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Urotensin Ⅱ increases endothelin production by vascular smooth muscle cells in rats

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Chinese science Bulletin 2002年第12期47卷 1007-1010页

作者： Ql Yongfen, BU Dingfang, YANG Jun, ZHANG Zhaokang, NIU Dadi, SHI Yanrong, ZHANG Zhenghao, TANG Chaoshu & DU JunbaoInstitute of Cardiovascular Diseases, The First Hospital of Peking University, Beijing 100083, China department of physiology, health science Institute of Cardiovascular Diseases First Hospital of Peking University Beijing 100083 China

The aim of this study was to observe the effects of urotensin Ⅱ (UII) on production of endothelin (ET) in rat aortic vascular smooth muscle cells (VSMC). Cultured VSMCs incubated with various concentrations of UII were used to measure the YSMC 3H-TdR incorporation, the amount of ET mRNA and ET production in VSMCs. In this work we found that UII (10-10-10-8 mol/L) promoted VSMC 3H-TdR incorporation (47%-83%, P<0.01) and increased the amount of ET mRNA by 17.1% (P < 0.05) to 112.8% (P < 0.01), respectively, in a concentration dependent manner compared with control. After 4 and 8 h incubation, 10-10-10-8 mol/L of UII elevated the ET synthesis and release in a concentration dependent manner. After 4 h incubation, the content of ET in medium was 4.9, 5.36 and 7.12 pg/mL (P < 0.01). After 8 h incubation, the ET content released from VSMCs was 12.6, 12.07 and 17.17 pg/mL (P < 0.01). In addition, it was found that BQ123, a specific ETA receptor antagonist, obviously decreased the VSMC DNA synthesis induced by

关键词： urotensin II endothelin mRNA peptide/interaction.

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Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

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Cell Research 2003年第5期13卷 385-391页

作者： JIAN WEN DONG, HAI FENG ZHU, WEI ZHONG ZHU, HAI LEI DING, TIE MIN MA, ZHAO NIAN ZHOU 1 Laboratory of Hypoxic Cardiovascular physiology, Shanghai Institutes for Biological sciences, Chinese Academy of sciences, Shanghai 200031, China.2 department of physiology and Pathophysiology, health science Center Peking University, Beijing 100083 China Laboratory of Hypoxic Cardiovascular physiology Shanghai Institutes for Biological SciencesChinese Academy of Sciences Shanghai China department of physiology and Pathophysiology Health Science Center Peking University Beijing China

Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury. Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. Adult male Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h/day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Isolated perfused hearts from both groups were subjected to 30 min of global ischemia followed by 60 min reperfusion. Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling （TUNEL） and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins, Bax and Bcl-2, in cytosolic and membrane fraction were detected by Western Blotting. After ischemia/reperfusion, enhanced recovery of ca

关键词： intermittent hypoxia apoptosis cardiac myocytes Bax Bcl-2.

Sodium hydrosulfide alleviated pulmonary vascular structural remodeling induced by high pulmonary blood flow in rats

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Acta Pharmacologica Sinica 2006年第8期27卷 971-980页

作者： Xiao-hui LI~2 Jun-bao DU~(2,6) Ding-fang BU~3 Xiu-ying TANG~4 Chao-shu TANG~5 ~1department of Pediatrics,Peking University First Hospital,Key Laboratory of Molecular Cardiovascular Diseases,Ministry of Education ~3 Laboratory Center ~4Laboratory of Electron Microscopy,Peking University First Hospital,Beijing 100034,China ~5department of physiology,Peking University health science Center,Beijing 100083,China department of Pediatrics Peking University First Hospital Key Laboratory of Molecular Cardiovascular Diseases Ministry of Education Beijing China Laboratory Center Peking University First Hospital Beijing China Laboratory of Electron Microscopy Peking University First Hospital Beijing China department of physiology Peking University Health Science Center Beijing China

