K, Akt, eNOS p-Akt, p-eNOS, IL-6 and IL-1 were detected by western blotting or immunofluorescence.Principal findingsPRP promoted HUVEC proliferation in a non-linear pattern, protected HUVECs against oX-LDL-induced apoptosis and attenuated oX-LDL-mediated inhibition of HUVEC migration and vasculogenesis. Additionally, compared to the PPP group, PRP downregulated pro-apoptotic proteins (ratio of Bax/Bcl-2, caspase-3 and cleaved caspase-3) as well as IL-6 and IL-1. Moreover, the PI3K/Akt/eNOS pathway was activated by PRP and inactivated by oX-LDL.ConclusionsIt was demonstrated that PRP protected HUVECs against oX-LDL-induced injury and that the PI3K/Akt/eNOS pathway was activated in this process.

scholarly journals Gambogic acid protects LPS-induced apoptosis and inflammation in a cell model of neonatal pneumonia through the regulation of TrkA/Akt signaling pathway

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xu Gao ◽  
Jingya Dai ◽  
Guifang Li ◽  
Xinya Dai
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Cell Model ◽  
Akt Signaling ◽  
Gambogic Acid ◽  
Akt Signaling Pathway ◽  
Western Blot Assay ◽  
A Cell ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation

Abstract Objective In this work, we investigated the effects of gambogic acid (GA) on lipopolysaccharide (LPS)-induced apoptosis and inflammation in a cell model of neonatal pneumonia. Method Human WI-38 cells were maintained in vitro and incubated with various concentrations of GA to examine WI-38 survival. GA-preincubated WI-38 cells were then treated with LPS to investigate the protective effects of GA on LPS-induced death, apoptosis and inflammation. Western blot assay was utilized to analyze the effect of GA on tropomyosin receptor kinase A (TrkA) signaling pathway in LPS-treated WI-38 cells. In addition, human AKT serine/threonine kinase 1 (Akt) gene was knocked down in WI-38 cells to further investigate the associated genetic mechanisms of GA in protecting LPS-induced inflammation and apoptosis. Results Pre-incubating WI-38 cells with low and medium concentrations GA protected LPS-induced cell death, apoptosis and inflammatory protein productions of IL-6 and MCP-1. Using western blot assay, it was demonstrated that GA promoted TrkA phosphorylation and Akt activation in LPS-treated WI-38 cells. Knocking down Akt gene in WI-38 cells showed that GA-associated protections against LPS-induced apoptosis and inflammation were significantly reduced. Conclusions GA protected LPS-induced apoptosis and inflammation, possibly through the activations of TrkA and Akt signaling pathway. This work may broaden our understanding on the molecular mechanisms of human neonatal pneumonia.

scholarly journals The relationship of the serum endocan level with the CHA2DS2-VASc score in patients with paroxysmal atrial fibrillation

2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Gökhan Ceyhun
Keyword(s):  
Atrial Fibrillation ◽  
Paroxysmal Atrial Fibrillation ◽  
Stroke Risk ◽  
Low Density Lipoprotein ◽  
Multivariate Logistic Regression Analysis ◽  
Density Lipoprotein ◽  
Roc Curve Analysis ◽  
Reactive Protein ◽  
Relationship Of ◽  
The Relationship

Abstract Background In this study considering the relationship between serum endocan and CHA2DS2-VASc score, we assumed that endocan level could be a new biomarker for stroke risk in patients with paroxysmal atrial fibrillation (PAF). It was examined that endocan could be an alternative to determine the risk of stroke and anticoagulation strategy in patients with PAF. The CHA2DS2-VASc scores were calculated for 192 patients with PAF, and their serum endocan levels were measured. The patients were divided into two groups as those with low to moderate (0-1) and those with high (≥ 2) CHA2DS2-VASc scores, and the endocan levels were compared between these two groups. Results The serum endocan level was significantly higher in the high CHA2DS2-VASc score group (p < 0.001). In the multivariate logistic regression analysis, endocan, C-reactive protein, and low-density lipoprotein were found to be independent determinants of the CHA2DS2-VASc score. The predictive value of endocan was analyzed using the ROC curve analysis, which revealed that endocan predicted a high stroke risk (CHA2DS2-VASc ≥ 2) at 82.5% sensitivity and 71.2% specificity at the cutoff value of 1.342. Conclusion This study indicates that endocan is significantly associated with CHA2DS2-VASc score. We demonstrated that endocan could be a new biomarker for the prediction of a high stroke risk among patients diagnosed with PAF.

