作者机构：
[Kai; ChaoKe] Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, Life Science Research Center, University of South China, Hengyang, China
通讯机构：
[ChaoKe Tang] I;Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, Life Science Research Center, University of South China, Hengyang, China
关键词：
Human Umbilical Vein Endothelial Cell;Berberine;Paraoxon;Percutaneous Coronary Interven;Cholesteryl Ester Hydrolase
摘要：
Atherosclerosis-related cardiovascular disease is one of the leading causes of death in China [1]. With advances in our understanding of the molecular mechanisms of atherosclerosis vascular inflammation, lipid metabolism dysfunction, and hypertension are regarded as the main pathogenetic pathways of both early atherogenesis and advanced plaque rupture [2,3]. Currently, much attention is being paid to the control of these pathways, which offers the potential for development of novel therapeutic approaches in the treatment of cardiovascular disease in China.
摘要：
The development of cancer is a pathological process involving multiple environmental carcinogenic factors and genetic alterations. For decades, cancer researchers have focused on genomic and transcriptomic analyses. The completion of the Human Genome Project has opened the door to the post-genome era and oncoproteomics. Proteins play a critical role in tumorigenesis and influence the differences between normal cells and malignant cells. This report proposes the concept that cancer is a proteomic disease. This concept is based on examining protein expression profiles, post-translational modifications, and protein-protein interactions in carcinogenesis using recent advances in comparative, functional and structural proteomics. This approach provides a new way of viewing carcinogenesis, presents new clues in biomarker discovery for cancer diagnosis and therapy, and reveals important scientific findings and their significance to clinical applications.
期刊：
Lipids in Health and Disease,2011年10(1):1-10 ISSN：1476-511X
通讯作者：
Fu, Mingde
作者机构：
[Tian, Li; Fu, Mingde; Liu, Yinghui] Sichuan Univ, W China Hosp, Lab Endocrinol & Metab, Chengdu 610041, Sichuan, Peoples R China.;[Xu, Yanhua] Chengdu Hoist Biotechnol Co LTD, Chengdu 610075, Sichuan, Peoples R China.;[Peng, Tao] Chengdu Univ, Affiliated Hosp Tradit Chinese Med, Chengdu 610072, Sichuan, Peoples R China.;[Long, Shiyin] Univ S China, Dept Biochem & Mol Biol, Hengyang, Hunan, Peoples R China.
通讯机构：
[Fu, Mingde] S;Sichuan Univ, W China Hosp, Lab Endocrinol & Metab, Chengdu 610041, Sichuan, Peoples R China.
关键词：
High Density Lipoprotein;Cholesteryl Ester Transfer Protein;Reverse Cholesterol Transport;High Density Lipoprotein Particle;High Density Lipoprotein Cholesterol Concentration
摘要：
To investigate the effect of triglyceride (TG) integrates with plasma major components of apolipoproteins in HDL subclasses distribution and further elicited the TG-apolipoproteins (apos) interaction in the processes of high density lipoprotein (HDL) mature metabolic and atherosclerosis related diseases. Contents of plasma HDL subclasses were quantities by two-dimensional gel electrophoresis associated with immunodetection in 500 Chinese subjects. Contents of preβ1-HDL, HDL3a, and apoB-100 level along with apoB-100/A-I ratio were significantly increased, whereas there was a significant reduction in the contents of HDL2, apoA-I level as well as apoC-III/C-II ratio with increased TG concentration. Moreover, preβ1-HDL contents is elevated about 9 mg/L and HDL2b contents can be reduced 21 mg/L for 0.5 mmol/L increment in TG concentration. Moreover, with increase of apoA-I levels, HDL2b contents were marginally elevated in any TG concentration group. Furthermore, despite of in the apoB-100/A-I < 0.9 group, the contents of preβ1-HDL increased, and those of HDL2b decreased significantly for subjects in both high and very high TG levels compared to that in normal TG levels. Similarly, in the apoB-100/A-I ≥ 0.9 group, the distribution of HDL subclasses also showed abnormality for subjects with normal TG levels. The particle size of HDL subclasses tend to small with TG levels increased which indicated that HDL maturation might be impeded and efficiency of reverse cholesterol transport(RCT) might be weakened. These data suggest that TG levels were not only significantly associated with but liner with the contents of preβ1-HDL and HDL2b. They also raise the possibility that the TG levels effect on HDL maturation metabolism are subjected to plasma apolipoproteins and apolipoproteins ratios.
