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Chinese Journal of Integrative Medicine 2015年第3期21卷 204-210页

作者：许晓乐黄燕娟凌丹彦张伟 Department of Pharmacology Nantong University Pharmacy College Shanghai Health Vocational and Technical College

Objective：To investigate the effect of 2,3,4’,5-tetrahydroxystilbene-2-0- p-D-glucoside（TSG）,an active component extracted from the root of Polygonum multiflorum,on angiotensin Ⅱ（Ang Ⅱ）-induced proliferation of cultured rat vascular smooth muscle cells（VSMCs） and to identify the potential ***：Cell proliferation and cell cycle were determined by cell counting,5-bromo-2’-deoxyuridine incorporation assay,proliferating cell nuclear antigen protein expression and flow *** of phosphorylated extracellular signal-regulated kinase 1/2（ERK1/2）,mitogenic extracellular kinase 1/2（MEK1/2） and Src in VSMCs were measured by Western *** expression of c-fos,c-jun and c-myc mRNA were measured by reverse transcription polymerase chain reaction（RT-PCR）.Intracellular reactive oxygen species（ROS） was measured by fluorescence ***：TSG significantly inhibited Ang Ⅱ-induced VSMCs proliferation and arrested cells in the G1/S checkpoint（P〈0.05 or P〈0.01）.TSG decreased the levels of phosphorylated ERK1/2,MEK1/2 and Src in VSMCs（P〈0.05 or P〈0.01）.TSG also suppressed c-fos,c-jun and c-myc mRNA expression（P〈0.05 or P〈0.01）.In addition,the intracellular ROS was reduced by TSG（P〈0.01）.Conclusions：TSG inhibited Ang Ⅱ-induced VSMCs *** antiproliferative effect might be associated with down-regulation of intracellular ROS,followed by the suppression of the Src-MEK1/2-ERK1/2 signal pathway,and hence,blocking cell cycle progression.

关键词： 2,3,4’,5-tetrahydroxystilbene-2-O-β-D-glucoside vascular smooth muscle cells proliferation angiotensin Ⅱ Chinese medicine Polygonum multiflorum

Electroacupuncture Attenuated Phenotype Transformation of vascular smooth muscle cells via PI3K/Akt and MAPK Signaling Pathways in Spontaneous Hypertensive Rats

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Chinese Journal of Integrative Medicine 2022年第4期28卷 357-365页

作者： CHEN Xin-yu YANG Lu-ping ZHENG Ya-ling LI Yu-xi ZHONG Dong-ling JIN Rong-jiang LI Juan School of Health Preservation and Rehabilitation Chengdu University of Traditional Chinese MedicineChengdu610072China Food Science and Nutrition School University of LeedsLeedsLS29JTUK Department of Rehabilitation the Second People’s Hospital of ChengduChengdu610072China School of Acupuncture-Moxibustion and Tuina Chengdu University of Traditional Chinese MedicineChengdu610072China

Objective:To investigate whether the antihypertensive mechanism of electroacupuncture(EA)is associated with attenuating phenotype transformation of vascular smooth muscle cells(VSMCs)via phosphoinositide3-kinase(PI3K)/protein kinase B(Akt)and mitogen-activated protein kinase(MAPK)signaling ***:Eight Wistar-ktoyo(WKY)rats were set as normal blood pressure group(normal group).A total of 32 spontaneous hypertensive rats(SHRs)were randomly divided into 4 groups using random number tables:a model group,an EA group,an EA+PI3K antagonist group(EA+P group),and an EA+p38 MAPK agonist+extracellular signal-regulated kinase(ERK)agonist group(EA+M group)(n=8/group).SHRs in EA group,EA+P group and EA+M group received EA treatment 5 sessions per week for continuous 4 weeks,while rats in the normal and model groups were bundled in same *** systolic blood pressure(SBP),diastolic blood pressure(DBP),and mean arterial pressure(MAP)of each rat was measured at 0 week and the 4th *** 4-week intervention,thoracic aorta was collected for hematoxylin-eosin(HE)staining,immunohistochemistry[the contractile markersα-smooth muscle actin(α-SMA)and calponin and the synthetic marker osteopontin(OPN)]and Western blot[α-SMA,calponin,OPN,PI3K,phosphorylated-Akt(p-Akt),Akt,p-p42/44 ERK,total p42/44 ERK,p-p38 MAPK and total p38 MAPK].Results:EA significantly reduced SBP,DBP and MAP(P<0.01).HE staining showed that the wall thickness of thoracic aorta in EA group was significantly decreased(P<0.01).From results of immunohistochemistry and Western blot,EA increased the expression ofα-SMA and calponin,and decreased the expression of OPN(P<0.01).In addition,the expression of PI3K and p-Akt increased(P<0.01),while the expression of p-p42/44 ERK and p-p38 MAPK decreased in EA group(P<0.01).However,these effects were reversed by PI3K antagonist,p38 MAPK agonist and ERK ***:EA was an effective treatment for BP *** antihypertensive effect of EA may be rela

