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

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

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Regulation of intracellular Ca2+and calcineurin by NO/PKG in proliferation of vascular smooth muscle cells

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Acta Pharmacologica Sinica 2005年第3期26卷 323-328页

作者： Shi-jun LI Ning-ling SUN~1 Department of Cardiology,People’s Hospital,Peking University,Beijing 100044,China Department of Cardiology People's Hospital Peking University Beijing China

Aim:To determine whether Ca2+/calcineurin mediated the inhibitory effects ofnitric oxide/cGMP-dependent protein kinase (NO/PKG) on the proliferation ofvascular smooth muscle cells (VSMC).Methods:Proliferation and viability ofprimary VSMC from rat aorta were measured using [3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide] (MTT) assay and acridine orange and ethidiumbromide staining,respectively.Cytosolic Ca2+was determined by Fluo-3/AM.Calcineurin protein and its activity were assayed using immunoblotting and freeinorganic phosphate analysis,respectively.Results:(e)-S-nitroso-N-acetyl-penicillamine (SNAP) and Sp-8-(4-chlorophenylthio)-guanosine-3′,5′-cyclicmonophosphorothioate (Sp-8-pCPT-cGMPS) decreased phenylephrine (PE)-in-duced proliferation of VSMC by 27.3% and 36.6%,respectively,but Rp-8-[(4-chlorophenyl)thio]-guanosine-3′,5′-cyclic monophosphorothioate (Rp-8-pCPT-cGMPS) increased PE-induced proliferation of VSMC.SNAP,Sp-8-pCPT-cGMPS,and Rp-8-pCPT-cGMPS did not affect the viability of VSMC.Calcineurin proteinwas decreased by 63.1% and its activity was decreased by 59.7% in smooth musclecells (SMC) pretreated with verapamil (Ver) and then stimulated by PE.In SMCpretreated with Vet,the absorbance of cells stimulated by PE decreased by 22.0%and was further inhibited by the additional treatment of SNAP and Sp-8-pCPT-cGMPS.In SMC pretreated with cyclosporin A (CsA),the absorbance of cellsstimulated by PE decreased by 36.7%,but could not be further altered by theadditional treatment of SNAP,Sp-8-pCPT-cGMPS,and Rp-8-pCPT-cGMPS.Inaddition,Ver inhibited PE-induced intracellular Ca2+variations,which could befurther inhibited by SNAP and Sp-8-pCPT-cGMPS,but not by Rp-8-pCPT-cGMPS.Moreover,the increase in calcineurin activity induced by PE was inhibited bySNAP and Sp-8-pCPT-cGMPS,but was promoted by Rp-8-pCPT-cGMPS.Conclusion:NO/PKG regulates calcineurin activity via the modulation of intracel-lular Ca2+concentration,and thus partially inhibits the proliferation of VSMCwithout affecting their viability.

关键词： calcium calcineurin nitric oxide cGMP-dependent protein kinase vascular smooth muscle

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Onychin inhibits proliferation of vascular smooth muscle cells by regulating cell cycle

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Acta Pharmacologica Sinica 2005年第2期26卷 205-211页

作者： Ming YANG~2,Hong-lin HUANG~2,Bing-yang ZHU,Qin-hui TUO,Duan-fang LIAO~3Institute of Pharmacy and Pharmacology,Nanhua University,Hengyang 421001,China Institute of Pharmacy and Pharmacology Nanhua University Hengyang China

Aim:To investigate the effects of onychin on the proliferation of cultured ratartery vascular smooth muscle cells(VSMCs)in the presence of 10% new-borncalf serum(NCS).Methods:Rat VSMCs were incubated with onychin 1-50μmol/L or genistein 10μmol/L in the presence of 10% NCS for 24 h.The prolif-eration of VSMCs was measured by cell counting and MTS/PMS colorimetricassays.Cell cycle progression was evaluated by flow cytometry.Retinoblastoma(Rb)phosphorylation,and expression of cyclin D1and cyclin E were measured byWestern blot assays.The tyrosine phosphorylation of ERK1/2 was examined byimmunoprecipitation techniques using anti-phospho-tyrosine antibodies.Results:The proliferation of VSMCs was accelerated significantly in the presence of 10%NCS.Onychin reduced the metabolic rate of MTS and the cell number of VSMCsin the presence of 10% NCS in a dose-dependent manner.Flow cytometry analy-sis revealed that the G1-phase fraction ratio in the onychin group was higher thanthat in the 10% NCS group(85.2% vs 70.0%,P<0.01),while the S-phase fractionratio in the onychin group was lower than that in 10% NCS group(4.3% vs16.4%,P<0.01).Western blot analysis showed that onychin inhibited Rb phos-phorylation and reduced the expression of cyclin D1and cyclin E.The effects ofonychin on proliferation,the cell cycle and the expression of cyclins in VSMCswere similar to those of genistein,an inhibitor of tyrosine kinase.Furthermoreimmunoprecipitation studies showed that both onychin and genistein markedlyinhibited the tyrosine phosphorylation of ERK1/2 induced by 10% NCS.Conclusion:Onychin inhibits the proliferation of VSMCs through G1phase cellcycle arrest by decreasing the tyrosine phosphorylation of ERK1/2,and the ex-pression of cyclin D1and cyclin E,and sequentially inhibiting Rb phosphorylation.