作者机构：
[Zhou, Shouhong; Tian, Shaowen; Ouyang, Xinping; Qiao, Ge; Wang, Ling] Univ S China, Coll Med, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.;[Li, Peng] Univ S China, Coll Life Sci & Technol, Dept Biol, Hengyang 421001, Hunan, Peoples R China.;[Tang, Chaoke; Ouyang, Xinping] Univ S China, Life Sci Res Ctr, Inst Cardiovasc Dis, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Tian, Shaowen] U;Univ S China, Coll Med, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.
关键词：
Behavioral sensitization;Memory;Morphine;Rapid eye movement sleep deprivation;Sleep
摘要：
Previous studies have shown that behavioral sensitization is modulated by drug-associated context, in which memory processes may be critically involved. Sleep has been suggested to play an important role in memory processes. However, the relationship between sleep and context-modulated effects on behavioral sensitization remains to be elucidated. In the present study, we designed three experiments to explore the effects of rapid eye movement sleep deprivation (RSD) on context-modulated effects on morphine locomotor sensitization in mice. Mice were subjected to 6 h RSD starting either immediately after morphine pairing training or 6 h later. The control mice were returned to their home cages immediately after pairing training and left undisturbed. In experiment 1, RSD from 0 to 6h but not from 7 to 12 h disrupted paired context-modulated enhancement of locomotor activity. In experiment 2, RSD from 0 to 6 h but not from 7 to 12 h disrupted unpaired context-modulated suppression of locomotor activity. In experiment 3, RSD from either 0 to 6h or 7 to 12 h had no effect on conditioned locomotor activity. Our findings suggest that sleep plays a critical role in memory processes underlying context-modulated effects on morphine locomotor sensitization. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
摘要：
Background: Numerous man-made pollutants activate the aryl hydrocarbon receptor (AhR) and are risk factors for type 2 diabetes. AhR signaling also affects molecular clock genes to influence glucose metabolism. Objective: We investigated mechanisms by which AhR activation affects glucose metabolism. Methods: Glucose tolerance, insulin resistance, and expression of peroxisome proliferator-activated receptor-α (PPAR α) and genes affecting glucose metabolism or fatty acid oxidation and clock gene rhythms were investigated in wild-type (WT) and AhR-deficient [knockout (KO)] mice. AhR agonists and small interfering RNA (siRNA) were used to examine the effect of AhR on PPAR α expression and glycolysis in the liver cell line Hepa-1c1c7 (c7) and its c12 and c4 derivatives. Brain, muscle ARNT-like protein 1 (Bmal1) siRNA and Ahr or Bmal1 expression plasmids were used to analyze the effect of BMAL1 on PPAR α expression in c7 cells. Results: KO mice displayed enhanced insulin sensitivity and improved glucose tolerance, accompanied by decreased PPAR α and key gluconeogenic and fatty acid oxidation enzymes. AhR agonists increased PPAR α expression in c7 cells. Both Ahr and Bmal1 siRNA reduced PPAR α and metabolism genes. Moreover, rhythms of BMAL1 and blood glucose were altered in KO mice. Conclusions: These results indicate a link between AhR signaling, circadian rhythms, and glucose metabolism. Furthermore, hepatic activation of the PPAR α pathway provides a mechanism underlying AhR-mediated insulin resistance.
作者机构：
[Huang, Fulian; Zhou, Shouhong; Tian, Shaowen; Yang, Yufeng; Deng, Haifeng; Li, Zhenbang] Univ S China, Coll Med, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.;[Li, Peng] Univ S China, Coll Life Sci & Technol, Dept Biol, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Tian, Shaowen] U;Univ S China, Coll Med, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.
关键词：
Nicotine;Learning and memory;Contextual fear memory;Reconsolidation;Rats
摘要：
There is increasing evidence that nicotine is involved in learning and memory. However, there remains no study that has explored the relationship between nicotine and memory reconsolidation. At present study, we tested the effects of nicotine on the reconsolidation of contextual fear memory in rats. Behavior procedure involved four training phases: habituation (Day 0), fear conditioning (Day 1), reactivation (Day 2) and test (Day 3). Rats were injected saline or nicotine (0.25, 0.5 and 1.0mg/kg) immediately after reactivation. Percent of time spent freezing was used to measure conditioned fear response. Results showed that compared with saline rats, rats with nicotine at 1.0mg/kg presented a significant increase of freezing response on Day 3. Nicotine at 1.0mg/kg was ineffective when injected 6h after reactivation. Further results showed that the enhancement of freezing response induced by nicotine at 1.0mg/kg was dependent on fear memory reconsolidation, and was not attributed to an enhancement of the nonspecific freezing response 24h after nicotine administration. The results suggest that nicotine administration immediately after reactivation enhances contextual fear memory reconsolidation. Our present finding extends previous research on the nicotinic effects on learning and memory.