关键词： electroacupuncture hypertension vascular smooth muscle cells PI3K/Akt signaling pathway MAPK signaling pathway

Heat shock protein 90 acts as a molecular chaperone in late-phase activation of extracellular signal-regulated kinase 1/2 stimulated by oxidative stress in vascular smooth muscle cells

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Acta Pharmacologica Sinica 2007年第12期28卷 1907-1913页

作者： Dai-hua LIU~2,Hao-yu YUAN~2,Chun-ya CAO,Zhi-ping GAO,Bing-yang ZHU,Hong-lin HUANG~3,Duan-fang LIAO~3Division of Pharmacoproteomics,Institute of Pharmacy and Pharmacology,School of Life Science and Technology,University of SouthChina,Hengyang 421001,China DivisionofPharmacoproteomics InstituteofPharmacyandPharmacologySchoolofLifeScienceandTechnologyUniversityofSouthChinaHengyang421001China

Aim:To investigate whether cytosolic heat shock protein 90 (HSP90) acts as amolecular chaperone on the activated extracellular signal-regulated kinase 1/2(ERK1/2) and cell proliferation stimulated by reactive oxygen species (ROS) in ratvascular smooth muscle cells (VSMC).Methods:VSMC were exposed to 1 μmol/LLY83583 (6-anilinoquinoline-5,8-quinolinedione,producer of ROS) for 120 min inthe presence or absence of 5 μmol/L geldanamycin,a specific inhibitor of *** the total,soluble,and insoluble proteins of the cells were ***90,ERK1/2,and phosphor-ERK1/2 in the cell lysate were measured by Western *** interaction of HSP90 and phosphor-ERK1/2 was analyzed by immunoprecipi-tation assay,and the nuclear phosphor-ERK1/2 was measured by Western blot-ting and *** proliferation was tested by cell counting and3-(4,5-dimethylthiazol-2-yl)-3,5-di-phenyltetrazolium bromide (MTT).Results:Thecytosolic HSP90 of VSMC was upregulated by LY83583 in a time-dependent man-ner with the peak at 120 min,which is consistent with the late peak of phosphor-ERK1/*** and Western blotting analyses showed that LY83583increased the interaction of HSP90 with phosphor-ERK 1/2,the phosphor-ERK 1/2level,and the soluble phosphor-ERK1/2 level by 1.8-,2.5-,and 2.9-fold,*** contrast,the insoluble phosphor-ERK1/2 of VSMC was ***,LY83583 treatment promoted the nuclear phosphor-ERK1/2 by 7.6-fold as con-firmed by Western blotting and immunofluorescence ***,cellcounting and the MTT assay showed that LY83583 stimulated VSMC prolifera-tion with the increased expression of HSP90 and levels of soluble and nuclearphosphor-ERK1/*** of geldanamycin antagonized the effect ***:HSP90 could mediate the oxidative stress-stimulated,late-phase activation of ERK1/2 and VSMC proliferation by promoting the ERK1/2phosphorylation,the association of itself with phosphor-ERK1/2,and the solubil-ity

