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Endothelin-1 induces intracellular [Ca^(2+)] increase via Ca^(2+) influx through the L-type Ca^(2+) channel, Ca^(2+)-induced Ca^(2+) release and a pathway involving ET_A receptors, PKC, PKA and AT1 receptors in cardiomyocytes

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Science china(Life sciences) 2009年第4期52卷 360-370页

作者： ZENG QingHua1, LI XingTing1, ZHONG GuoGan2, ZHANG WenJie2 & SUN ChengWen3 1 Laboratory of Molecular & Cellular physiology, school of Life sciences, Northeast Normal university, changchun 130024, china 2 department of physiology, school of basic medical sciences, jilin university, changchun 130021, china 3 department of Pharmaceutical sciences, North Dakota State university, Fargo, NorthDakota, USA Laboratory of Molecular & Cellular physiology School of Life Sciences Northeast Normal University Changchun 130024 China department of physiology School of Basic Medical Sciences Jilin University Changchun 130021 China department of Pharmaceutical sciences North Dakota State University Fargo NorthDakota USA

Using fura-2-acetoxymethyl ester (AM) fluorescence imaging and patch clamp techniques, we found that endothelin-1 (ET-1) significantly elevated the intracellular calcium level ([Ca2+]i) in a dose-dependent manner and activated the L-type Ca2+ channel in cardiomyocytes isolated from rats. The effect of ET-1 on [Ca2+]i elevation was abolished in the presence of the ETA receptor blocker BQ123, but was not affected by the ETB receptor blocker BQ788. ET-1-induced an increase in [Ca2+]i, which was inhibited 46.7% by pretreatment with a high concentration of ryanodine (10 μmol/L), a blocker of the ryanodine receptor. The ET-1-induced [Ca2+]i increase was also inhibited by the inhibitors of protein kinase A (PKA), protein kinase C (PKC) and angiotensin type 1 receptor (AT1 receptor). We found that ET-1 induced an enhancement of the amplitude of the whole cell L-type Ca2+ channel current and an increase of open-state probability (NPo) of an L-type single Ca2+ channel. BQ123 completely blocked the ET-1-induced increase in calcium channel open-state probability. In this study we demonstrated that ET-1 regulates calcium overload through a series of mechanisms that include L-type Ca2+ channel activation and Ca2+-induced Ca2+ release (CICR). ETA receptors, PKC, PKA and AT1 receptors may also contribute to this pathway.

关键词： endothelin-1(ET-1) cardiomyocytes intracellular calcium concentration ([Ca2+]i) L-type Ca2+ channel current (ICaL) Ca2+-induced Ca2+ release (CICR) ETA receptors PKC PKA AT1 receptors

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Cloning of the full-length gene of activin receptor-interacting protein2a and characterization of its interaction with ActR Ⅱ A

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Progress in Natural Science:Materials International 2007年第2期17卷 172-176页

作者： CUI Xueling, TAI Guixiang, ZHANG Hongjun, FANG Lin and LIU Zhonghui (school of basic medical sciences, jilin university, changchun 130021, china) school of basic medical sciences Jilin University Changchun 130021 China

To investigate the mechanism of intracellular signal transduction mediated by activin receptors, the full-length gene encoding a novel activin receptor-interacting protein2a (ARIP2a) was identified from a mouse brain cDNA library. The sequences of ARIP2a and ARIP2, distribution of ARIP2a and ARIP2 mRNA in mouse tissues, and expression of ARIP2a and ARIP2 in activin-induced RAW264.7 cell were compared, and the interaction between ARIP2a and ActRIIA was confirmed. The sequence analysis revealed that the full-length gene of ARIP2a, which composed of 1008 bp and encoded 153 amino acid residues, shared high sequence identity with ARIP2 except the position of the 99th amino acid. RT-PCR assay showed that ARIP2a mRNA was highly expressed in brain, pituitary and testis, and moderately in pancreas and ovary, but undetectable in other tissues. Whereas, ARIP2 mRNA was widely distributed in all mouse tissues that we tested. Moreover, expression of ARIP2a mRNA was significantly decreased in activin-stimulated RAW264. 7 cells; however, the expression of ARIP2 mRNA was increased. Additionally, the interaction between ARIP2a and activin type IIA receptor (ActRIIA) was further demonstrated by mammalian two-hybrid assays and pull-down assays. Taken together, those results indicate that although ARIP2a is homologous to ARIP2, they are different in tissue distribution and responses to activin. ARIP2a could also interact with activin type II receptor as a novel member of ARIP family.

