Wen-Jing Fan’s research while affiliated with University of South China and other places

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Publications (4)


Role of autophagy in advanced atherosclerosis (Review)
  • Literature Review

March 2017

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34 Reads

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17 Citations

Molecular Medicine Reports

Yu-Ning Zhu

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Wen-Jing Fan

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[...]

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Shun-Lin Qu

Atherosclerosis (AS) remains the leading cause for global cardiovascular disease morbidity and mortality, and a major cause of cardiopathy, myocardial infarction and peripheral vascular diseases. Macrophages serve a critical role in atherosclerotic plaque stabilization and rupture, and the selective removal of macrophages may be beneficial in improving plaque stability. Autophagy is a process of self?feeding, during which cytoplasmic proteins or organelles are packaged into vesicles and fused with the lysosome to form an autophagosome. The newly formed autophagosome can degrade internalized proteins, and this process may be used to serve the metabolic and self?renewal requirements of the cell. Autophagy serves an important role in maintaining cell homeostasis and promoting cell survival, and therefore an imbalance in autophagy is closely associated with multiple diseases.


Fig. 1. oxLDL increases the expression of Mipu1. (A,E) Time course of oxLDL-induced Mipu1 mRNA expression levels. oxLDL (75 mg/L) was added for the indicated periods of time. Total RNA was isolated from each sample, and real-time RT-PCR was performed to quantify Mipu1 mRNA expression levels, shown as the relative difference from the control normalized to GAPDH expression levels. (B,F) Concentration-response effect of oxLDL on Mipu1 mRNA expression. RAW264.7 cells were treated as described above and with the indicated concentrations of oxLDL for 24 h. (C,G) Time course of oxLDL-induced Mipu1 protein expression levels. (D,H) Concentration-response effect of oxLDL on Mipu1 protein expression. All data represent three independent experiments. *P<0.05 versus control. A-D, RAW264.7 cells; E-H, THP-1 cells. (I)LDL (75 mg/L) was added for the indicated periods of time in RAW264.7 cells. (J) RAW264.7 cells were treated with the indicated concentrations of LDL for 24 h. All data represent three independent experiments. *P<0.05 versus control. 
Fig. 3. The mouse CD36 gene promoter is transcriptional target of Mipu1. A, Mouse CD36 promoter region from-1200 to +299bp was cloned. RAW264.7 cells were treated with oxLDL for 24 h, then luciferase assays were performed. B, Mouse CD36 promoter analysis by series of deletion. C, The mutated sequences of MRE-Ⅱ(from-1200 to +299bp) are presented. The sequence of the Mut-Luc construct was identical to the Wt-Luc construct except for the mutated sequences (GACTTACT). D, Chromatin immunoprecipitation 
Fig. 4. Mipu1 downregulation increases oxLDL-induced lipid accumulation in RAW264.7 cells. A, protein expression of Mipu1 in RAW264.7 cells transfected with Mipu1 siRNA were analyzed by western blot. B, RAW264.7-Ctrl siRNA and RAW264.7-Mipu1 siRNA cells were treated with 75 mg/L ox-LDL for 24 h, and the intracellular cholesterol content was measured via HPLC. C, under the same conditions as in (B), cells were incubated with Dil-labeled oxLDL (75 mg/L) for 24 h, and uptake of oxLDL identified by Dil-ox-LDL fluorescence intensity. Data are presented as the mean±SEM of at least four independent experiments. *P<0.05 vs. pcDNA3.1 group. 
Fig. 6. Overexpression of CD36 rescues lipid accumulation in RAW264.7-Mipu1 cells. A, Intracellular cholesterol content was measured via HPLC after treatment with ox-LDL (75μg/ml) for 24 h. B, Fluorescence intensity was detected after incubation with Dil-labeled ox-LDL (75μg/ml) for 24 h. Mipu1:RAW264.7-Mipu1 cells; Mipu1+CD36:RAW264.7-Mipu1 cells were transfected with CD36 plamid. Data are presented as the mean±SEM of at least four independent experiments. *P<0.05 vs. Mipu1 group. 
Mipul Inhibits Lipid Accumulation Through Down-Regulation of CD36 in RAW264.7 Cells
  • Article
  • Full-text available

September 2015

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86 Reads

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6 Citations

Cellular Physiology and Biochemistry

Background/Aims: Our recent data indicated that Mipu1 overexpression reduces lipid intake and CD36 expression of macrophages in the presence of oxLDL. However, the mechanism of Mipu1 inhibiting lipid accumulation in macrophages is not elucidated. Methods: Real-time quantitative polymerase chain reaction (PCR) and western blot analysis were used to detect expression of Mipu1 and CD36. The promoter activity of CD36 was studied using luciferase assays. Chromatin immunoprecipitation (ChIP) was used to show the recruitment of Mipu1 onto the CD36 promoter. High-performance liquid chromatography and Dil-labeled lipoprotein were used to detect cholesterol accumulation. Results: Here, we show that CD36 overexpression rescues oxLDL-induced cholesterol accumulation in RAW264.7-Mipu1 cells. Analysis of the mouse CD36 promoter revealed two potential Mipu1-response elements (MRE), one of which (from -237bp to -244bp, ACTTAC) was shown, using mutagenesis and deletion analysis, to be functional. Mipu1 was demonstrated to bind to CD36 promoter, and oxLDL treatment resulted in increases in their interaction as assessed by ChIP. Conclusions: It was demonstrated that Mipu1 inhibited the lipid accumulation of macrophages and it down-regulated CD36 expression in the presence of oxLDL.