关键词： heat shock protein 90 extracellular signalregulated kinase 1/2 reactive oxygen species vascular smooth muscle cells

Ginsenoside Rg1 inhibits proliferation of vascular smooth muscle cells stimulated by tumor necrosis factor-α

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Acta Pharmacologica Sinica 2006年第8期27卷 1000-1006页

作者： Zeng-chun MA Yue GAO~2 Yu-guang WANG Hong-ling TAN Cheng-rong XIAO Sheng-qi WANG Institute of Radiation Medicine Sciences,Academy of Military Medical Sciences,Beijing 100850,China InstituteofRadiationMedicineSciences AcademyofMilitaryMedicalSciencesBeijing100850China

Aim:To investigate the proliferation of vascular smooth muscle cells(VSMC)affected by ginsenoside Rg1 and further explore the molecular mechanism ofginsenoside Rg1 using ***:The proliferation of VSMC wasmeasured by MTS assay kit and flow *** alterations were ana-lyzed using two-dimensional electrophoresis and peptide mass *** proteins found in proteomics were confirmed by ***:The proliferation of VSMC was enhanced significantly after tumor necrosis fac-tor-α(TNF-α)treatment,and ginsenoside Rg1 treatment inhibited proliferation ina dose-dependent *** analysis showed 24 protein spots werechanged,including 17 spots that were increased and 7 spots that were *** Rg1 could restore the expression levels of these proteins,at leastpartly,to basic levels of untreated *** expression of G-protein coupledreceptor kinase,protein kinase C(PKC)-ζ,N-ras protein were decreased,whilecycle related protein p21 was increased by ginsenoside Rgl in TNF-α ***:PKC-ζ and p21 pathway might be the mechanism for inhibi-tory effects of ginsenoside Rg1 on proliferation of VSMC.

关键词： cell cycle ginsenoside Rg1 proteomics tumor necrosis factor-α vascular smooth muscle cells

Spontaneous Ca2+ oscillations in subcellular compartments of vascular smooth muscle cells rely on different Ca2+ pools

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Cell Research 2004年第5期14卷 379-388页

作者： Olesya D. FEDORYAK,Yvonne SEARLS,Irina V. SMIRNOVA,Douglas M. BURNS,Lisa STEHNO-BITTEL Departments of Physical Therapy and Rehabilitation Sciences University of Kansas Medical Center Kansas City KS 66160 USA Departments of Physical Therapy and Rehabilitation Sciences University of Kansas Medical Center Kansas City KS 66160 USA Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City KS 66160 USA Departments of Physical Therapy and Rehabilitation Sciences University of Kansas Medical Center Kansas City KS 66160 USA VA Medical Center Kansas City MO 64128 USA Departments of Physical Therapy and Rehabilitation Sciences University of Kansas Medical Center Kansas City KS 66160 USA Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City KS 66160 USA

Spontaneous Ca2+ oscillations in vascular smooth muscle cells have been modeled using a single Ca2+ pool. This report describes spontaneous Ca2+ oscillations dependent on two separate Ca2+ sources for the nuclear versus cytoplas- mic compartments. Changes in free intracellular Ca2+ were monitored with ratiometric Ca2+- fluorophores using confo- cal microscopy. On average, spontaneous oscillations developed in 79% of rat aortic smooth muscle cells that were synchronous between the cytoplasm and nucleus. Reduction of extracellular Ca2+ (cells that had spontaneously developed prior oscillations. Conversely, cells in the same conditions lacking oscillations had a greater AVP-induced Ca2+ transient in the cytoplasm (4.99 ± 0.66, n = 17) than in the nucleus (2.67 ± 0.29). Pre-treatment with Ca2+ channel blockers depressed the AVP responses in both compartments with the cytoplasmic Ca2+ most diminished. Depletion of internal Ca2+ stores prior to AVP exposure blunted the nuclear response, mimicking the response of cells that lacked prior oscillations. Spontaneous oscillating cells had a greater sarcoplasmic reticulum network than cells that did not oscillate. We propose that sponta- neous nuclear oscillations rely on perinuclear sarcoplasmic reticulum stores, while the cytoplasmic oscillations rely on Ca2+ influx.