关键词： activin receptor-interacting protein tissue distribution.

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Surface electrocardiogram and action potential in mice lacking urea transporter UT-B

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Science china(Life sciences) 2009年第5期52卷 474-478页

作者： MENG Yan1, ZHAO ChunYan2, ZHANG XueXin2, ZHAO HuaShan1, GUO LiRong1, Lü Bin1, ZHAO XueJian1& YANG BaoXue1,3 1 department of Pathophysiology, school of basic Medicine, jilin university, changchun 130021, china 2 department of physiology, school of basic Medicine, jilin university, changchun 130021, china 3 department of Medicine, university of California, San Francisco CA 94143, USA department of Pathophysiology School of Basic Medicine Jilin University Changchun 130021 China department of physiology School of Basic Medicine Jilin University Changchun 130021 China department of Medicine University of California San Francisco CA 94143 USA

UT-B is a urea transporter protein expressed in the kidney and in many non-renal tissues including erythrocytes, brain, heart, bladder and the testis. The objective of this study was to determine the phenotype of UT-B deletion in the heart. UT-B expression in the heart was studied in wild-type mice vs UT-B null mice by utilizing RT-PCR and Western blot. A surface electrocardiogram (ECG) recording (lead II) was measured in wild-type mice and UT-B null mice at the ages of 6, 16 and 52 weeks. For the action potential recording, the ventricular myocytes of 16 w mice were isolated and recorded by floating microelectrode method. The sodium current was recorded by the patch clamp technique. RT-PCR and Western blot showed the UT-B expression in the heart of wild-type mice. No UT-B transcript and protein was found in UT-B null mice. The ECG recording showed that the P-R interval was significantly prolonged in UT-B null mice ((43.5 ± 4.2), (45.5 ± 6.9) and (43.8 ± 7.6) ms at ages of 6, 16 and 52 weeks) vs wild-type mice ((38.6 ± 2.9), (38.7 ± 5.6) and (38.2 ± 7.3) ms, P2 w old). The amplitude of action potential and Vmax decreased significantly in UT-B null mice ((92.17 ± 10.56) and (101.89 ± 9.54) mV/s) vs those in wild-type mice (vs (110.51 ± 10.38) and (109.53 ± 10.64) mV/s, P23.83 ± 11.17) and (195.43 ± 16.41) ms) vs that in wild-type mice ((108.27 ± 10.85) and (171.00 ± 15.53) ms, P2) nA vs that in wild-type mice ((-5.98 ± 1.07) nA, P<0.05). These results provide the first evidence that UT-B deletion causes progressive heart block in mice.

关键词： urea transporter heart block electrocardiogram

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Expression of ATP synthase 6 in breast cancer cell line, T47D cells, induced by heregulin β1

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吉林大学学报（医学版） 2002年第2期28卷 111-114页

作者： SUN Yan bo,YANG Gui zhen (Dept.of Immunology, school of basic medical sciences,jilin university ,changchun 130021 china) Dept. of Immunology School of Basic Medical Sciences Jilin University Changchun 130021

目的 :探讨 Heregulinβ1诱导乳腺癌细胞 T47D相关基因的表达。方法 :应用差减杂交和斑点杂交技术检测乳腺癌细胞在 Heregulinβ1 ( 30 μg· L-1)作用 1 8h后 ,相关基因的表达情况。结果 :线粒体 ATP合成酶 6m RNA的表达在 1～ 6h明显... 详细信息

目的 :探讨 Heregulinβ1诱导乳腺癌细胞 T47D相关基因的表达。方法 :应用差减杂交和斑点杂交技术检测乳腺癌细胞在 Heregulinβ1 ( 30 μg· L-1)作用 1 8h后 ,相关基因的表达情况。结果 :线粒体 ATP合成酶 6m RNA的表达在 1～ 6h明显增高。结论 :乳腺癌细胞 T47D在 Here-gulinβ1刺激后 ,细胞 ATP酶

