Li Zhang

Chongqing Normal University, Ch’ung-ch’ing-shih, Chongqing Shi, China

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Publications (393)1644.72 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: An ultrasensitive protocol for surface plasma resonance (SPR) detection of adenosine is designed with the aptamer-based target-triggering cascade multiple cycle amplification, and streptavidin-coated Au-NPs (Au NPs-SA) enhancement to enhance the SPR signals. The cascade amplification process consists of the aptamer-based target-triggering nicking enzyme signaling amplification (T-NESA), the nicking enzyme signaling amplification (NESA) and the hybridization chain reaction (HCR), the whole circle amplification process is triggered by the target recognition of adenosine. Upon recognition of the aptamer to target adenosine, DNA s1 is released from the aptamer and then hybridizes with hairpin DNA (HP1). The DNA s1 can be dissociated from HP1 under the reaction of nicking endonuclease to initiate the next hybridization and cleavage process. Moreover, the products of the upstream cycle (T-NESA) (DNA s2 and s3) could act as the "DNA trigger" of the downstream cycle (NESA and HCR) to generate further signal amplification, resulting in the immobilization of abundant Au NPs-SA on the gold substrate, and thus significant SPR enhancement is achieved due to the electronic coupling interaction between the localized surface plasma of Au NPs and the surface plasma wave. This detection method exhibits excellent specificity and sensitivity towards adenosine with a detection limit of 4 fM. The high sensitivity and specificity make this method a great potential for detecting biomolecules with trace amounts in bioanalysis and clinical biomedicine.
    Analytical chemistry. 12/2014;
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    ABSTRACT: Autoimmune pancreatitis (AIP) is a chronic inflammatory disease of pancreas. We evaluated the clinical manifestations, imaging, and histological presentations of AIP in Chinese patients, and investigated the roles of immunoglobulin E (IgE) and allergic diseases in the diagnosis and pathogenesis of AIP. The clinical records of 22 patients diagnosed with AIP were reviewed and analyzed. All patients with AIP fulfilled the 2006 revised diagnostic criteria proposed by Japan Pancreas Society or the Korean Criteria for AIP. Half (11/22) of AIP patients had allergic diseases. Twenty-one patients had elevated serum IgE levels, and 14 patients had IgE levels more than 3 times that of normal. There were no significant differences between the patients with higher or lower IgE, with or without allergic disease, in clinical features, laboratory tests, diffuse or focal lesions, or the choice of treatment methods; however, more complaints of body weight loss were observed in patients with higher IgE levels. Patients with higher IgE levels and with allergic diseases were more likely to have onset in March, April, May, August, September, or October. IgE levels decreased after therapy, but increased again during recurrence. Increased number of mast cells was found in the pancreatic tissue in AIP. IgE maybe a useful marker for monitoring therapeutic response and recurrence of AIP. Allergic processes may play an important role in the pathogenesis of AIP.
    Chinese medical journal. 12/2014; 127(23):4104-9.
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    ABSTRACT: An exonuclease III-assisted recycling amplification (ERA) coupled with fluorescent DNA-scaffolded silver nanoclusters (Ag NCs) for sensitive determination of hepatitis B virus (HBV) DNA is proposed. The sensing mechanism is based on the employment of two different molecular beacons (MBs), MB1 and MB2. In the absence of targets, the MBs self-hybridize into stable stem-loop structures with exonuclease III (Exo III) cleaving resistance, and the MB2 containing a C-rich loop can be utilized to synthesize Ag NCs with high fluorescence signal. In the presence of targets, the targets can bind with MB1 to form partly duplex structure. With the cleaving of Exo III, the liberated target DNA can initiate the cycle of MB1-target hybridization, while the generated trigger DNA can hybridize with MB2, inducing a conformational change of MB2 from hairpin to single-stranded structure. The structural change of MB2 would influence the formation of Ag NCs, thus producing weak fluorescence signal, and the released trigger DNA could activate the cycle of MB2-trigger hybridization. The present method for HBV DNA analysis exhibits a detection limit of 0.97 nM (S/N = 3) with high specificity, and demonstrates its applicability for the HBV detection in human serum.