关键词： oscillations vascular smooth muscle cells nuclear Ca2+ vasopressin thapsigargin diltiazem nimodipine.

Endogenous tissue factor pathway inhibitor in vascular smooth muscle cells inhibits arterial thrombosis

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Frontiers of Medicine 2017年第3期11卷 403-409页

作者： Jichun Yang Kaiyue Jin Jiajun Xiao Jing Ma Duan Ma Institute of Biomedical Sciences Fudan University Shanghai 200032 China Key Laboratory of Metabolism and Molecular Medicine Ministry o~f Education Department of Biochemis[ry and -Molecular Biology Institute of Biomedical Sciences School of Basic Medical Sciences Fudan University Shanghai 200032 China

Tissue factor pathway inhibitor （TFPI） is the main inhibitor of tissue factor-mediated coagulation. TFPI is expressed by endothelial and smooth muscle cells in the vasculature. Endothefium-derived TFPI has been reported to play a regulatory role in arterial thrombosis. However, the role of endogenous TFPI in vascular smooth muscle cells （VSMCs） in thrombosis and vascular disease development has yet to be elucidated. In this TFPI^Flox mice crossbred with Sma-Cre mice were utilized to establish TFPI conditional knockout mice and to examine the effects of VSMC-directed TFPI deletion on development, hemostasis, and thrombosis. The mice with deleted TFPI in VSMCs （TFP^Sma） reproduced viable offspring. Plasma TFPI concentration was reduced 7.2% in the TFPIsma mice compared with TFPI^Flox littermate controls. Plasma TFPI concentration was also detected in the TFPI^Tle2 （mice deleted TFPI in endothefial ceils and cells of hematopoietic origin） mice. Plasma TFPI concentration of the TFPI^Tle2 mice was 80.4% lower （P 〈 0.001） than that of the TFPI^Flox mice. No difference in hemostatic measures （PT, APTT, and tail bleeding） was observed between TFPIsma and TFPI^Flox mice. However, TFP^Sma mice had increased ferric chloride-indueed arterial thrombosis compared with TFPI^Flox littermate controls. Taken together, these data indicated that endogenous TFPI from VSMCs inhibited ferric chloride-induced arterial thrombosis without causing hemostatic effects.

关键词： arterial thrombosis conditional knockout mice tissue factor pathway inhibitor vascular smooth muscle cells

Inhibitory Effects of Saponins From Anemarrhena asphodeloides Bunge on the Growth of vascular smooth muscle cells

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Biomedical and Environmental Sciences 2006年第3期19卷 185-191页

作者： SHANG-ZHI XIAO MING-EN XU YA-KUN GE GUI-FENG XIAO Department of Biomedical Engineering Zhejiang University （Yuquan Campus） Hangzhou 310027 Zhejiang China

Objective To investigate the effects of saponins from Anemarrhena asphodeloides Bunge （SAaB）（Botanical Name： Anemarrhena Asphodeloidis Rhizoma） on the growth of vascular smooth muscle cells （VSMCs）. Methods Cell proliferation was measured by a newly developed cell proliferation reagent, WST-1. Cell apoptosis was assayed by flow cytometry through detecting annexin V. Nitric oxide production was evaluated using confocal laser scanning microscopy with diaminofluorescein diacetate （DAF-2, DA）. Cell aldose reductase （AR） activity, as well as the effect of Epalrestat and interleukin-1β were also explored. Results WST assay showed that cell proliferation induced by serum was significantly inhibited by SAaB （P〈0.01）. Flow cytometry analysis revealed that SAaB could enhance apoptotic rate of VSMCs （P〈0.01）. Nitric oxide production was significantly enhanced after administration of SAaB and interleukin-Iβ Moreover, AR activity of VSMCs was also remarkably inhibited by both SAaB and Epalrestat （P〈 0.01）. Conclusion SAaB can inhibit proliferation and enhance apoptosis of VSMCs. It may protect vascular cells by inhibiting VSMC proliferation and augmenting apoptotic rate of VSMCs via NO-dependent pathway.