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Mipu1 Overexpression Protects Macrophages from oxLDL-Induced Foam Cell Formation and Cell Apoptosis

August 2014

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22 Reads

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8 Citations

DNA and cell biology

Mipu1 (myocardial ischemic preconditioning upregulated protein 1) is a novel N-terminal Kruppel-associated box (KRAB)/C2H2 zinc finger superfamily protein, that displays a powerful effect in protecting H9c2 cells from oxidative stress-induced cell apoptosis. The present study aims to investigate the effect of Mipu1 overexpression on oxidized low-density lipoprotein (oxLDL)-induced foam cell formation, cell apoptosis, and its possible mechanisms. New Zealand healthy rabbits were used to establish atherosclerosis model, and serum levels of triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol were detected by an automatic biochemical analyzer. Sudan IV staining was used to detect atherosclerotic lesions. The RAW264.7 macrophage cell line was selected as the experimental material. Oil red O staining, high-performance liquid chromatography, and Dil-labeled lipoprotein were used to detect cholesterol accumulation qualitatively and quantitatively, respectively. Flow cytometry was used to determine cell apoptosis. Real-time quantitative PCR was used to detect the mRNA expression of the main proteins that are associated with the transport of cholesterol, such as ABCA1, ABCG1, SR-BI, and CD36. Western blot analysis was used to detect the protein expression of Mipu1. There were atherosclerotic lesions in the high-fat diet group with Sudan IV staining. High-fat diet decreased Mipu1 expression and increased CD36 expression significantly at the 10th week compared with standard-diet rabbits. Mipu1 overexpression decreased oxLDL-induced cholesterol accumulation, oxLDL uptake, cell apoptosis, and cleaved caspase-3. Mipu1 overexpression inhibited the oxLDL-induced CD36 mRNA and protein expression, but it did not significantly inhibit the mRNA expression of ABCA1, ABCG1, and SR-BI. Mipu1 overexpression inhibits oxLDL-induced foam cell formation and cell apoptosis. Mipu1 overexpression reduces the lipid intake of macrophages and might be associated with the downregulation of CD36 expression in the presence of oxLDL.


H2S, a novel therapeutic target in renal-associated diseases?

August 2014

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25 Reads

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6 Citations

Clinica Chimica Acta

For more than a century, hydrogen sulfide (H2S) has been regarded as a toxic gas. Recently, the understanding of the biological effects of H2S has been changed. This review surveys the growing recognition of H2S as an endogenous signaling molecule in mammals, with emphasis on its physiological and pathological pathways in the urinary system. This article reviews recent progress of basic and pharmacological researches related to endogenous H2S in urinary system, including the regulatory effects of H2S in the process of antioxidant, inflammation, cellular matrix remodeling and ion channels, and the role of endogenous H2S pathway in the pathogenesis of renal and urogenital disorders.

Citations (4)


... 10 In contrast, autophagy, a cellular process responsible for maintaining cellular homeostasis and plaque stability, is involved in the accumulation of oxidized lipids, inflammation, and the formation of foam cells, which have been implicated in atherosclerosis. 12,13 Furthermore, the transcription factor Nrf2 has emerged as playing a major role in the complex interplay of cellular activities. Nrf2 has been shown to be involved in regulating autophagy activity by promoting autophagy efflux and is also closely associated with the Keap1/p62 pathway, which mediates proteasomal activity. ...

Reference:

Nrf2 Connects Cellular Autophagy and Vascular Senescence in Atherosclerosis: A Mini-Review
Role of autophagy in advanced atherosclerosis (Review)
  • Citing Article
  • March 2017

Molecular Medicine Reports

... ZNF667 (zinc finger protein 667, also referred to as Mipu1) participates in cell growth, apoptosis, oxidative stress, and lipid accumulation. In a study on laryngeal squamous cell carcinoma (LSCC), it was found that ZNF667 is a tumor-suppressing gene [64][65][66][67][68]. ZNF667 can regulate P-selectin expression in specific cells and leukocyte-endothelial adhesion after hypoxia [69]. ...

Mipul Inhibits Lipid Accumulation Through Down-Regulation of CD36 in RAW264.7 Cells

Cellular Physiology and Biochemistry

... H 2 S has been considered as a highly toxic gas for a long time [5,23]; however, researchers have found that H 2 S also provides biological protective functions, to a certain extent [24,25]. Specifically, in Wistar rats (weight, 200-250 g) exposed to 300 ppm H 2 S for 60 min, the mitochondria of myocardial cells swelled and alveolar epithelial cells disappeared, showing a crescent apoptosis [26]. ...

H2S, a novel therapeutic target in renal-associated diseases?
  • Citing Article
  • August 2014

Clinica Chimica Acta

... ZNF667 also mediates cytoprotection of HIF1 against hydrogen peroxide-mediated injury in H9c2 cells through transcriptional repression of BAX (25). In addition, ZNF667 can inhibit oxLdL-induced foam cell formation, cell apoptosis and lipid accumulation in macrophages by directly inhibiting the transcription of cd36 (38,39). Nonetheless, to date, no angiogenesis-related gene has been identified as the direct target gene of ZNF667. ...

Mipu1 Overexpression Protects Macrophages from oxLDL-Induced Foam Cell Formation and Cell Apoptosis
  • Citing Article
  • August 2014

DNA and cell biology