    Sensors and Actuators B Chemical 12/2014; 205:219–226. · 3.84 Impact Factor
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    ABSTRACT: In the present study, the key genes and biological functions associated with insulin resistance were investigated by comparing the gene expression profiles of adipose tissue obtained from insulin‑sensitive and insulin‑resistant patients. The gene expression data set GSE20950 was downloaded from the Gene Expression Omnibus, including 39 adipose tissue samples obtained from insulin‑sensitive and insulin‑resistant patients undergoing gastric bypass surgery. Adipose samples were divided into two groups (the insulin‑sensitive and insulin‑resistant groups) and the differentially expressed genes (DEGs) were screened out with packages of R. The interactions among DEGs were retrieved with Osprey and functional enrichment analysis was performed with the WebGestalt system. Information regarding the interaction network and enriched biological functions was combined to construct a functional interaction network. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was then conducted using the Database for Annotation, Visualization and Integrated Discovery. A total of 170 DEGs were detected in the insulin‑sensitive group, 8 downregulated and 162 upregulated. Response to glucose stimulus was the most significantly over‑represented functional term. The focal adhesion pathway was identified to be significant in the genes of the functional interaction network. The present study revealed key biological functions and DEGs in adipose tissues associated with insulin resistance, which may facilitate the development of novel therapies for insulin resistance and diabetes.
    Molecular Medicine Reports 11/2014; · 1.17 Impact Factor
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    ABSTRACT: Objective: The aim of the study was to estimate long-term cost effectiveness of a hepatitis B vaccination catch-up program among children born between 1994 and 2001 (when they were 8 15 years old) in Shandong province, China, to provide information for nationwide evaluation and future policy making. Methods: We determined the cost-effectiveness of the catch-up program compared with the status quo (no catch-up program). We combined a Decision Tree model and a Markov model to simulate vaccination and clinical progression after hepatitis B virus (HBV) infection. Parameters in the models were from the literature, a field survey, program files, and the National Notifiable Disease Reporting System (NNDRS). The incremental cost effectiveness ratio (ICER) was used to compare the two alternative strategies. One-way sensitivity analysis, two-way sensitivity analysis, and probability sensitivity analysis were used to assess parameter uncertainties. Results: The catch-up program was dominant compared with the status quo. Using a total of 5.53 million doses of vaccines, the catch-up program could prevent 21,865 cases of symptomatic acute hepatitis B, 3,088 carrier states with positive hepatitis B surface antigen (HBsAg), and 812 deaths due to HBV infection. The catch-up program could add 28,888 quality-adjusted life years (QALYs) and save $192.01 million in the targeted population in the future. The models were robust, considering parameter uncertainties. Conclusion: The catch-up program in Shandong province among children born between 1994 and 2002 2001 was 'very cost-saving.' It could save life years and reduce total future costs. Our study supported the desirability and impact of such a catch-up program throughout China.
    Human vaccines & immunotherapeutics. 11/2014;
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    ABSTRACT: A facile and quick route for the chemical reduction of graphene oxide (GO) using In powder as a reductant has been established. The reduction of GO by In powder is traced by UV-visible absorption spectroscopy, and the obtained reduced graphene oxide (rGO) is analyzed. The In3+ ions produced during the reaction between the GO and the In powder are chemically transformed to In2O3 and then form In2O3/rGO hybrids. The In2O3/rGO hybrids are used as electrode materials and their electrochemical performance are studied using cyclic voltammetry and galvanostatic charge/discharge. The In2O3/rGO hybrids demonstrate excellent electrochemical performance and their highest specific capacitance is 178.8 F g-1 which is much higher than that of either In2O3 or rGO. In addition, the In2O3/rGO hybrids are also very stable.
    10/2014;
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    ABSTRACT: Curcumin, traditionally used as food and medicinal purposes, has recently been reported to have protective efficacy against hypoxia. Hypoxia is one of the important reactive factors in tumor metastasis, which is a key problem in clinical thyroid cancer therapy. In present study, we investigate the anti-metastatic effect of curcumin on the K1 papillary thyroid cancer cells as well as its potential mechanisms. The results show that curcumin effectively inhibits hypoxia-induced reactive oxygen species (ROS) upregulation and significantly decreases the mRNA and protein expression levels of hypoxia-inducible factor-1α (HIF-1α) in K1 cells. Curcumin also decreases the DNA binding ability of HIF-1α to hypoxia response element (HRE). Furthermore, curcumin enhances E-cadherin expression, inhibits metalloproteinase-9 (MMP-9) enzyme activity, and weakens K1 cells migration under hypoxic conditions. In summary, these results indicate that curcumin possesses a potent anti-metastatic effect and might be an effective tumoristatic agent for the treatment of aggressive papillary thyroid cancers.