关键词： onych(?)n vascular smooth muscle cell cycle retinoblastoma cyclin D1 cyclin E tyrosine kinase mitogen-activated protein kmase

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vascular smooth muscle Cell Development and Cardiovascular Malformations

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Cardiology Discovery 2021年第4期1卷 259-268页

作者： Lihua Qi Wei Kong Yi Fu Department of Human Anatomy Histology and EmbryologySchool of Basic Medical SciencesPeking University Health Science CenterBeijing 100191China Department of Physiology and Pathophysiology School of Basic Medical SciencesPeking University Health Science CenterBeijing 100191China Key Laboratory of Molecular Cardiovascular Science Ministry of EducationBeijing 100191China Beijing Key Laboratory of Cardiovascular Receptors Research Beijing 100191China

vascular smooth muscle cells(VSMCs)have diverse biological functions that include maintaining the vascular structure and recruiting progenitors to form the embryonic vascular system.Accumulating evidence suggests that the VSMCs are not just derived from the mesoderm,as previously thought,but have diverse developmental origins.Lineage tracing analysis indicates that VSMCs have at least 7 different origins,thereby giving it the characteristic of a mosaic tissue.The crucial role of the diverse origins of the VSMCs has been recognized in relation to blood vessel function and diseases such as arteriosclerosis.The VSMC distribution in cardiovascular development and whether and how their heterogeneous origins contribute to the overall cardiovascular development continue to be topics of research.Here,we review the current state of research,mainly focusing on the role of VSMCs in cardiovascular development.We emphasize the following biological pathways:(1)normal course of development of VSMCs and their diverse origins in relation to cardiovascular development,(2)signaling regulation of progenitor cell development and differentiation into VSMCs,and(3)abnormal development of vascular smooth muscle and the associated cardiovascular malformations.

关键词： vascular smooth muscle Development Diverse progenitor Signaling pathway Cardiovascular malformation

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Blockade of L-type calcium channel in myocardium and calcium-induced contractions of vascular smooth muscle by CPU 86017

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Acta Pharmacologica Sinica 2004年第4期 18-25页

作者： De-zai DAI2, Hui-juan HU3, JingZHAO, Xue-mei HAO4, Dong-mei YANG4, Pei-ai ZHOU4,Cai-hong WU4 Research Division of Pharmacology, China Pharmaceutical University, Nanjing, 210009 4National Laboratoryof Biomembrane and Membrane Biotechnology, Peking University, Beijing 100871, China

AIM: To assess the blockade by CPU 86017 on the L-type calcium channels in the myocardium and on the Ca2+- related contractions of vascular smooth muscle. METHODS: The whole-cell patch-clamp was applied to investi- gate the blocking effect of CPU 86017 on the L-type calcium current in isolated guinea pig myocytes and contrac- tions by KCl or phenylephrine (Phe) of the isolated rat tail arteries were measured. RESULTS: Suppression of the L-type current of the isolated myocytes by CPU 86017 was moderate, in time- and concentration-dependent man- ner and with no influence on the activation and inactivation curves. The IC50was 11.5 μmol/L. Suppressive effect of CPU 86017 on vaso-contractions induced by KCl 100 mmol/L, phenylephrine 1 μmol/Lin KH solution (phase 1), Ca2+ free KH solution ( phase 2) , and by addition of CaCl2 into Ca2+-free KH solution (phase 3) were observed. The IC50 to suppress vaso-contractions by calcium entry via the receptor operated channel (ROC) and voltage-depen- dent channel (VDC) was 0.324 μmol/L and 16.3 μmol/L, respectively. The relative potency of CPU 86017 to suppress vascular tone by Ca2+ entry through ROC and VDC is 1/187 of prazosin and 1/37 of verapamil, respectively. CONCLUSION: The blocking effects of CPU 86017 on the L-type calcium channel of myocardium and vessel are moderate and non-selective. CPU 86017 is approximately 50 times more potent in inhibiting ROC than VDC.