关键词：乳腺癌 T47D 基因表达线粒体 ATP

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Taurine Inhibits Myocardial Fibrosis via PKC-ERK1/2 Signaling Pathways

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Chemical Research in Chinese Universities 2012年第1期28卷 84-90页

作者： WANG Li-ying1,2, LI Hong1 and YANG Shi-jie1 1. department of Pharmacology, Norman Bethune College of Medicine, jilin university, changchun 130021, P. R. china 2. department of physiology, basic Medicine College, Beihua university, jilin 132013, P. R. china jilin Univ Norman Bethune Coll Med Dept Pharmacol Changchun 130021 Peoples R China Beihua Univ Basic Med Coll Dept Physiol Jilin 132013 Jilin Peoples R China

Previous studies have demonstrated the important role of taurine in inhibiting proliferation of myofibrob lasts（myoFb） and myocardial fibrosis. However, the underlying mechanisms are unclear. The present study was de signed to shed light on this issue through exploring the signal pathways via in vitro experiments. Angiotension II （AngII） treatment significantly increased myoFb proliferation and the levels of collagens I and III（P〈0.05）, whereas taurine, PKCα（PKC： protein kinase C） specific inhibitor L-threo-dihydro-sphingosine（D4681）, ERK1/2 inhibitor （PD98095） abrogated myoFb proliferation and collagen levels（P〈0.05, P〈0.01, respectively）, and increased the G0/G1 phase rate and decreased S phase rate. Immunocytochemistry, confocal fluorescence staining and image analy sis showed that taurine could inhibit the translocation and expression of p-PKCαin membrane, and then inhibit nuc lear translocation and expression of p-ERK1/2. These results have statistically significant differences compared with those of AngII group（P〈0.01）. Western blot results also show that taurine could inhibit the protein expression of p-PKCα and p-ERK1/2. We used p-PKCα specific inhibitor D4681 in order to elucidate the relationship between p-PKCα and p-ERK1/2 in signal transduction pathways. Finally, the results show that the protein expression of p-ERK1/2 and nuclear translocation were suppressed in D4681 group.

关键词： Taurine Myocardial fibrosis Proliferation Signal transduction Cardiac remodeling

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Calcitonin gene-related peptide inhibits interleukin-1β-induced interleukin-8 secretion in human type Ⅱ alveolar epithelial cells

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Acta Pharmacologica Sinica 2006年第10期27卷 1340-1345页

作者： Wen-jing LI Teng-ke WANG Xian WANG~2 department of physiology,school of basic medical sciences,Peking university,Key Laboratory of Molecular Cardiovascular Science,Ministry of Education,Beijing 100083,china department of physiology School of Basic Medical Sciences Peking University Key Laboratory of Molecular Cardiovascular Science Ministry of Education Beijing 100083 China

Aim:Our previous data have shown that type Ⅱ alveolar epithelial(AEⅡ)cellsexpress neuropeptide calcitonin gene-related peptide(CGRP),and that pro-in-flammatory factor interleukin 1-β(IL-1β)induces CGRP secretion in the A549 hu-man AEⅡ cell *** the present study,we investigated the effect of endogenousand exogenous CGRP on IL-1β-induced chemokine interleukin-8(IL-8)***:We used enzyme-linked immunosorbent assay(ELISA)and RT-PCR todetect IL-8 protein and mRNA levels,respectively,siRNA and the stably trans-fected cell line were used to knock down and overexpress the CGRP gene,respectively,and chemiluminescence assay was used to detect reactive oxygenspecies(ROS)***:CGRP-1 receptor antagonist hCGRP8-37(0.1-1nmol·L-1)greatly amplified IL-1β-induced IL-8 *** inhibition of CGRPexpression by siRNA significantly increased IL-8 secretion upon IL-1β ***,cell clones stably transfected with CGRP showed significantly inhibitedmRNA and protein levels of IL-8 induced by 1L-1β.Conclusion:These data implythat AEⅡ cell-derived CGRP suppress IL-1β-induced IL-8 secretion in an autocrine/paracrine *** investigation showed that CGRP attenuated IL-1β-arousedROS formation,which is an early indication of pro-inflammatory factor signaling.