    Experimental biology and medicine (Maywood, N.J.). 10/2014;
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    ABSTRACT: The relationship between hydrophobicity and the protective effect of whey protein hydrolysates (WPHs) against oxidative stress was studied. Whey protein was first hydrolysed by pepsin and trypsin to obtain WPHs. After absorbed by macroporous adsorption resin DA201-C, three fractions named as M20, M40, and M60 were eluted by various concentrations of ethanol. The hydrophobicity showed a trend of increase from M20 to M60. Antioxidant ability test in vitro indicated that all the three components of WPHs displayed reasonably good antioxidant ability. Moreover, with the increase of hydrophobicity, antioxidant ability of WPHs improved significantly. Then rat pheochromocytoma line 12 (PC12) cells oxidative model was built to evaluate the suppression of oxidative stress of three components on PC12 cells induced by H2O2. Morphological alterations, cell viability, apoptosis rate, and intracellular antioxidase system tests all indicated that WPHs exert significant protection on PC cells against H2O2-induced damage. Among them, M60 had the highest protective effect by increasing 19·3% cell survival and reducing 28·6% cell apoptosis. These results suggested hydrophobicity of WPHs was contributing to the antioxidant ability and the protective effect against oxidative damage.
    Journal of Dairy Research 10/2014; · 1.34 Impact Factor
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    ABSTRACT: The fuzzy c-means (FCM) algorithm is a widely applied clustering technique, but the implicit assumption that each attribute of the object data has equal importance affects the clustering performance. At present, attribute weighted fuzzy clustering has became a very active area of research, and numerous approaches that develop numerical weights have been combined into fuzzy clustering. In this paper, interval number is introduced for attribute weighting in the weighted fuzzy c-means (WFCM) clustering, and it is illustrated that interval weighting can obtain appropriate weights more easily from the viewpoint of geometric probability. Moreover, a genetic heuristic strategy for attribute weight searching is proposed to guide the alternating optimization (AO) of WFCM, and improved attribute weights in interval-constrained ranges and reasonable data partition can be obtained simultaneously. The experimental results demonstrate that the proposed algorithm is superior in clustering performance. It reveals that the interval weighted clustering can act as an optimization operator on the basis of the traditional numerical weighted clustering, and the effects of interval weight perturbation on clustering performance can be decreased.
    Expert Systems with Applications 10/2014; 41(13):5960–5971. · 1.85 Impact Factor
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    ABSTRACT: A label-free, sensitive and simple method to detect protein kinase based on the selective aggregation of phosphorylated peptide-gold nanoclusters (peptide-AuNCs) triggered by Zr(4+) ion coordination is developed. The AuNCs were synthesized by peptide without any strong reducing agents, which prevent peptides from being disrupted. Under optimal conditions, a linear relationship between the decreased PL intensity of peptide-AuNCs and the concentration of casein kinase II (CK2) in the range of 0.08-2.0unitmL(-1) with a detection limit of 0.027unitmL(-1) (3σ) was obtained. The feasibility of this AuNCs-based sensor was further demonstrated by the assessment of kinase inhibition by ellagic acid, 5,6-dichlorobenzimidazole-1-β-d-ribofuranoside, emodin, and quercetin in human serum. As expected, the PL intensity increased with increasing inhibitor efficiency in the presence of inhibitors. The IC50 value (inhibitor concentration producing 50% inhibition) for ellagic acid was estimated to be 0.045μM. With more sophisticated design of the peptide substrate sequences, the detection of other enzymes will be realized. With characteristics of homogeneous, facile, universal, label-free, and applicable for kinase assay, the proposed sensor provides potential application in kinase-related biochemical fundamental research and inhibitor screening.
