PTPRO Promotes Oxidized Low-Density Lipoprotein Induced Oxidative Stress and Cell Apoptosis through Toll-Like Receptor 4/Nuclear Factor κB Pathway

Liang, Caihong; Wang, X; Hu, Jianping; Lian, Xiaoqing; Zhu, Tiantian; Hui, Zhang; Gu, Ning; Li, Jun

doi:10.1159/000477596

Cited by 36 publications

(37 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Luo et al [63] observed that pycnogenol, another kind of flavonoid compound, can decrease lipid droplet formation and mitigate LPStriggered atherosclerotic development by repressing TLR4/NF-κB pathway in human THP-1 monocytes. Liang et al found that phosphatase receptor type O (PTPRO) plays an unfavorable role in atherogenesis by stimulating ox-LDL-induced cell apoptosis and oxidative stress through activation of the TLR4/NF-κB pathway in RAW264.7 macrophages [64]. Based on these findings, we hypothesized that TLR-4/NF-κB pathway may be implicated in apigenininduced athero-protection.…”

Section: Discussionmentioning

confidence: 77%

Apigenin Retards Atherogenesis by Promoting ABCA1-Mediated Cholesterol Efflux and Suppressing Inflammation

Ren

Jiang

Zhou

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: The development of atherosclerosis is accompanied by escalating inflammation and lipid accumulation within blood vessel walls. ABCA1 plays a crucial role in mediating cholesterol efflux from macrophages, which protects against atherogenesis. This research was designed to explore the effects and underlying mechanisms of apigenin (4’, 5, 7-trihydroxyflavone) on ABCA1-mediated cellular cholesterol efflux and LPS-stimulated inflammation in RAW264.7 macrophages and apoE^-/- mice. Methods: Expression of genes or proteins was examined by RT-PCR or western blot analysis. Liquid scintillation counting was used to detect percent cholesterol efflux. Cellular cholesterol content was measured using HPLC assay. The secretion levels of pro-inflammatory cytokines were quantified by ELISA assay. Atherosclerotic lesion sizes were determined with Oil Red O staining. The contents of macrophages and smooth muscle cells in atherosclerotic lesion were evaluated using immunohistochemistry. Plasma TC, TG, HDL-C and LDL-C levels in apoE^-/- mice were evaluated using commercial test kits. Results: Apigenin potently increased ABCA1 expression through miR-33 repression in a dose- and time-dependent manner. Treatment with apigenin significantly increased ABCA1-mediated cholesterol efflux, and reduced TC, FC and CE levels in macrophage-derived foam cells. In LPS-treated macrophages, the expression levels of TLR-4, MyD88 and p-IκB-α as well as nuclear NF-κB p65 were decreased by the addition of apigenin. Moreover, apigenin markedly decreased secretion levels of several pro-inflammatory cytokines. Lastly, in LPS-challenged apoE^-/- mice, apigenin administration augmented ABCA1 expression, decreased the contents of macrophages and smooth muscle cells in atherosclerotic lesion, reduced miR-33, TLR-4, and NF-κB p65 levels, improved plasma lipid profile and relieved inflammation, which results in less atherosclerotic lesion size. Conclusions: Taken together, these results suggest that apigenin may attenuate atherogenesis through up-regulating ABCA1-mediated cholesterol efflux and inhibiting inflammation.

show abstract

Section: Discussionmentioning

confidence: 77%

Apigenin Retards Atherogenesis by Promoting ABCA1-Mediated Cholesterol Efflux and Suppressing Inflammation

Ren

Jiang

Zhou

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…The MDA concentration in kidney tissues was detected with a commercial MDA assay kit (Beyotime Biotechnology, Shanghai, China) according to the manufacturer's instructions [ 28 ]. MDA values were normalized to the protein concentrations and expressed as nmoL/mg protein.…”

Section: Methodsmentioning

confidence: 99%

Celastrol ameliorates cisplatin nephrotoxicity by inhibiting NF-κB and improving mitochondrial function

