Publications by authors named "Dong-juan Zhang"

8 Publications

  • Page 1 of 1

[Study on the authenticity of immunization coverage on the routine immunization coverage surveillance system of Fujian province].

Zhonghua Liu Xing Bing Xue Za Zhi 2011 Sep;32(9):946-8

Fuijian Provincial Center for Disease Control and Prevention, Fuzhou 350004, China.

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September 2011

Proteomic analysis of glutathione S-transferase isoforms in mouse liver mitochondria.

World J Gastroenterol 2012 Jul;18(26):3435-42

Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 101318, China.

Aim: To survey glutathione (GSH) S-transferase (GST) isoforms in mitochondria and to reveal the isoforms' biological significance in diabetic mice.

Methods: The presence of GSTs in mouse liver mitochondria was systematically screened by two proteomic approaches, namely, GSH affinity chromatography/two dimensional electrophoresis (2DE/MALDI TOF/TOF MS) and SDS-PAGE/LC ESI MS/MS. The proteomic results were further confirmed by Western blotting using monoclonal antibodies against GSTs. To evaluate the liver mitochondrial GSTs quantitatively, calibration curves were generated by the loading amounts of individual recombinant GST protein vs the relative intensities elicited from the Western blotting. An extensive comparison of the liver mitochondrial GSTs was conducted between normal and db/db diabetic mice. Student's t test was adopted for the estimation of regression and significant difference.

Results: Using GSH affinity/2DE/MALDI TOF/TOF MS, three GSTs, namely, alpha3, mu1 and pi1, were identified; whereas five GSTs, alpha3, mu1, pi1, kappa1 and zeta1, were detected in mouse liver mitochondria using SDS-PAGE/LC ESI MS/MS, of these GSTs, GST kappa1 was reported as a specific mitochondrial GST. The R² values of regression ranged between values of about 0.86 and 0.98, which were acceptable for the quantification. Based on the measurement of the GST abundances in liver mitochondria of normal and diabetic mice, the four GSTs, alpha3, kappa1, mu1 and zeta1, were found to be almost comparable between the two sets of animals, whereas, lower GST pi1 was detected in the diabetic mice compared with normal ones, the signal of Western blotting in control and db/db diabetic mice liver mitochondria is 134.61 ± 53.84 vs 99.74 ± 46.2, with P < 0.05.

Conclusion: Our results indicate that GSTs exist widely in mitochondria and its abundances of mitochondrial GSTs might be tissue-dependent and disease-related.
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http://dx.doi.org/10.3748/wjg.v18.i26.3435DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3396197PMC
July 2012

[Determination of process variable pH in solid-state fermentation by FT-NIR spectroscopy and extreme learning machine (ELM)].

Guang Pu Xue Yu Guang Pu Fen Xi 2012 Apr;32(4):970-3

School of Electrical and Information Engineering, Jiangsu University, Zhenjiang 212013, China.

Fourier transform near-infrared (FT-NIR) spectroscopy was attempted to determine pH, which is one of the key process parameters in solid-state fermentation of crop straws. First, near infrared spectra of 140 solid-state fermented product samples were obtained by near infrared spectroscopy system in the wavelength range of 10 000-4 000 cm(-1), and then the reference measurement results of pH were achieved by pH meter. Thereafter, the extreme learning machine (ELM) was employed to calibrate model. In the calibration model, the optimal number of PCs and the optimal number of hidden-layer nodes of ELM network were determined by the cross-validation. Experimental results showed that the optimal ELM model was achieved with 1040-1 topology construction as follows: R(p) = 0.961 8 and RMSEP = 0.104 4 in the prediction set. The research achievement could provide technological basis for the on-line measurement of the process parameters in solid-state fermentation.
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April 2012

[Proteinomics study in diabetes nephropathy].

Sheng Li Ke Xue Jin Zhan 2010 Apr;41(2):129-32

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April 2010

Enhanced pressor response to acute Ang II infusion in mice lacking membrane-associated prostaglandin E2 synthase-1.

