Yan Liu

Hebei Medical University, Chentow, Hebei, China

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Publications (13)36.21 Total impact

  • Yue Cao · Xinli Jiang · Huijie Ma · Yuling Wang · Peng Xue · Yan Liu ·
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    ABSTRACT: Sirtuin 1 (SIRT1) is a prototype mammalian NAD(+)-dependent protein deacetylase that has emerged as a key metabolic sensor in various metabolic tissues. Growing evidence suggests that SIRT1 regulates glucose and lipid metabolism through its deacetylase activity. In this review, we have summarized the recent progress in SIRT1 research with a particular focus on the role of SIRT1 in insulin resistance at different metabolic tissues. Recent data indicate that activated SIRT1 improves the insulin sensitivity of liver, skeletal muscle and adipose tissues and protects the function and cell mass of pancreatic β-cells. These findings suggest that SIRT1 might be a new therapeutic target for the prevention of disease related to insulin resistance, such as metabolic syndrome and type 2 diabetes mellitus.
    Journal of diabetes and its complications 09/2015; DOI:10.1016/j.jdiacomp.2015.08.022 · 3.01 Impact Factor
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    ABSTRACT: The regulation of vascular smooth muscle cell (VSMC) proliferation is an important issue because it has major implications for the prevention of pathological vascular conditions. Using microRNA array screen and found the expression levels of 200 unique miRNAs in hyperplasic tissues. Among them, miR-200c expression substantially was down-regulated. The objective of this work was to assess the function of miR-200c and SUMOylated Krϋppel-like transcription factor 4 (KLF4) in the regulation of VSMC proliferation inboth cultured cells and animal models of balloon injury.Under basal conditions,we found that miR-200c inhibited the expression of KLF4 and the SUMO-conjugating enzyme Ubc9. Upon PDGF-BB treatment, Ubc9 interacted with and promoted the SUMOylation of KLF4, which allowed the recruitment of transcriptional corepressors (e.g., nuclear receptor co-repressor (NCoR) and HDAC2) to the miR-200c promoter. The reduction in miR-200c levels led to increased target gene expression (e.g., Ubc9 and KLF4), which further repressed miR-200c levels and accelerated VSMC proliferation. These results demonstrate that induction of a miR-200c-SUMOylated KLF4 feedback loop is a significant aspect of the PDGF-BB proliferative response in VSMCs and that targeting Ubc9 represents a novel approach for the prevention of restenosis. Copyright © 2015. Published by Elsevier Ltd.
    Journal of Molecular and Cellular Cardiology 03/2015; 82. DOI:10.1016/j.yjmcc.2015.03.011 · 4.66 Impact Factor
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    ABSTRACT: This study investigated the anti-arrhythmic effects from chronic intermittent hypobaric hypoxia (CIHH) and the cellular mechanisms in rats with metabolic syndrome. Male Sprague-Dawley rats were randomly distributed among the control, fructose-fed (fed with 10% fructose in the drinking water to induce metabolic syndrome), CIHH (42 days of hypobaric hypoxia treatment simulating an altitude of 5000 m a.s.l.: PB = 404 mm Hg, PO2 = 84 mm Hg, 6 h per day), and the CIHH plus fructose (CIHH-F) groups. In anesthetized rats, the arrhythmia score was determined after 30 min of cardiac ischemia followed by 120 min of reperfusion. Action potentials (AP) were recorded from isolated ventricular papillary muscles. The arrhythmia score was much lower in CIHH-F rats than in the fructose-fed rats. Under basic conditions, AP duration (APD) was significantly shortened in fructose-fed rats, but obviously prolonged in CIHH rats compared with that of the control rats. During ischemia, the AP amplitude, the maximal rate of rise of phase 0, APD, and resting potential, were lower in the control, fructose-fed, and CIHH-F groups, but were not changed in the CIHH rats. The lower AP during ischemia did not recover after washout for the fructose-fed rats. In conclusion, CIHH protects the heart against ischemia-reperfusion induced arrhythmia in rats with metabolic syndrome. This effect of CIHH is possibly related to baseline prolongation of the AP and attenuation of AP reduction during ischemia-reperfusion.