    Biosensors & Bioelectronics 09/2014; 64C:234-240. · 6.45 Impact Factor
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    ABSTRACT: Podocyte damage and loss together have an important role in the pathogenesis and progression of glomerulonephritis. Glomerulonephritis patients and healthy controls were enrolled in this study. Biochemical, clinical and experimental procedures included measurement of total urinary protein, renal biopsy and gene expression analysis of the receptor activator of NF-kappaB (RANK). The urinary mRNA levels of RANK were significantly higher in the glomerulonephritis group compared to the controls. The urinary RANK level of glomerular subtypes was correlated significantly with proteinuria. The calculated area of RANK mRNA levels under the curve was 0.61 for minimal change disease (MCD), 0.97 for membranous nephropathy (MN), 0.65 for IgA nephropathy (IgAN), 0.70 for lupus nephritis (LN) and 0.70 for focal segmental glomerulosclerosis (FSGS). The urinary mRNA of RANK might be used to differentiate histologic subtypes of glomerulonephritis, particularly between MCD and MN.
    Biomarkers 08/2014; · 1.88 Impact Factor
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    ABSTRACT: A series of lanthanide thiogermanates [Ln(dien)3]2[Ge2S6]Cl2 [Ln = Pr (Ia), Sm (Ib), Gd (Ic), Dy (Id); dien = diethylenetriamine], [Er2(dien)4(μ-OH)2][Ge2S6] (II) and [Ho(trien)(en)GeS3(SH)] (III, trien = triethylenetetramine, en = ethylenediamine) have been hydrothermally synthesized and structurally characterized. The structures of Ia–d consist of isolated [Ln(dien)3]3+ cations, [Ge2S6]4− anions built up from the connection of two [GeS4] tetrahedra sharing a common edge and Cl− ions. II contains binuclear [Er2(dien)4(μ-OH)2]4+ cations constructed by the linkage of [Er(dien)2]3+ ions and –OH bridging groups, and [Ge2S6]4− anions. III contains neutral holmium-centred complexes, where the unusual protonated tetrahedral anion [GeS3(SH)]3− acts as a chelating ligand to complex the [Ho(en)(trien)]3+ cation. A systematic investigation of six lanthanide thiogermanates and four reported compounds revealed that both the well-known lanthanide contraction and different chelating organic amines have a significant influence on the formation of lanthanide thiogermanates under solvothermal conditions. Density functional theory calculation for III has also been performed and the absorption edges of all compounds have been investigated by UV-vis spectroscopy.
    RSC Advances 08/2014; 4(73). · 3.71 Impact Factor
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    ABSTRACT: Post-exposure prophylaxis with hepatitis B vaccine (HepB) alone is highly effective in preventing perinatal hepatitis B virus (HBV) transmission and the World Health Organization recommends administering HepB to all infants within 24 h after delivery. Maternal screening for HBsAg and administration of hepatitis B immune globulin (HBIG) in addition to HepB for infants born to HBsAg-positive pregnant women can increase the effectiveness of post-exposure prophylaxis for perinatal HBV transmission. In Shangdong Province, China which has a high prevalence of chronic HBV infection, HepB birth dose and HBIG were integrated into the routine childhood immunization program in 2002 and July 2011 respectively. We assessed progress toward implementation of these measures. Hospital-based reporting demonstrated an increase in maternal screening from 70.7% to 96.9% from 2004-2012; HepB birth dose coverage (within 24 h) remained high (96.3-97.1%) during this period. For infants with known HBsAg-positive mothers, the coverage of HBIG increased from 85.0% (before July 2011) to 92.1% (after July 2011). However, HBIG coverage in western areas of Shandong Province remained at 81.1% among infants with known HBsAg-positive mothers. Preterm/low-birth-weight and illness after birth were the most commonly reported reasons for delay in the first dose of HepB to >24 h of birth. Additional education on the safety and immune protection from HepB and HBIG might help to correct delays in administering the HepB birth dose and low HBIG coverage in the western areas of the Shandong Province.