关键词： chlorobenzyltetrahydroberine myocardium vascular smooth muscle patch-clamp techniques berberine calcium

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Aged Garlic Extract and One of the Constituent, (+)-(2S,3R)-Dehydrodiconiferyl Alcohol, Inhibits Alkaline Phosphatase Activity Induced by Inflammation Factors in Human vascular smooth muscle Cells

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Food and Nutrition Sciences 2014年第2期5卷 177-184页

作者： Takahiro Yamakawa Toshiaki Matsutomo Thomas Hofmann Yukihiro Kodera Central Research Institute of Wakunaga Pharmaceutical Co.Ltd. HiroshimaJapan Technische Universitat München FreisingGermany

Previous clinical study showed that aged garlic extract (AGE) has a preventive effect of vascular calcification in patients with coronary artery diseases. It has been reported that vascular smooth muscle cells (VSMC) and inflammatory cells including macrophages and lymphocytes migrate to sub-intimal region where atherosclerotic plaques are formed, and VSMC can differentiate into osteoblast-like cells, which are represented by the induction of alkaline phosphatase (ALP). We found that primary human coronary artery smooth muscle cells (HCASMC) showed the increased ALP activity, when cultured in the medium containing ascorbic acid, β-glycerophosphate, dexamethasone (IM), and supplemented with conditioned medium from macrophages (MCM). Then we tested the effect of AGE subdivided fractions and several compounds found in AGE, and then found that ((+)-(2S,3R)-Dehydrodiconiferyl alcohol, a dilignol compound existed in hydrophobic fraction of AGE, inhibited ALP activity in HCASMC.

关键词： vascular smooth muscle Alkaline Phosphatase Aged Garlic Extract Dehydrodiconiferyl Alcohol

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Expression of Inositol 1,4,5-trisphosphate Receptor mRNA in Myocardium of Spontaneous Hypertension Rats and Cultured vascular smooth muscle Cells of Rats

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Journal of Nanjing Medical University 2002年第2期16卷 75-79页

作者：刘乃丰张寄南耿茜杨笛董莉马文珠 Division of Cardiology Zhongda Hospital Southeast University Nanjing 210009 Research Institute of Cardiovascular Diseases NJMU Nanjing 210029 P. R. China

Objective\ To investigate expression of inositol 1,4,5 trisphosphate receptor (IP\-3R) mRNA on sacroplasmic reticular in myocardium of spontaneous hypertension rats (SHRs) and cultured vascular smooth muscle cells (VSMC) of rats and effects of perindopril and urapidil on them. Methods\ SHRs were orally given perindopril (1.0 mg·kg\+\{ 1\}·d\+\{ 1\}) or urapidil (15 mg·kg\+\{ 1\}·d\+\{ 1\}) for 24 weeks, respectively. Expression of IP\-3R mRNA was examined by semi quantitative reverse transcription polymers chain reaction (RT PCR) using three oligonuclotide primers for each subtype of IP\-3R with β actin as internal label. Results\ All subtypes of IP\-3R were expressed in myocardium of SHR, WKY and cultured VSMC. Expression of IP\-3R mRNA in left ventricle of SHR was markedly enhanced. Urapidil could down regulate expression of IP\-3R Ⅰand IP\-3R Ⅲ, perindopril slightly increased expression of IP\-3R Ⅱ and decreased expression of IP\-3R Ⅰand IP\-3R Ⅲ in myocardium of SHR. Conclusion\ Our results suggest that expression of IP\-3R mRNA in cardiovascular system could be regulated by urapidil and perindopril.

关键词： calcium release channel signal transduction inositol 1,4,5 trisphosphate receptor spontaneous hypertension rat vascular smooth muscle cultured cells polymers chain reaction

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Urocortin and cardiovascular protection

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Acta Pharmacologica Sinica 2004年第3期25卷 3-11页

作者： Chi-wai LAU Yau-chi CHAN Suk-ying TSANG Franky Leung CHAN China Department of Anatomy The Chinese University of Hong Kong

Urocortin and other hypothalamus corticotropin-releasing factor (CRF) polypeptides play biologically diverse roles in the stress, cardiovascular and inflammatory responses by acting on central and peripheral CRF receptors. Urocortin shows a significantly high sequence homology to CRF, and the concurrent expression of type-2 CRF (CRF2) receptors with urocortin in the heart suggests that urocortin may play a physiological role in the cardiac function. Urocortin is thought to be the endogenous agonist producing the cardiovascular actions previously attributed to CRF. This review highlights the current novel findings on the molecular and cellular mechanisms by which urocortin may exert its cardiovascular protective action.