    Canadian Journal of Physiology and Pharmacology 12/2014; 93(4):1-6. DOI:10.1139/cjpp-2014-0343 · 1.77 Impact Factor

  • Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 03/2014; 42(3):262-5. DOI:10.3760/cma.j.issn.0253-3758.2014.03.019
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    Xinli Jiang · Huijie Ma · Yan Wang · Yan Liu ·
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    ABSTRACT: Type 2 diabetes mellitus (T2DM) is a multifactorial disease, and its aetiology involves a complex interplay between genetic, epigenetic, and environmental factors. In recent years, evidences from both human and animal experiments have correlated early life factors with programming diabetes risk in adult life. Fetal and neonatal period is crucial for organ development. Many maternal factors during pregnancy may increase the risk of diabetes of offsprings in later life, which include malnutrition, healthy (hyperglycemia and obesity), behavior (smoking, drinking, and junk food diet), hormone administration, and even stress. In neonates, catch-up growth, lactation, glucocorticoids administration, and stress have all been found to increase the risk of insulin resistance or T2DM. Unfavorable environments (socioeconomic situation and famine) or obesity also has long-term negative effects on children by causing increased susceptibility to T2DM in adults. We also address the potential mechanisms that may underlie the developmental programming of T2DM. Therefore, it might be possible to prevent or delay the risk for T2DM by improving pre- and/or postnatal factors.
    Journal of Diabetes Research 12/2013; 2013(1):485082. DOI:10.1155/2013/485082 · 2.16 Impact Factor
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    ABSTRACT: Previous studies have demonstrated that both retinoids and apelin possess potent cardiovascular properties and that retinoids can mediate the expression of many genes in the cardiovascular system. However, it is not clear whether and how retinoids regulate apelin expression in rat vascular smooth muscle cells (VSMCs). In this study, we investigated the molecular mechanism of apelin expression regulation by synthetic retinoid Am80 in VSMCs. The results showed that Am80 markedly upregulated apelin mRNA and protein levels in VSMCs. Furthermore, KLF5 and Sp1 cooperatively mediated Am80-induced apelin expression through their direct binding to the TGF-β control element (TCE) on the apelin promoter. Interestingly, upon Am80 stimulation, the retinoic acid receptor alpha (RARα) was recruited to the apelin promoter by interacting with KLF5 and Sp1 prebound to the TCE site of the apelin promoter to form a transcriptional activation complex, subsequently leading to the upregulation of apelin expression in VSMCs. Thus, these results describe a novel mechanism of apelin regulation by Am80 and further expand the network of RARα in the retinoid pathway.
    Biochemical Journal 08/2013; 456(1). DOI:10.1042/BJ20130418 · 4.40 Impact Factor
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    ABSTRACT: The Krüppel-like factor 4 is a DNA-binding transcriptional regulator that regulates a diverse array of cellular processes, including development, differentiation, proliferation, and apoptosis. The previous studies about KLF4 functions mainly focused on its role as a transcription factor, its functions in the cytoplasm are still unknown. In this study, we found that PDGF-BB could prompt the translocation of KLF4 to the cytoplasm through CRM1-mediated nuclear export pathway in vascular smooth muscle cells (VSMCs) and increased the interaction of KLF4 with actin in the cytoplasm. Further study showed that both KLF4 phosphorylation and SUMOylation induced by PDGF-BB participates in regulation of cytoskeletal organization by stabilizng the actin cytoskeleton in VSMCs. In conclusion, these results identify that KLF4 participates in the cytoskeletal organization by stabilizing cytoskeleton in the cytoplasm of VSMCs.