    Human vaccines & immunotherapeutics. 08/2014;
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    ABSTRACT: Hepatocellular carcinoma (HCC) represents a major health problem worldwide. Prostaglandin E2 (PGE2), the predominant product of cyclooxygenase-2, has been implicated in hepatocarcinogenesis. However, the underlying molecular mechanisms remain to be further elucidated. c-myc, a cellular proto-oncogene, is activated or overexpressed in many types of human cancer, including HCC. The present study was designed to investigate the internal relationship and molecular mechanisms between PGE2 and c-Myc in HCC, and to define its role in HCC cell growth and invasion. Our results showed that PGE2 significantly upregulated c-Myc expression at both the mRNA and protein levels, and knockdown of c-Myc blocked PGE2-induced HCC cell growth and invasive ability in human HCC Huh-7 cells. The effect of PGE2 on c-Myc expression was mainly through the EP4 receptor, and EP4 receptor-mediated c-Myc protein upregulation largely depended on de novo biosynthesis of c-Myc mRNA and its protein. EP4 receptor signaling activated GS/AC and increased the intracellular cAMP level in Huh-7 cells. The adenylate cyclase (AC) activator forskolin mimicked the effects of the EP4 receptor agonist on c-Myc expression, while the AC inhibitor SQ22536 reduced EP4 receptor-mediated c-Myc upregulation. These data confirm the involvement of the GS/AC/cAMP pathway in EP4 receptor-mediated c-Myc upregulation. Moreover, the phosphorylation levels of CREB protein were markedly elevated by EP4 receptor signaling, and by using specific inhibitor and siRNA interference, we demonstrated that PKA/CREB was also involved in the EP4 receptor-mediated c-Myc upregulation. In summary, the present study revealed that PGE2 significantly upregulates c-Myc expression at both mRNA and protein levels through the EP4R/GS/AC/cAMP/PKA/CREB signaling pathway, thus promoting cell growth and invasion in HCC cells. Targeting of the PGE2/EP4R/c-Myc pathway may be a new therapeutic strategy to prevent and cure human HCC.
    Oncology reports. 08/2014;
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    ABSTRACT: Astrocytic excitatory amino acid transporters (EAATs) regulate extracellular glutamate concentrations and play a role in preventing neuroexcitotoxicity. Since δ-opioid receptor (DOR) is neuroprotective against excitotoxic injury, we asked if DOR activation upregulates EAAT expression and function.
    British Journal of Pharmacology 07/2014; · 5.07 Impact Factor
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    ABSTRACT: -The KCNH2 gene encodes the Kv11.1 potassium channel that conducts the rapidly activating delayed rectifier current in the heart. The relative expression of the full-length Kv11.1a isoform and the C-terminally truncated Kv11.1a-USO isoform play an important role in regulation of channel function. The formation of C-terminal isoforms is determined by competition between the splicing and alternative polyadenylation of KCNH2 intron 9. It is not known whether changes in the relative expression of Kv11.1a and Kv11.1a-USO can cause long QT syndrome.
    Circulation Cardiovascular Genetics 07/2014; · 6.73 Impact Factor
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    ABSTRACT: A horseradish peroxidase (HRP)-mimicking DNAzyme sequence is first blocked by the triplex-based molecular beacon (tMB). Upon hybridization with single-stranded DNA inputs, triplex–helix molecular switch occurs, and the released product strand self-assembles into the hemin/G-quadruplex-HRP-mimicking DNAzyme that biocatalyzes the formation of a colored product and provides an output signal for the different logic gates. On the basis of this principle, a series of logic gates (OR, XOR, INHIBIT, and AND) have been developed. Moreover, a multilevel circuit (MC) that enforces an overall OR Boolean behavior is developed by connecting the AND and XOR logic gates. The logic output signals can be recognized by naked eyes, thus providing a flexible, secure, economic, and simple method for designing a complex DNA-based logic device.
    The Journal of Physical Chemistry C 06/2014; 118(26):14410–14417. · 4.84 Impact Factor
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    ABSTRACT: A simple method to fabricate Bi nanoparticles by using redox reactions between sodium borohydride and ammonium bismuth citrate in the presence of soluble starch in water phase was developed. The results show that soluble starch is better than PVP in stabilizing Bi nanoparticles. The as-prepared Bi nanoparticles were characterized by Fourier transform infrared spectroscopy, transmission electron microscopy, energy-dispersive X-ray, and powder X-ray diffraction. The catalytic performance of the Bi nanoparticles for the reduction of 4-nitrophenol (4-NP) to 4-aminophenol (4-AP) in the presence of sodium borohydride was studied. The effects of sodium borohydride concentration, initial 4-NP concentration, catalyst dose, and reduction temperature were also investigated.
    Industrial & Engineering Chemistry Research. 06/2014; 53(26):10576–10582.