Aim:To explore the possible role of endogenous hydrogen sulfide （H2S）,a novelgasotransmitter,in the pathogenesis of pulmonary vascular structural remodeling（PVSR） induced by high pulmonary blood ***:Thirty-two Sprague-Dawley male rats were randomly divided into sham,shunt,sham+NaHS （a H2Sdonor） and shunt+NaHS *** in shunt and shunt+NaHS groups under-went an abdominal aorta-inferior vena cava shunt,and rats in shunt+NaHS andsham+NaHS groups were intraperitoneally injected with *** was inves-tigated using optical microscope and transmission electron *** H2S was evaluated by sulfide-sensitive *** oxide synthase（NOS）,heme oxygenase （HO-1）,proliferative cell nuclear antigen （PCNA） andextracellular signal-regulated kinase （ERK） activation were analyzed by ***:After 11 weeks of shunting,PVSR developed with a decrease inlung tissue H2S production and an increase in nitric oxide （NO）.However,lungtissue carbon monoxide （CO） did not *** the treatment with NaHS for11 weeks,H2S donor ameliorated PVSR and downregulated PCNA expression andERK activation with an increase in lung tissue CO production and HO-1 proteinexpression but a decrease in NO production,NOS activity and eNOS proteinexpression in shunted ***:H2S exerted a regulatory effect on PVSRinduced by high pulmonary blood ***,H2S down-regulated theERK/MAPK signal pathway,inhibited the NO/NOS pathway and enhanced theCO/HO pathway in rats with high pulmonary blood flow.

关键词： hydrogen sulfide pulmonary hypertension structure remodeling nitric oxide/nitric oxide synthase carbon monoxide/heme oxygenase

Mechanism of Calcitonin Gene-related Peptide Modulating Apoptosis of Vascular Smooth Muscle Cells

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Mechanism of Calcitonin Gene-related Peptide Modulating Apop...

Taurine antagonized oxidative stress injury induced by homocysteine in rat vascular smooth muscle cells

2002全国青年药理学英文学术会议

作者： WANG Wang, WANG Xian (department of physiology, health science Center, Peking University, Beijing, 100083)

AIM: Atherosclerosis (AS) is one of the major threatens of the health and life of human being. Accumulating data have supported the idea that the pathogenesis of AS includes a set of inflammatory and immune responses. The migration, proliferation and apoptosis of smooth muscle cells (SMC) also play an important role. Calcitonin gene-related peptide (CGRP) is a neuropeptide with potent vasodilatory effect. CGRP and its receptors are widely expressed throughout the cardiovascular system. Recently, more and more vasodilators have been found to have antiproliferative effects on SMC. Our previous data

关键词： Calcitonin Gene-related Peptide /Vascular Smooth Muscle Cells /Apoptosis

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Acta Pharmacologica Sinica 2004年第3期25卷 87-92页

作者： Lin CHANG2,3,Jian-xin XU4,Jing ZHAO5,Yong-zheng PANG2,3,Chao-shu TANG2,3,Yong-fen QI5,6 2Institute of Cardiovascular Diseases,the FirstHospital,Peking University,Beijing 100034 3Institute of Cardiovascular Diseases,Peking University,Beijing 100083 4Instituteof Biophysics,Chinese Academy of sciences,Beijing 100101 5department of physiology,health science Center,Peking University,Beijing 100083,China Institute of Cardiovascular Diseases the First Hospital Peking University 北京 100034 Institute of Biophysics Chinese Academy of Sciences 北京 100101 department of physiology Health Science Center Peking University 北京 100083

AIM: To observe protective effects of taurine on reactive oxygen species generation induced by homocysteine in rat vascular smooth muscle cells (VSMC). METHODS: Rat VSMC was incubated with various concentrations of homocysteine and taurine. The lactate dehydrogenase (LDH) activity which released into culture medium was elevated as an indicator for VSMC injury. The reactive oxygen species (ROS) — hydrogen peroxide (H2O2) and superoxide anion (O2ˉ· )were measured with luminol or lucigenin chemiluminescences method, and the mitochondria Mn-superoxide dismutase (Mn-SOD) and catalase (CAT) were also measured in treated VSMC. RESULTS: LDH leakage from cultured VSMC treated with homocystenie, was increased (P0.05 vs control). In this study, the superoxide anion in VSMC was not detectable by chemiluminent method. In addition, treatment of VSMC with taurine increased mitochondria Mn-SOD and CAT activity in a concentration dependent manner (P<0.05), but homocysteine decreased mitochondria Mn-SOD and CAT activity (P<0.01 vs control). In addition, co-administration of taurine markedly ameliorated homocysteine-induced inhibition of Mn-SOD and CAT activity in VSMC (P<0.01 vs homocysteine alone group). CONCLUSION: Taurine antagonized the effects of homocysteine on ROS generation and anti-oxidant enzyme activities in rat VSMC in vitro.