    Biochemical and Biophysical Research Communications 05/2013; 436(2). DOI:10.1016/j.bbrc.2013.05.067 · 2.30 Impact Factor
  • Peng Xue · Xuelun Wu · Lixin Zhou · Huan Ma · Yan Wang · Yan Liu · Jianxia Ma · Yukun Li ·
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    ABSTRACT: Whether Insulin-like growth factor 1 (IGF1) inhibits or promotes the osteogenic differentiation in vitro remains controversial. Moreover, the biological mechanisms and signaling pathways by which IGF1 affects osteogenic differentiation remain obscure. Transcriptional coactivator with PDZ-binding motif (TAZ) plays a vital role in the osteogenic differentiation of mesenchymal stem cells (MSCs), and strongly activates runt related transcription factor 2 (RUNX2)-driven genes during the terminal osteogenic differentiation. In the present study, we found that IGF1 increased the ALP activities and calcium depositions of MSCs derived from rat bone marrow dose-dependently, with a peak at 100-200 ng/ml. IGF1 increased TAZ and RUNX2 expression mainly at the early stage of osteogenic differentiation, but increased OCN expression at the late stage. Our data further demonstrated that down-regulation of TAZ expression by siRNA inhibited the IGF1 induced increase in osteogenic differentiation. Moreover, UO126 (MEK-ERK inhibitor), not LY294002 (PI3K-Akt inhibitor), inhibited the IGF1 induced increase in TAZ expression. Taken together, we provide evidence to demonstrate that IGF1 promotes the osteogenic differentiation of rat MSCs by increasing TAZ expression, and that the increased TAZ expression induced by IGF1 is mostly mediated by MEK-ERK pathway.
    Biochemical and Biophysical Research Communications 03/2013; 433(2). DOI:10.1016/j.bbrc.2013.02.088 · 2.30 Impact Factor
  • Yan Wang · Baoxin Li · Wei Zhang · Yan Liu · Peng Xue · Jianxia Ma · Yukun Li ·
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    ABSTRACT: It is well established that estrogen deficiency is strongly linked to the development of insulin resistance (IR), but the mechanism is still unclear. Since IR is characterized by a marked reduction in insulin-stimulated PI3 K-mediated activation of Akt in liver and skeletal muscle, we hypothesized that ovariectomized rats (OVX) would exhibit reductions in the expression of proteins in PI3 K signaling pathway, including PI3 K and Akt. As hypothesized, after observing for 12 weeks, compared with the SHAM rats, ovariectomy led to decreased plasma estrogen level and increased HOMA-IR index; in addition, ovariectomy also caused decreased PI3 K and Akt expression levels in the liver and skeletal muscle. Interestingly, the expression patterns differed in tissue-dependent fashion: Akt1 was only found reduction in liver, whereas Akt2 decreased in muscle; these changes can be reversed by estrogen supplement (OVXE). In conclusion, data demonstrate that estrogen withdrawals may cause IR at least in part by impaired PI3 K/Akt signaling proteins in liver and skeletal muscle, and Akt1 and Akt2 might be tissue-specific expressions.