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    ABSTRACT: Aging is associated with exacerbated brain injury after ischemic stroke. Herein, we explored the possible mechanisms underlying the age-associated exacerbated brain injury after ischemic stroke and determined whether therapeutic intervention with anesthetic post-conditioning would provide neuroprotection in aged rats. Male Fisher 344 rats (young, 4 months; aged, 24 months) underwent 2 h of middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion, with or without sevoflurane post-conditioning for 15 min immediately at the onset of reperfusion. Compared with young rats, aged rats showed larger infarct size, worse neurological scores and more TUNEL positive cells in the penumbral cerebral cortex at 24 h after MCAO. However, edema formation and motor coordination were similar in both groups. Sevoflurane reduced the infarct size, edema formation, and TUNEL positive cells, and improved the neurological outcome in young rats but not in aged rats. Molecular studies revealed that basal expression of the anti-apoptotic molecule B-cell lymphoma-2 (Bcl-2) in the brain was lower in aged rats compared with young rats before MCAO, while basal expression of the pro-apoptotic molecule Bcl-2 associated X protein (Bax) showed similar levels in both groups. MCAO reduced Bcl-2 expression and increased Bax expression in both groups; however, Bax increase was more pronounced in aged rats. In young rats, sevoflurane reversed the above MCAO-induced changes. In contrast, sevoflurane failed to enhance Bcl-2 expression but decreased Bax expression in aged rats. These findings suggest that aging-associated reduction in basal Bcl-2 expression in the brain contributes to increased neuronal injury by enhancing cell apoptosis after ischemic stroke. Sevoflurane post-conditioning failed to provide neuroprotection in aged rats, probably due to its inability to increase Bcl-2 levels and prevent apoptosis in the brain.
    Neuroscience 06/2014; · 3.12 Impact Factor
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    ABSTRACT: Oxidative stress has been implicated in both normal aging and various neurodegenerative disorders and it may be a major cause of neuronal death. Chaperone-mediated autophagy (CMA) targets selective cytoplasmic proteins for degradation by lysosomes and protects neurons against various extracellular stimuli including oxidative stress. MEF2A (myocyte enhancer factor 2A), a key transcription factor, protects primary neurons from oxidative stress-induced cell damage. However, the precise mechanisms of how the protein stability and the transcriptional activity of MEF2A are regulated under oxidative stress remain unknown. In this study, we report that MEF2A is physiologically degraded through the CMA pathway. In pathological conditions, mild oxidative stress (200 μM H 2O 2) enhances the degradation of MEF2A as well as its activity, whereas excessive oxidative stress (> 400 μM H 2O 2) disrupts its degradation process and leads to the accumulation of nonfunctional MEF2A. Under excessive oxidative stress, an N-terminal HDAC4 (histone deacetylase 4) cleavage product (HDAC4-NT), is significantly induced by lysosomal serine proteases released from ruptured lysosomes in a PRKACA (protein kinase, cAMP-dependent, catalytic, α)-independent manner. The production of HDAC4-NT, as a MEF2 repressor, may account for the reduced DNA-binding and transcriptional activity of MEF2A. Our work provides reliable evidence for the first time that MEF2A is targeted to lysosomes for CMA degradation; oxidative stress-induced lysosome destabilization leads to the disruption of MEF2A degradation as well as the dysregulation of its function. These findings may shed light on the underlying mechanisms of pathogenic processes of neuronal damage in various neurodegenerative-related diseases.