作者：
Yan, Limei;Hao, Hong;Elton, Terry S.;Liu, Zhenguo*;Ou, Hesheng
期刊：
Molecular and Cellular Biochemistry,2011年357(1-2):9-19 ISSN：0300-8177
通讯作者：
Liu, Zhenguo
作者机构：
[Yan, Limei] Univ S China, Biochem Res Ctr, Hengyang 421001, Hunan, Peoples R China.;[Liu, Zhenguo; Hao, Hong; Elton, Terry S.; Ou, Hesheng] Ohio State Univ, Med Ctr, Davis Heart & Lung Res Inst, Columbus, OH 43210 USA.;[Liu, Zhenguo; Hao, Hong; Elton, Terry S.; Ou, Hesheng] Ohio State Univ, Med Ctr, Div Cardiovasc Med, Columbus, OH 43210 USA.;[Ou, Hesheng] Guangxi Med Univ, Coll Pharm, Nanning 530021, Peoples R China.;[Liu, Zhenguo] Ohio State Univ, Med Ctr, Davis Heart & Lung Res Inst, DHLRI Suite 200,473 W 12th Ave, Columbus, OH 43210 USA.
通讯机构：
[Liu, Zhenguo] O;Ohio State Univ, Med Ctr, Davis Heart & Lung Res Inst, DHLRI Suite 200,473 W 12th Ave, Columbus, OH 43210 USA.
摘要：
Intronic microRNA (miRNAs) suppressed the expression of endothelial nitric oxide synthase (eNOS) gene in endothelial cells (ECs). This study was to investigate the role of signal transducer and activator of transcription 3 (STAT3) in the regulation of eNOS expression and vascular EC proliferation by the intronic 27-nucleotide (nt) miRNA derived from the 27-base pair repeats in intron 4 of eNOS gene. A detectable level of the 27-nt miRNA was present in the control ECs. Overexpression of the 27-nt miRNA dramatically suppressed the expression of eNOS and STAT3 at both transcription and translation levels in ECs in association with significant inhibition of EC proliferation. Mutation of the 27-nt miRNA at the 3'-terminal region resulted in substantial reduction of the inhibitory effect of miRNA on eNOS and STAT3 expression, and EC proliferation. Overexpression of active STAT3 significantly reversed the inhibitory effect of the 27-nt miRNA on eNOS expression and EC proliferation. In summary, we demonstrated that the 27-nt intronic miRNA functioned as a negative regulator for the expression of its host gene eNOS and cell proliferation in ECs. The sequence in 3'-terminal region played a key role in the function of the 27-nt miRNA. The regulatory effect of the intronic miRNA on eNOS gene expression was associated with miRNA polymorphisms, and mediated through inhibition of STAT3 signaling in ECs.
关键词：
Human telomerase reverse transcriptase;Lung adenocarcinoma;RNAi;Telomerase;siRNA
摘要：
Human telomerase reverse transcriptase (hTERT) is the catalytic subunit and the activity determinant factor of the telomerase enzyme which maintains the length of human chromosomes. In recent years it has become an attractive molecular target for cancer gene therapy. In the present study, we show that hTERT siRNA effectively suppressed the expression of hTERT mRNA and hTERT protein levels, reduced telomerase activity, and induced apoptosis of A549 lung adenocarcinoma cells (P<0.05). In vivo, tumors treated with the hTERT siRNA were of reduced sizes, indicating that the hTERT siRNA also reduced the tumorigenic potential of lung adenocarcinoma cells (P<0.05). These results demonstrate that hTERT siRNA can cause effective suppression of telomerase and lead to apoptosis in A549 lung adenocarcinoma cells. hTERT siRNA may, therefore, be a strong candidate for highly selective therapy for chemoprevention and treatment of lung adenocarcinoma.