关键词： Anemarrhena asphodeloides Bunge Saponins vascular smooth muscle cells Proliferation

Glycation of high-density lipoprotein triggers oxidative stress and promotes the proliferation and migration of vascular smooth muscle cells

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Journal of Geriatric Cardiology 2017年第7期14卷 473-480页

作者： Qian DU Ming-Ming QIAN Pin-Li LIU Le ZHANG Yan WANG Dong-Hui LIU Department of Cardiology the Affiliated Cardiovascular Hospital of Xiamen University Medical College of Xiamen University Xiamen China Department of Endocrinology the Second Hospital of Hebei Medical University Shijiazhuang China

Background In type 2 diabetes mellitus （T2DM）, high-density lipoprotein （HDL） impairs its anti-atherogenic properties and even develops to a pro-inflammatory and pro-atherogenic phenotype because of abnormal compositions and modifications. In this study, we ex- amined the effects and the related mechanisms of glycation of HDL on the proliferation and migration of vascular smooth muscle cells （VSMCs）. Methods ＆ Results Glycated HDL （G-HDL） was modified with D-glucose （25 mmol/L） in vitro. Diabetic HDL （D-HDL） was isolated from T2DM patients. Rat VSMCs were isolated from the thoracic aortas. Human VSMCs were obtained from ScienCell Research Laboratories. Alpha-actin was detected through immunofiuorescence. VSMC proliferation was assayed by Cell Count. VSMC migration was determined by transwell chamber and scratch-wound assay. Intracellular reactive oxygen species （ROS） was detected based on ROS-medi- ated 2＇,7＇-dichlorofluorescein （DCFH-DA） fluorescence. Compared to native HDL （N-HDL）, G-HDL remarkably promoted VSMC prolif- eration and migration in the dose and time-dependent manners. In addition, G-HDL enhanced ROS generation in VSMCs. However, the ROS scavenger, N-acetylcysteine, efficiently decreased ROS production and subsequently inhibited the proliferation of VSMCs induced by G-HDL. Similarly, D-HDL from T2DM patients also promoted ROS release and VSMC proliferation and migration. Conclusions HDL either glycated in vitro or isolated from T2DM patients triggered VSMC proliferation, migration, and oxidative stress. These results might partly interpret the higher morbidity of cardiovascular disease in T2DM patients.

关键词： High-density lipoprotein Glycation Migration Proliferation vascular smooth muscle cells

Inhibitory Effects of Suppressor of Cytokine Signaling 3 on Inflammatory Cytokine Expression and Migration and Proliferation of IL-6/IFN-γ-induced vascular smooth muscle cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2013年第5期33卷 615-622页

作者：向水董念国刘金平王玉史嘉玮魏战杰胡行健龚立 Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Department of Cardiothoracic Surgery Central Hospital of Enshi Autonomous Prefecture Department of Biochemistry and Molecular Biology Tongji Medical College Huazhong University of Science and Technology