Acta Pharmacol Sin 2010 Oct 27;31(10):1284-92. Epub 2010 Sep 27.

Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing, China.

Aim: To examine the contribution of vascular membrane-associated prostaglandin E2 synthase-1 (mPGES-1) to acute blood pressure homeostasis.

Methods: Angiotensin II (AngII, 75 pmol·kg⁻¹·min⁻¹) was continuously infused via the jugular vein into wild-type and mPGES-1(-/-) mice for 30 min, and blood pressure was measured by carotid arterial catheterization. RT-PCR and immunohistochemistry were performed to detect the expression and localization of mPGES-1 in the mouse arterial vessels. Mesenteric arteries were dissected from mice of both genotypes to study vessel tension and measure vascular PGE2 levels.

Results: Wild-type and mPGES-1(-/-) mice showed similar blood pressure levels at baseline, and the acute intravenous infusion of AngII caused a greater increase in mean arterial pressure in the mPGES-1(-/-) group, with a similar diuretic and natriuretic response in both groups. mPGES-1 was constitutively expressed in the aortic and mesenteric arteries and vascular smooth muscle cells of wild-type mice. Strong staining was detected in the smooth muscle layer of arterial vessels. Ex vivo treatment of mesenteric arteries with AngII produced more vasodilatory PGE2 in wild-type than in mPGES-1(-/-) mice. In vitro tension assays further revealed that the mesenteric arteries of mPGES-1(-/-) mice exhibited a greater vasopressor response to AngII than those arteries of wild-type mice.

Conclusion: Vascular mPGES-1 acts as an important tonic vasodilator, contributing to acute blood pressure regulation.
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http://dx.doi.org/10.1038/aps.2010.99DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895497PMC
October 2010

[Role of increased activity of carbohydrate response element binding protein in excessive lipid accumulation in the liver of type 2 diabetic db/db mouse].

Beijing Da Xue Xue Bao Yi Xue Ban 2009 Jun;41(3):307-12

Department of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences; Key Laboratory of Molecular Cardiology, Ministry of Education; Peking University Diabetes Center, Beijing 100191, China.

Objective: To study the role of the carbohydrate response element binding protein (ChREBP) in excessive lipid deposition in the liver of db/db mouse.

Methods: The deposition of neutral lipids in the liver was evaluated by Oil Red O staining. Immunohistochemical assay was utilized to determine the localization of ChREBP protein expression in mouse liver. The expressions of ChREBP and its target genes including acetyl-coenzyme A carboxylase 1 (Acc-1), fatty acid synthase (Fas), glycerol-3-phosphate acyltransferase (Gpat) were analyzed by Real-time PCR and Western blot.

Results: Significant lipid droplet deposition was detected in the livers of db/db mice. ChREBP was diffusely expressed in heptocytes with relative higher expression levels around portal and central veins. ChREBP was predominantly located in the cytosol in non-diabetic db/m mice, but was translocated to the nucleus in db/db mice. Nuclear ChREBP protein levels were 8.2-fold higher in db/db mice than in db/m mice(P<0.01). In contrast, another lipogenic transcription factor, sterol regulatory element binding protein-1(SREBP-1), remained unchanged. Consistent with increased nuclear ChREBP levels, expressions of ChREBP target genes involved in lipogenesis including Acc-1, Fas and Gpat were upregulated by 2-fold(P<0.05),1.7-fold (P<0.05) and 4.2-fold(P<0.05), respectively, in db/db mice.

Conclusion: The db/db mouse exhibits significantly higher liver ChREBP activity, which may be associated with the development of hepatic steatosis frequently occurring in type 2 diabetes. Targeting ChREBP might represent a new intervention strategy for fatty liver.
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June 2009

[Activation of liver X receptor regulates fatty acid synthase expression in diabetic liver].

Zhonghua Yi Xue Za Zhi 2008 Mar;88(12):848-52

Second Affiliated Hospital, Dalian Medical University , Dalian 116027, China.