    Endocrine 02/2013; 44(3). DOI:10.1007/s12020-013-9894-1 · 3.88 Impact Factor
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    Hui-Jie Ma · Xin-Li Huang · Yan Liu · Ya-Min Fan ·
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    ABSTRACT: We speculated that the enhanced apoptosis of polymorphonuclear neutrophil (PMN) might be responsible for the inhibition of PMN infiltration in the lung. This study was designed to investigate the effects of sulfur dioxide (SO(2)) on PMN apoptosis in vivo and in vitro, which may mediate the protective action of SO(2) on pulmonary diseases. Acute lung injury (ALI) was induced by intratracheally instillation of lipopolysaccharide (LPS, 100 μg/100 g, in 200 μL saline) in adult male SD rats. SO(2) solution (25 μmol/kg) was administered intraperitoneally 30 min before LPS treatment. The rats were killed 6 h after LPS treatment. Lung tissues were collected for histopathologic study and SO(2) concentration assay. Bronchoalveolar lavage fluid (BALF) was collected for the measurement of PMN apoptosis. For in vitro experiments, rat peripheral blood PMNs were cultured and treated with LPS (30 mg/L) and SO(2) (10, 20 and 30 μmol/L) for 6 h, and apoptosis-related protein expression was detected by Western blotting, and apoptosis rate was measured with flow cytometry. LPS treatment significantly reduced the SO(2) concentrations in the lung tissue and peripheral blood, as compared with the control group. Pretreatment with SO(2) prevented LPS-induced reduction of the SO(2) concentration in the lung tissue and peripheral blood. LPS treatment significantly reduced PMN apoptosis both in vivo and in vitro, which could be prevented by the pretreatment with SO(2). The protein levels of Caspase-3 and Bax was significantly increased, but Bcl-2 was decreased by the pretreatment with SO(2), as compared with LPS administration alone. SO(2) plays an important role as the modulator of PMN apoptosis during LPS-induced ALI, which might be one of the mechanisms underlying the protective action of SO(2) on pulmonary diseases.
    Acta Pharmacologica Sinica 07/2012; 33(8):983-90. DOI:10.1038/aps.2012.70 · 2.91 Impact Factor
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    ABSTRACT: Krüppel-like factor 5 (KLF5) plays an important role in cellular proliferation and differentiation. In this study, we show that adenovirus-mediated overexpression of KLF5 increased neointimal formation, while human heart LIM protein (hhLIM) decreased neointimal formation following vascular injury. Interestingly, neointimal formation was significantly increased in the animals where both hhLIM and KLF5 were introduced, suggesting that KLF5 can reverse hhLIM function in cell proliferation on the coexpression with hhLIM. These results were also confirmed the cellular level. Further mechanistic studies suggested that PDGF-BB promoted the interaction between hhLIM and KLF5 through stimulating hhLIM binding to TGF-β control element (TCE) on the cyclin E promoter in a KLF5-dependent manner. Failure of KLF5 binding to the TCE, on the knockdown of KLF5 by transfecting siRNA, not only prevented the recruitment of hhLIM to the cyclin E promoter but also affected activation of the cyclin E promoter by KLF5. These data suggest that KLF5 reverses hhLIM function from anti-proliferation to pro-proliferation through its interaction with hhLIM on the cyclin E promoter.
    Molecular and Cellular Biochemistry 05/2012; 367(1-2):185-94. DOI:10.1007/s11010-012-1332-9 · 2.39 Impact Factor
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    ABSTRACT: Diabetes Mellitus (DM) is an important risk factor of erectile dysfunction (ED). We sought to investigate the nature and mechanism of the vasoreactivity in Akita (Ins2 [WT/C96Y]) mice, a model of genetic nonobese Type 1 diabetes that recapitulates human Type 1 diabetes. Eight wild-type (WT) mice (group 1) and 8 Akita mice (group 2) were used for this study. Corporal tissues were harvested and studied for endothelium-dependent and endothelium-independent vasoreactivities by isometric tension study; levels of vascular endothelial growth factor (VEGF) and cyclic guanosine monophosphate (cGMP) were studied with the use of enzyme-linked immunosorbent assay (ELISA). Endothelium-dependent and endothelium-independent vasoreactivities, cGMP, and VEGF were significantly decreased in the corporal tissues of Akita mice. Corporal tissues from Akita mice demonstrate many of the major functional and biochemical changes found in humans with ED. This model could serve as a valuable tool for advancing our understanding of the role DM plays in the pathogenesis of ED.
    Journal of Andrology 11/2010; 31(6):547-51. DOI:10.2164/jandrol.110.010223 · 2.47 Impact Factor
  • Yukuin Li · Yan Wang · Fan Wu · Baoxin Li · Yi Haung · Yan Liu ·

    Bone 10/2008; 43. DOI:10.1016/j.bone.2008.08.031 · 3.97 Impact Factor