作者机构：
[Li, Wenjuan; Zhang, Zuping; Li, Xiaoling; Wang, Wei; Ma, Jian; Xiong, Wei; Wu, Minghua; Liao, Qianjin; Xiang, Bo; Li, Guiyuan; Yi, Mei] Cent S Univ, Xiangya Sch Med, Canc Res Inst, Changsha 410078, Hunan, Peoples R China.;[Li, Xiayu] Cent S Univ, Xiangya Hosp 3, Dept Gastroenterol, Changsha 410013, Hunan, Peoples R China.;[Tan, Yixin] Cent S Univ, Xiangya Hosp 2, Dept Dermatol, Changsha 410008, Hunan, Peoples R China.;[Yi, Mei] Cent S Univ, Xiangya Hosp, Dept Dermatol, Changsha 410008, Hunan, Peoples R China.;[McCarthy, James B.; Yang, Jianbo] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
通讯机构：
[Xiang, Bo] C;Cent S Univ, Xiangya Sch Med, Canc Res Inst, Xiangya Rd, Changsha 410078, Hunan, Peoples R China.
摘要：
Promoter hypermethylation-mediated silencing of tumor suppressor genes (TSGs) is a hallmark of oncogenesis. Oxidored-nitro domain-containing protein 1 (NOR1) is a candidate TSG that is downregulated in nasopharyngeal carcinoma (NPC). In the present study, we identified a functional NOR1 promoter that is regulated by heat shock factor 1 and nuclear respiratory factor 1. The promoter is located within a CpG island. Hypermethylation of this CpG island was found in NPC tissue samples and cancer cell lines, whereas no aberrant promoter methylation was detected in non-cancerous nasopharyngeal tissue samples or normal nasopharyngeal epithelial cells. Treatment of NPC 6-10B cells and leukemia HL60 cells with 5′-aza-2′-deoxycytidine increased endogenous levels of NOR1 messenger RNA. Ectopic expression of NOR1 in NPC HNE1 cells inhibited tumor cell colony formation and viability. These findings suggest that promoter hypermethylation may participate in transcriptional inactivation of the NOR1 gene in NPC. Frequent epigenetic inactivation of the NOR1 gene in NPC suggests that it may be a critical tumor suppressor involved in the development of NPC.
作者机构：
[Xiao, Guohua; Wang, Zongbao; Yu, Jian; Zhang, Yali; Zhang, Sujun; Yin, Weidong; Wang, Yueting] Univ S China, Inst Biochem & Mol Biol, Hengyang 421001, Peoples R China.;[Wang, Zongbao] Univ S China, Dept Lab Anim Sci, Hengyang 421001, Peoples R China.;[Zeng, Huaicai] Univ S China, Sch Publ Hlth, Hengyang 421001, Peoples R China.
通讯机构：
[Wang, Zongbao] U;Univ S China, Inst Biochem & Mol Biol, Hengyang 421001, Peoples R China.
摘要：
Objective: Endothelial dysfunction is a key event in the onset and progression of atherosclerosis associated with diabetes. Increasing cell apoptosis may lead to endothelial dysfunction and contribute to vascular complications. Therefore, we aimed to elucidate the possible role and mechanism of ibrolipim in preventing endothelial dysfunction induced by high glucose. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured respectively under normal glucose level (5.5 mM), high glucose level (33 mM), and high glucose level with ibrolipim treatment. Endothelial dysfunction was identified by the expression of ET-1 and vWF through reverse transcription PCR (RT-PCR). HUVECs apoptosis was assessed by fluorescent staining with Hoechst 33258. Akt activity was analyzed by western blot. Results: High glucose condition significantly increased the rate of apoptotic cells, weakened cell viability, and decreased the expression of ET-1 and vWF. Ibrolipim treatment significantly attenuated these alterations of endothelial dysfunction. The lower concentrations (2, 4, 8 μM) of ibrolipim inhibited apoptosis of cultured HUVECs, improved cell viability, down-regulated the mRNA levels of ET-1, vWF, and attenuated the cytotoxicity; however, higher concentration (16, 32 μM) of ibrolipim aggravated the damage of HUVECs cultured under high glucose level. Meanwhile, high glucose induced a decrease of Akt activity which led to apoptosis, and ibrolipim prevented the decrease and attenuated apoptotic effect induced by high glucose. Furthermore, the PI3K inhibitor LY294002 significantly abolished the anti-apoptotic effect of ibrolipim, and decreased Akt phosphorylation. Although, the expression of Akt mRNA and total protein were not altered in cultured HUVECs. Conclusion: Ibrolipim at lower concentrations can inhibit high glucose-induced apoptosis in cultured HUVECs, which might be related to the alternation of Akt activity. Ibrolipim has the potential to attenuate endothelial dysfunction and lower the risk of diabetes-associated vascular diseases. And it might be a therapeutic agent for diabetic vascular complications.