Objective: To investigate the effects of liver X receptor (LXR) on the expression of fatty acid synthase (FAS) in diabetic liver.

Methods: Sixteen-week-old male db/db mice with C57BL/6 background were administered via gavaging of T0901317 (TO), a LXR synthetic agonist, at the dose of 3 mg x kg(-1) x d(-1) or dimethyl sulfide (DMSO), a vehicle alone for 7 days. Then the mice were killed with their livers taken out to undergo immunohistochemistry to observe the distribution of FAS protein. Human hepatocellular liver carcinoma cell of the line HepG2 were cultured with TO (10 micromol/L) or DMSO for 24 hours. Another HepG2 cells were transfected with mouse FAS promoter-luciferase reporter recombinants with or without pcDNA3.1, LXR expression vector, or an active sterol regulatory element binding protein-1c (SREBP-1c) expression vector for 12 hours. Real-time PCR and Western blotting were used to detect the levels of mRNA and protein of FAS and SREBP-1c respectively. Luciferase reporter assay was utilized to examine the activity of mouse FAS promoter.

Results: FAS was abundantly expressed in the mouse livers, especially in the cytoplasm of liver cells. The FAS mRNA levels of the livers of the db/db mice was about 5.5 times as high as that of the db/m mice (P < 0.01). The FAS protein levels in the livers of db/db and db/m mice treated with TO were 1.7 and 3.5 times higher than those of the control mice (both P < 0.05). The SREBP-1 mRNA levels in the liver of the db/m and db/db mice treated with TO were 2.4 and 2.1 times higher compared with the control mice (P < 0.05, P < 0.01). Luciferase test showed that the FAS promoter activity of the HepG2 cells treated with TO was 1.5 times that of the control cells (P < 0.01). The FAS promoter activities of the HepG2 cells transfected with LXR and SREBP-1c were 1.9 and 1.6 times those of the control cells (botn P < 0.01).

Conclusion: LXRE directly or indirect (via SREBP-lc) upregulates the expression of FAS gene in the diabetic liver. LXR may mediate the lipid accumulation in liver of diabetes.
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March 2008

[High glucose downregulates the expression of podocalyxin protein in glomerular podocytes of mice].

Beijing Da Xue Xue Bao Yi Xue Ban 2007 Apr;39(2):167-70

Division of Nephrology, Peking University First Hospital, Beijing 100034, China.

Objective: To examine the expression of podocalyxin protein in glomerular podocytes by long-term high glucose exposure in vitro and in vivo.

Methods: Immunohistochemical staining and computer image analysis were applied to detect the expression of podocalyxin protein in glomeruli from db/db mice and Wt mice. The effects of high glucose on the expression of podocalyxin protein were analyzed by Western blotting. The activation of MAPKS signaling pathway (ERK, p38 and JNK) by high glucose was also examined.

Results: The expressions of podocalyxin protein in db/db mice were obviously less than that in Wt mice [(0.18+/-0.07) vs (0.25+/-0.05),P<0.05] assessed by immunostaining and semiquantitative analysis. Basal levels of podocalyxin protein were observed in cultured mouse podocytes. The level of podocalyxin protein declined at each time point by high glucose incubation, reached the lowest level on the 6th day (5.5% of control group, P<0.01), but no significant changes were observed in normal glucose and mannitol glucose incubation groups. High glucose medium induced phosphorylation of ERK1/2 as early as 30 minutes, reached the peak at hour 6; maintained the activation from hour 12 to 24, and declined to the basal level at hour 48. However, activation of ERK1/2 was not detected in normal glucose and mannitol glucose groups. Blockade of activation of ERK1/2 with PD98059, a specific ERK1/2 activation inhibitor, attenuated the high glucose-induced expression of podocalyxin protein on the 6th day.

Conclusion: High ambient glucose decreases the protein level of podocalyxin by podocyte in vitro and in vivo, and the decrease in podocalyxin protein is ERK1/2jdependent in cultured podocytes.
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April 2007