关键词： urocortin corticotropin-releasing hormone vascular smooth muscle heart vasodilaion second messenger system protein kinases

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Opioid receptor antagonists increase [Ca2+]i in rat arterial smooth muscle cells in hemorrhagic shock

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Acta Pharmacologica Sinica 2004年第3期25卷 141-146页

作者： Li KAI,Zhong-feng WANG2,Yu-liang SHI2,3,Liang-ming LIU,De-yao HU Institute of Surgery,Department of Pharmacology,Third Military Medical University,Chongqing 400042 Key Laboratory of 2 Neurobiology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China Institute of Surgery Department of Pharmacology Third Military Medical University 重庆 400042 中科院上海生命科学院 Key Laboratory of Neurobiology CAS 上海 200031

AIM: To examine the effects of opioid receptor antagonists and norepinephrine on intracellular free Ca2+ concentra- tion ([Ca2+]i) in mesenteric arterial (MA) smooth muscle cells (SMC) isolated from normal and hemorrhagic shocked rats in the vascular hyporesponse stage. METHODS: The rat model of hemorrhagic shock was made by withdrawing blood to decrease the artery mean blood pressure to 3.73-4.26 kPa and keeping at the level for 3 h. [Ca2+]i of vascular smooth muscle cells (VSMC) were detected by the laser scan confocal microscopy. RESULTS: In the hyporesponse VMSC of rats in hemorrhagic shock, selective δ-, κ-, and μ-opioid receptor antagonists (naltrindole, nor-binaltorphimine, and β-funaltrexamine, 100 nmol/L) as well as norepinephrine 5 μmol/L significantly increased [Ca2+]i by 47 %±13 %, 37 %±14 %, 33 %±10 %, and 54 %±17 %, respectively, although their effects were lower than those in the normal rat cells (the increased values were 148 %±54 %, 130 %±44 %, 63 %±17 % and 110 %±38 %, respectively); and the norepinephrine-induced increase in [Ca2+]i was further augmented by three δ-, κ-, and μ-opioid receptor antagonists (50 nmol/L, respectively) application (from 52 %±16 % to 99 %±29 %, 146 %±54 % and 137 %±47 %, respectively). CONCLUSION: The disorder of [Ca2+]i regulation induced by hemorrhagic shock was mediated by opioid receptor and α-adrenoceptor, which may be partly responsible for the vascular hyporesponse, and the opioid receptor antagonists improved the response of resistance arteries to vascu- lar stimulants in decompensatory stage of hemorrhagic shock.

关键词： hemorrhagic shock vascular smooth muscle opioid receptors calcium

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Melatonin reduces peroxynitrite-induced injury in aortic smooth muscle cells

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Acta Pharmacologica Sinica 2004年第2期25卷 60-64页

作者： Jun-lin ZHOU1, Xiao-guang ZHU1, Yi-ling LING2, Qing LI3 Department of Hand Suegery, Third Affiliated Hospital, Hebei Medical University, Shijiazhuang 050051 2Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017 3Department of Physiology, Hebei Medical University, Shijiazhuang 050017,China Department of Hand Suegery Third Affiliated Hospital Hebei Medical University Shijiazhuang 050051 Department of Pathophysiology Hebei Medical University Shijiazhuang 050017 Department of Physiology Hebei Medical University Shijiazhuang 050017

AIM: To study the protective role of melatonin (MT) in peroxynitrite-induced injury in cultured aortic smooth muscular cells (ASMC). METHODS: Peroxynitrite was synthesized chemically with a quenched flow reaction. Cells were exposed to peroxynitrite 500 μmol/L for 1 h in the absence or presence of various concentrations of MT 100, 300, and 500 μmol/L. Nitrotyrosine (NT), a specific “footprint” of peroxynitrite formation, was detected by immunohistochemical technique. The DNA damage was assayed by TUNEL technique. The levels of MDA in the medium and cell viability were measured. RESULTS: Incubation of ASMC with peroxynitrite 500 μmol/L for 1 h elicited the increase in the extent of immunostaining for NT, the rate of the TUNEL-positive cell, the content of MDA in the medium, and the number of dead cell. Pretreatment of ASMC with MT 100-500 μmol/L decreased these peroxynitrite-induced changes in a concentration-dependent manner. CONCLUSION: MT attenuated the injury induced by peroxynitrite in ASMC.

关键词： melatonin nitrates nitric oxide free radicals vascular smooth muscle

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