关键词： homocysteine taurine vascular smooth muscle mitochondria reactive oxygen species

Proteomic analysis of lipid raft proteins in human endothelial cells after atorvastatin treatment

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Proteomic analysis of lipid raft proteins in human endotheli...

Identification of over-expressed genes in human renal cell carcinoma by combining suppression subtractive hybridi-zation and cDNA library array

中国生理学会第23届全国会员代表大会暨生理学学术大会

作者： Ming-Xia GU,Ying-Jian HOU,Yi FU,Cheng-Hong LI,Yi ZHU department of physiology and Pathophysiology,health science Center,Peking University,Beijing 100083,China

Background:Statins,as a HMG-CoA reductase inhibitor,have been used in clinical treatment extensively these years to help patients reduce plasma LDL cholesterol levels,thereby effectively cutting down the incidence of cardiovascular ***,accumulated evidence suggests that statins also exert other vascular protective effects beyond cholesterol reduction,such as anti-inflammatory and anti-oxidative ***, the acute effects of statins on endothelial cells(ECs) were still ***,we investigated the short-term beneficial effects of statins by modulating lipid rafts related protein translocation in ECs,which might offer another insight into the pleiotropic functions of *** and results:After treatment of human umbilical vein ECs (HUVECs) with atorvastatin for short times(30 min or 2 h),proteins on membrane lipid rafts were isolated through sucrose density gradient *** quantitative proteomics analysis(isobaric tagging for relative and absolute quantitation(iTRAQ labeling technique coupled with Nano-liquid chromatography/tandem mass spectrometry (LC/MS/MS)) was *** functional classification of more than 300 proteins obtained from proteomic analysis,we found that atorvastatin mainly increased anti-oxidative proteins and proteins enhancing cell barrier,and decreased proteins associated with mitochondrial function and cells adhesion in endothelial lipid rafts. These results indicating that atorvastatin played a protective role,at least partly,through regulating the protein translocation in lipid rafts in a short *** proteins were verified according to the results of *** anti-oxidative protein(ERp46),which was significantly increased in lipid rafts after atorvastatin treatment,was further *** results revealed that atorvastatin dramatically repressed cell membrane NADPH oxidase activation both under untreated condition and after angiotensinⅡ(AngⅡ) ***-IP and immunofluoresce

关键词： atorvastatin proteomics lipid raft ERp46 Nox2 anti-oxidant

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science China(Life sciences) 2004年第2期47卷 148-157页

作者： AI Junkui1, ZHANG Zhiwen2, XIN Dianqi1, ZHU Hongjian1, YAN Quanjian3, XIN Zhongcheng1, NA Yanqun1 & GUO Yinglu1 1. Institute of Urology, Peking University & department of Urology, First Hospital, Peking University, Beijing 100034, China 2. department of physiology, Peking University health science Center, Beijing 100083, China 3. department of Urology, Xijing Hospital, the 4th Military Medical University, Xi抋n 710033, China Institute of Urology Peking University & Department of Urology First Hospital Peking University Beijing 100034 China department of physiology Peking University Health Science Center Beijing 100083 China department of Urology Xijing Hospital the 4th Military Medical University Xi'an 710033 China

To isolate the over-expressed genes in human renal cell carcinoma (RCC) and analyze its molecular basis of carcinogenesis, we used the mRNA from human RCC tissues as tester and that from the matched normal kidney tissues as driver to construct the suppression subtractive hybridization library. 379 of the subtracted clones were arrayed onto a nylon mem-brane and the over-expressed genes were then screened by hybridizing the filter with radioac-tively labeled cDNA from RCC and matched normal kidney tissues. 67 clones over-expressed in RCC by a factor of 6 or more were sequenced and its identities were analyzed in GenBank da-tabase. 4 clones were previously unknown fragments and 2 clones represent KIAA genes. The rest clones were the known genes and some of them were RCC-related, including vascular en-dothelial growth factor, vimentin and tissue factor. Most of the known genes were the RCC-related genes previously unknown, including zinc ribbon domain-containing 1 protein (ZNRD1), pituitary tumor transforming gene1 (PTTG1). Northern blot and semi-quantitative RT-PCR confirmed that the mRNA levels of the 3 novel fragments and 1 KIAA and 3 known genes were significantly higher in RCC than in the matched normal kidney tissues. Immunohis-tochemical and Western blot analysis for PTTG1 and ZNRD1 revealed increased protein level in RCC. The over-expressed genes in RCC are the potential molecular targets for diagnosis and therapy and it is very important to understand the molecular mechanism of RCC through the profile of over-expressed genes.