Summary： The main pathogenesis of saphenous vein graft neointimal hyperplasia after coronary artery bypass grafting （CABG） is inflammation-caused migration and proliferation of vascular smooth muscle cells （VSMCs）. Janus kinase 2/signal transducer and activators of transcription 3 （JAK2/STAT3） path- way is an important signaling pathway through which VSMCs phenotype conversion occurs. Suppressor of cytokine signaling 3 （SOCS3） is the classic negative feedback inhibitor of JAK2/STAT3 pathway. Growing studies show that SOCS3 plays an important anti-inflammatory role in numerous autoimmune diseases, inflammatory diseases and inflammation-related tumors. However, the effect and mechanism of SOCS3 on vein graft disease is unclear. The purpose of this study was to investigate the effects of SOCS3 on the inflammation, migration and proliferation of VSMCs in vitro and the mechanism. The small interference RNA plasmid targeting rat SOCS3 （SiRNA-rSOCS3） and the recombinant adenovirus vector carrying rat SOCS3 gene （pYrAd-rSOCS3） were constructed, and the empty plamid （SiRNA-control） and vector （pYrAd-GFP） only carrying GFP reported gene were constructed as control. The rat VSMCs were cultured. There were two large groups of A （SOCS3 up-regulated）： control group, IL-6/IFN-γ group, IL-6/IFN-γ＋pYrAd-rSOCS3 group, IL-6/IFN-γ＋pYrAd-GFP group; and B （SOCS3 down-regulated）： control group, IL-6/IFN-γ group, IL-6/IFN-γ＋SiRNA-rSOCS3 group and IL-6/IFN -T＋SiRNA-control group. The pYrAd-rSOCS3 and SiRNA-rSOCS3 were transfected into VSMCs in- duced by IL-6/IFN-γ. After 24 h, real-time reverse transcription polymerase chain reaction （RT-PCR） and Western blotting were used to detect the mRNA and protein expression of SOCS3, STAT3 （only by Western blotting）, P-STAT3 （only by Western blotting）, IL-1β, IL-6, TNF-α, MCP-1 and ICAM-1. The MTT, Transwell assay and flow cytometry were used to examine VSMCs proliferation, migration and cell cycle progression, respectively. As compared with control

关键词： SOCS3 JAK2/STAT3 inflammatory cytokine vascular smooth muscle cells vein graftdisease

Influence of Osteopontin Short Hairpin RNA on the Proliferation and Activity of Rat vascular smooth muscle cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2009年第2期29卷 144-149页

作者：叶珊孙玉梅别爱桂周颖刘佳妮刘启功 Department of Cardiology Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology Zhongshan Hospital of Hubei Province

To investigate the influence of osteopontin （OPN） short hairpin RNA （shRNA） on the proliferation and activity of rat vascular smooth muscle cells （VSMCs）, the expressing vector of shRNA targeting OPN was constructed and transferred into the rat VSMCs. After amplification and purification, pGenesil-1/OPNshRNA1 （PG1）, pGenesil-1/OPNshRNA2 （PG2） and pGenesil-1/OPNshRNAHK （PGH） were transfected into the cultured rat VSMC by LipofectamineTM 2000. Transfected cells were visualized by using an inverted fluorescent microscope. VSMCs transfected by optimal recombined plasmid was selected by culturing in G418 48 h later. Nude cells and cells transfected by PGH were used as control. The expression levels of OPN mRNA and protein were assayed by RT-PCR and Western blotting. The OPN of VSMCs was suppressed by transfection of optimal recombined plasmid, and the changes in cell proliferation, adhesion and motility were evaluated by MTT, adhesion test and transwell chamber test. Levels of type I and Ⅲ collagen were measured with ELISA kit. Our results showed that VSMCs stably transfected by OPN shRNA accounted for over 50% of total cells. OPN mRNA and protein were reduced by 81% and 67% （P〈0.01） by PG1, 73% and 52% （P〈0.01） by PG2, respectively while no change was found in PGH and non-treated VSMCs. PG1 significantly suppressed the proliferation, adhesion, mobility of VSMCs and reduced the amount of type Ⅰ and Ⅲ collagen. It is concluded that recombinant plasmid can be success-fully transfected into VSMCs by LipofectamineTM 2000 and inhibit the expression of OPN. The proliferation, adhesion and mobility of VSMCs can be inhibited by knocking down OPN expression. Moreover, the transferring capability of cells is attenuated, and the secretion of type Ⅰ and Ⅲ collagen is inhibited aftter knocking-down of OPN expression. The study provides experimental evidence for clinical prevention of restenosis after percutaneous coronary intervention （PCI） by RNA interference （RNAi） technology.

关键词： osteopontin short hairpin RNA RNA interference vascular smooth muscle cells