Meng

et al. 2018

EBioMedicine

149

View full text Add to dashboard Cite

BackgroundCelastrol is an active ingredient of Chinese medicine Tripterygium wilfordii which is clinically used to treat the immune diseases. Currently, celastrol is documented as a potent agent for treating cancer and inflammatory disorders. This study was to investigate the effect of celastrol on cisplatin nephrotoxicity and the underlying mechanism.MethodsMale C57BL/6 mice were treated with cisplatin (20 mg/kg) with or without celastrol treatment (1 and 2 mg/kg/day). In vitro, human proximal tubule epithelial cell line (HK−2) and mouse renal tubule epithelial cells (RTECs) were treated with cisplatin (5 μg/mL) with or without celastrol administration. Then renal injury and cell damage were evaluated.FindingsIn vivo, after celastrol treatment, cisplatin-induced kidney injury was significantly ameliorated as shown by the improvement of renal function (BUN, serum creatinine, and cystatin C), kidney morphology (PAS staining) and oxidative stress (MDA) and the suppression of renal tubular injury markers of KIM-1 and NGAL. Meanwhile, the renal apoptosis and inflammation induced by cisplatin were also strikingly attenuated in celastrol-treated mice. In vitro, celastrol treatment markedly inhibited cisplatin-induced renal tubular cell apoptosis, suppressed NF-κB activation, and improved mitochondrial function evidenced by the restored mtDNA copy number, mitochondrial membrane potential, and OXPHOS activity in cisplatin-treated renal tubular epithelial cells.InterpretationThis work suggested that celastrol could protect against cisplatin-induced acute kidney injury possibly through suppressing NF-κB and improving mitochondrial function.FundThe National Natural Science Foundation of China, National Key Research and Development Program, and Natural Science Foundation of Jiangsu Province.

show abstract

“…A key aspect of atherosclerosis is the maladaptive inflammatory response to lipid accumulation in the artery and NF-κB activation as a pathological mechanism of lipid metabolism and atherosclerosis [29]. Our previous study also demonstrated that NF-κB pathway played vital roles in atherosclerosis via promoting oxidized low density lipoproteins induced oxidative stress and cell apoptosis in macrophages [30]. In humans, divergent lncRNAs, neighboring protein-coding genes were strongly enriched in nuclear functions, including transcription factor activity, sequence-specific DNA binding, and embryo development [22].…”

Section: Discussionmentioning

confidence: 87%

Circulating Exosomal SOCS2-AS1 Acts as a Novel Biomarker in Predicting the Diagnosis of Coronary Artery Disease

Liang

Zhang

Lian

et al. 2020

BioMed Research International

Self Cite

View full text Add to dashboard Cite

Background and Aims. Critical roles of circulating exosomal long noncoding RNAs (lncRNAs) have been implicated in multiple diseases. However, little is known about their roles in coronary artery disease (CAD). The aim of the present study was to investigate the relationships between circulating exosomal lncRNAs and CAD and identify the aberrantly expressed disease-related lncRNAs as biomarkers in diagnosing CAD. Methods. The aberrantly expressed lncRNAs in plasma exosomes from CAD patients and controls were identified by microarray analysis and verified by quantitative real-time PCR (qRT-PCR). Then, the correlation between the expression level of candidate biomarker and clinic features in CAD patients, mild coronary artery stenosis (mCAS) patients, and controls was analyzed. Finally, we used the receiver operating characteristic (ROC) curve to examine the diagnosis value of candidate biomarkers. Results. The downregulated SOCS2-AS1 was determined by microarray analysis and verified by qRT-PCR in plasma from CAD patients in contrast to controls. The SOCS2-AS1 expression level in plasma exosomes was negatively correlated with PLT and Lpa. Moreover, CAD patients with elevated levels of plasma exosome-encapsulated SOCS2-AS1 were susceptible to multicoronary artery lesions. Additionally, the area under ROC (AUC) of SOCS2-AS1 was 0.704 (95% CI = 0.607–0.801, P<0.001) for diagnosis of CAD. Conclusions. Plasma exosome-encapsulated SOCS2-AS1 was an independent protective factor against CAD and could be potentially used as a novel biomarker for the diagnosis of CAD.

show abstract

PTPRO Promotes Oxidized Low-Density Lipoprotein Induced Oxidative Stress and Cell Apoptosis through Toll-Like Receptor 4/Nuclear Factor κB Pathway

Cited by 36 publications

References 28 publications

Apigenin Retards Atherogenesis by Promoting ABCA1-Mediated Cholesterol Efflux and Suppressing Inflammation

Apigenin Retards Atherogenesis by Promoting ABCA1-Mediated Cholesterol Efflux and Suppressing Inflammation

Celastrol ameliorates cisplatin nephrotoxicity by inhibiting NF-κB and improving mitochondrial function

Circulating Exosomal SOCS2-AS1 Acts as a Novel Biomarker in Predicting the Diagnosis of Coronary Artery Disease

Contact Info

Product

Resources

About