关键词： suppression subtractive hybridization (SSH), cDNA microarray, renal cell carcinoma (RCC), gene, differential expression.

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Clinical practice guidelines for full-cycle standardized management of bone health in breast cancer patients

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Cancer Innovation 2024年第1期3卷 1-28页

作者： Committee of Full-cycle Standardized Management of Bone health in Breast Cancer Patients Fei Ma 不详 department of Medical Oncology National Cancer CenterNational Clinical Research Center for CancerCancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China

Bone health management for breast cancer spans the entire cycle of patient care,including the prevention and treatment of bone loss caused by early breast cancer treatment,the adjuvant application of bone-modifying agents to improve prognosis,and the diagnosis and treatment of advanced bone *** good bone health management means formulating appropriate treatment strategies and dealing with adverse drug reactions,and will help to improve patients'quality of life and survival *** Breast Cancer Expert Committee of the National Cancer Center for Quality Control organized relevant experts to conduct an in-depth discussion on the full-cycle management of breast cancer bone health based on evidence-based medicine,and put forward reasonable suggestions to guide clinicians to better deal with health issues in bone health clinics.

关键词： bone health bone-modifying drugs breast cancer guidelines

Peroxisome proliferator-activated receptor γ ligands induce cell cycle arrest and apoptosis in human renal carcinoma cell lines

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Acta Pharmacologica Sinica 2005年第6期26卷 753-761页

作者： Feng-guang YANG~2, Zhi-wen ZHANG~3, Dian-qi XIN~2, Chang-jin SHI~2, Jie-ping WU~2, Ying-lu GUO~(2,4), You-fei GUAN~(3,4) ~2 department of Molecular Biology, Institute of Urology Peking University First Hospital ~3 department of physiology and Pathophysiology, Peking University health science Center, Beijing 100034, China department of Molecular Biology Institute of Urology Peking University First Hospital Beijing China department of physiology and Pathophysiology Peking University Health Science Center Beijing China

Aim: To study the effect of peroxisome proliferator-actived receptor y （PPARγ） ligands on cell proliferation and apoptosis in human renal carcinoma cell lines. Methods: The expression of PPARγ was investigated by reverse transcriptase polymerase chain reaction （RT-PCR）, Western blot and immunohistochemistry. The effect of thiazolidinedione （TZD） PPARγ ligands on growth of renal cell carcinoma （RCC） cells was measured by MTT assay and flow cytometric analysis. Cell death ELISA, Hoechst 33342 fluorescent staining and DNA ladder assay were used to observe the effects of PPARγ ligands on apoptosis. Regulatory proteins of cell cycle and apoptosis were detected by Western blot analysis. Results: PPARγ was expressed at much higher levels in renal tumors than in the normal kidney （2.16±0.85 vs 0.90±0.73; P<0.01）. TZD PPARyligands inhibited RCC cell growth in a dose-dependent manner with IC50values of 7.08 μmol/L and 11.32 μmol/L for pioglitazone, and 5.71 μmol/L and 8.38 μmol/L for troglitazone in 786-0 and A498 cells, respectively. Cell cycle analysis showed a G0/G1arrest in human RCC cells following 24-h exposure to TZD. Analysis of cell cycle regulatory proteins revealed that TZD decreased the protein levels of proliferating cell nuclear antigen, pRb, cyclin D1, and Cdk4 but increased the levels of p21 and p27 in a time-dependent manner. Furthermore, high doses of TZD induced massive apoptosis in renal cancer cells, with increased Bax expression and decreased Bcl-2 expression. Conclusion: TZD PPARγligands showed potent inhibitory effect on proliferation, and could induce apoptosis in RCC cells. These results suggest that ligands for PPARγ have potential antitumor effects on renal carcinoma cells.

关键词： renal cell carcinoma peroxisome proliferator activated receptor γ cell cycle apoptosis cyclin cdk