scholarly journals CircLDLR Promotes Papillary Thyroid Carcinoma Tumorigenicity by Regulating miR-637/LMO4 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yuan-ming Jiang ◽  
Wei Liu ◽  
Ling Jiang ◽  
Hongbin Chang
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Papillary Thyroid ◽  
Induced Apoptosis

Background. Circular RNAs (circRNAs) have been reported to play important roles in the development and progression of papillary thyroid carcinoma (PTC). However, the function and molecular mechanism of circRNA low-density lipoprotein receptor (circLDLR) in the tumorigenesis of PTC remain unknown. Results. In this study, circLDLR was found to be markedly upregulated in PTC tissues and cell lines, and knockdown of circLDLR inhibited PTC cell proliferation, migration, and invasion but induced apoptosis in vitro. Moreover, circLDLR acted as a sponge for miR-637, and miR-637 interference reversed the anticancer effects of circLDLR knockdown on PTC cells. LMO4 was verified to be a target of miR-637; LMO4 upregulation abolished miR-637 mediated inhibition of cell growth and metastasis in PTC. Additionally, circLDLR could indirectly modulate LMO4 via acting as a sponge of miR-637 in PTC cells. Besides that, xenograft analysis showed that circLDLR knockdown suppressed tumor growth in vivo via regulating LMO4 and miR-637. Conclusion. Taken together, these results demonstrated that circLDLR promoted PTC tumorigenesis through miR-637/LMO4 axis, which may provide a novel insight into the understanding of PTC tumorigenesis and be useful in developing potential targets for PTC treatment.

Abstract 405: Utility of Very Low-density Lipoprotein Cholesterol to Total Triglyceride Ratio (VLDL-C/TG) and Non-VLDL TG to Quantify Remnant Lipoprotein Cholesterol (RLP-C): The Very Large Database of Lipids Study 7C

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Aditya D Hendrani ◽  
Renato Quispe ◽  
Seth S Martin ◽  
Krishnaji R Kulkarni ◽  
Peter P Toth ◽  
...  
Keyword(s):  
Diagnostic Criteria ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Type Iii ◽  
Very Large Database ◽  
Relationship Of

Background: RLP-C is comprised of atherogenic triglyceride- (TG-) rich lipoproteins, commonly defined as the sum of intermediate-density lipoprotein cholesterol (IDL-C) and very low-density lipoprotein cholesterol remnants (VLDL 3 -C). In clinical practice, the VLDL-C/TG ratio is used to diagnose type III dyslipidemia, a primary lipoprotein disorder characterized by high levels of RLP-C. Methods: Serum lipids of 556,307 U.S. adults with TG ≥130 mg/dL were analyzed by ultracentrifugation (VAP, Atherotech, Birmingham, AL). We estimated TG content in VLDL (VLDL-TG) as the product of VLDL-C and validated variable TG/VLDL-C factors. Non-VLDL-TG was then calculated as total TG minus VLDL-TG, for which negative values represented the presence of RLP-C. We examined the relationship of non-VLDL-TG to 1000 quantiles of VLDL-C/TG ratio. We defined a VLDL-C/TG ratio cutpoint for presence of RLP-C based on the quantile at which median non-VLDL-TG≤0. Results: We found median non-VLDL-TG≤0 at VLDL-C/TG = 0.18 (Figure) . There were 174,907 adults who did not meet diagnostic criteria for type III dyslipidemia (VLDL-C/TG 0.18 to <0.30), whose levels of RLP-C and non-VLDL-TG levels were 37 (31-46) and -20 (-40 to -8) mg/dL, respectively. A total of 1,550 adults met classical diagnostic criteria for type III dyslipidemia (VLDL-C/TG ≥0.3), whose plasma levels of RLP-C and non-VLDL-TG levels were 80 (67-101) and -187 (-290 to -129) mg/dL, respectively. Conclusion: A threshold of VLDL-C/TG ≥0.18 correlates with the accumulation of RLP-C in plasma. If validated in future studies, these findings will improve identification of individuals who are at greater risk for atherosclerotic disease.

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