    Autophagy 06/2014; 10(6):1015-1035. · 12.04 Impact Factor

Publication Stats

8k Citations
1,644.72 Total Impact Points

Institutions

  • 2014
    • Chongqing Normal University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
    • Fourth Military Medical University
      • School of Stomatology
      Xi’an, Liaoning, China
    • Guangdong Academy of Medical Sciences and General Hospital
      Shengcheng, Guangdong, China
    • Guangdong Center for Disease Control and Prevention
      Shengcheng, Guangdong, China
  • 2013–2014
    • Tianjin University
      • • Department of Chemistry
      • • School of Science
      T’ien-ching-shih, Tianjin Shi, China
    • Shanghai Jiao Tong University
      • Center of Instrumental Analysis
      Shanghai, Shanghai Shi, China
    • Southern Medical University
      Shengcheng, Guangdong, China
    • Xi'an Jiaotong University
      Ch’ang-an, Shaanxi, China
  • 2011–2014
    • Lankenau Institute for Medical Research
      Wynnewood, Oklahoma, United States
    • Nanchang University
      Nan-ch’ang-shih, Jiangxi Sheng, China
    • Liaoning University
      Feng-t’ien, Liaoning, China
    • Peking University Third Hospital
      Peping, Beijing, China
    • Peking University
      Peping, Beijing, China
    • Tohoku University
      • Department of Electronic Engineering
      Sendai, Kagoshima-ken, Japan
    • Loyola University Maryland
      Baltimore, Maryland, United States
  • 2009–2014
    • Shandong University
      • School of Public Health
      Chi-nan-shih, Shandong Sheng, China
    • Jiangsu Provincial Center for Disease Control and Prevention
      Chiang-tu, Jiangsu Sheng, China
    • Wenzhou Medical College
      • School of Pharmaceutical Science
      Yung-chia, Zhejiang Sheng, China
  • 2007–2014
    • China-Japan Friendship Hospital
      Peping, Beijing, China
    • Nanjing Medical University
      • • Department of Pathology
      • • Key Laboratory of Reproductive Medicine
      Nan-ching, Jiangsu Sheng, China
    • Jiangsu Institute of Nuclear Medicine
      Jiangqun, Qinghai Sheng, China
    • Tsinghua University
      • Department of Environmental Engineering
      Peping, Beijing, China
  • 2002–2014
    • Henry Ford Hospital
      • Department of Neurology
      Detroit, Michigan, United States
    • Polish Academy of Sciences
      Warszawa, Masovian Voivodeship, Poland
  • 2012–2013
    • Peking Union Medical College Hospital
      Peping, Beijing, China
    • Jiangnan University
      • School of Food Science and Technology
      Wuxi, Jiangsu Sheng, China
    • Sun Yat-Sen University
      Shengcheng, Guangdong, China
    • Logistical College of Chinese People's Armed Police Force
      T’ien-ching-shih, Tianjin Shi, China
  • 2010–2013
    • Chinese Center For Disease Control And Prevention
      Peping, Beijing, China
  • 2009–2013
    • Peking University People's Hospital
      • Heart Center
      Peping, Beijing, China
  • 2006–2013
    • University of Maryland, Baltimore
      • • Center for Vascular and Inflammatory Diseases
      • • Department of Physiology
      Baltimore, Maryland, United States
    • University Center Rochester
      • Department of Medicine
      Rochester, Minnesota, United States
  • 2010–2012
    • Oakland University
      • Department of Physics
      Rochester, MI, United States
  • 2006–2012
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
    • Northeast Institute of Geography and Agroecology
      • State Key Laboratory of Drug Research
      Beijing, Beijing Shi, China
  • 2001–2012
    • Henry Ford Health System
      • Department of Neurology
      Detroit, Michigan, United States
  • 2007–2011
    • Oregon Health and Science University
      • Division of Cardiovascular Medicine
      Portland, OR, United States
  • 2005–2011
    • Stanford University
      • • Department of Chemistry
      • • Department of Materials Science and Engineering
      Stanford, CA, United States
  • 2002–2010
    • University of Utah
      • • School of Medicine
      • • Department of Internal Medicine
      Salt Lake City, Utah, United States
  • 2007–2009
    • University of Science and Technology, Beijing
      Peping, Beijing, China
  • 2006–2009
    • Shanghai Institutes for Biological Sciences
      Shanghai, Shanghai Shi, China
    • Dalian University of Technology
      • School of Electronic and Information Engineering
      Dalian, Liaoning, China
  • 2008
    • Huazhong University of Science and Technology
      • Department of Dermatology
      Wuhan, Hubei, China
    • Case Western Reserve University
      Cleveland, Ohio, United States
    • University of Notre Dame
      • Department of Chemistry and Biochemistry
      United States
    • University of Kentucky
      • Department of Biology
      Lexington, KY, United States
  • 2005–2006
    • Nanjing University
      • State Key Laboratory of Pharmaceutical Biotechnology
      Nanjing, Jiangsu Sheng, China
  • 2003–2004
    • The University of Tokyo
      • • Department of Biotechnology
      • • Faculty & Graduate School of Medicine
      Tokyo, Tokyo-to, Japan
  • 2001–2004
    • University of Tsukuba
      • Institute of Applied Biochemistry
      Tsukuba, Ibaraki, Japan
  • 2000
    • Beijing University of Aeronautics and Astronautics (Beihang University)
      Peping, Beijing, China