关键词： type Ⅱ alveolar epithelial cells interleukinl interleukin-8 calcitonin gene-related peptide anti-inflammation lung reactive oxygen species

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A PSTAIRE CDK-like protein localizes in nuclei and cytoplasm of Physarum polycephalum and functions in the mitosis

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Cell Research 2004年第2期14卷 169-175页

作者： Gui Ying LI~(1,2), Miao XING~(1,*), Bo HU~(1,3) ~1College of Life Science, Shenzhen Key Laboratory of Microbial Gene Engineering, Shenzhen university, Shenzhen 518060, china. ~2department of Immunology, school of basic medical sciences, jilin university, changchun 130021, china ~3Institute of Genetics and Cytology, Northeast Normal university, changchun 130024, china. College of Life Science Shenzhen Key Laboratory of Microbial Gene Engineering Shenzhen University Shenzhen 518060 China.

CDKs play key roles in controlling cell cycle progression in all eukaryotes. In plants, multiple CDKs are present, among which the best characterized CDKs are PSTAIRE CDKs. In this study, we carried out Western blot, immunoelectron microscopy and antibody treatment with an anti-PSTAIRE monoclonal antibody to explore the subcellular localization and functions of PSTAIRE CDKs in Physarum polycephalum. The results of Western blot and immunoelectron microscopy showed that in P. polycephalum, a PSTAIRE CDK-like protein was 34 kD in molecular weight and located in both nuclei and cytoplasm. In nuclei, the protein was mainly associated with chromosomes and nucleoli. The expression of the PSTAIRE CDK-like protein in both the plasmodia and nuclei showed little fluctuation through the whole cell cycle. When treated with an anti-PSTAIRE monoclonal antibody at early S phase, the cells were arrested in S phase, and the mitotic onset of P. polycephalum was blocked for about 1 h when treated at early G2 phase. Our dat

关键词： PSTAIRE CDK-like protein Physarum polycephalum mitosis immunoelectron microscopy.

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The study on effect of long-termed administration of mixed rare earth Changle on rat liver

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吉林大学学报（医学版） 2002年第6期28卷 567-570页

作者： LIU Ying,CHEN Dong ,CHEN Ai jun,WANG Xiao ming,NIE Yu xiu (Dept. of Histology and Embryology,school of basic medical sciences,jilin university,changchun 130021, china) Dept. of Histology and Embryology School of Basic Medical Sciences Jilin University Changchun 130021

目的 :研究不同剂量的“常乐”对大鼠肝脏结构和功能的影响。方法 :采用健康 Wistar大鼠 1 80只 ,每组 30只 ,实验组分别以 0 .1、0 .2、2 .0、1 0 .0、2 0 .0 mg· kg-1常乐连续灌胃 6个月 ,每日 1次。应用常规组织化学、透射电镜技术... 详细信息

目的 :研究不同剂量的“常乐”对大鼠肝脏结构和功能的影响。方法 :采用健康 Wistar大鼠 1 80只 ,每组 30只 ,实验组分别以 0 .1、0 .2、2 .0、1 0 .0、2 0 .0 mg· kg-1常乐连续灌胃 6个月 ,每日 1次。应用常规组织化学、透射电镜技术及血清生化测定技术 ,观察动物肝脏的结构和功能变化。结果 :各实验组动物体重随染毒剂量的减少而呈线性增长。 2 0 .0 mg·kg-1组肝细胞内糖原颗粒减少 ,肝细胞核有不同程度的变形 ,门管区有炎细胞浸润 ,其余各组肝脏结构与对照组相比无明显改变。各实验组动物肝脏 Kupffer细胞及肝细胞中均可见到高电子密度的致密体及含电子密度较高颗粒的溶酶体 ,其数量随染毒剂量的增大而增多。 2 0 .0 mg· kg-1组血清 ALP及 GPT增高。结论 :2 0 .0 mg·kg-1“常乐”长期作用对大鼠肝脏结构和功能均有损害。

关键词：混和稀土制剂常乐长期用药鼠肝影响肝功能

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Effects of retinoic acid on proliferation,phenotype and expression of cyclin-dependent kinase inhibitors in TGF-β1-stimulated rat hepatic stellate cells

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World Journal of Gastroenterology 2000年第6期6卷 819-823页

作者： Guang Cun Huang Jin Sheng Zhang Yue E Zhang department of Pathology school of basic medical sciences,Fudan university.Shanghai 200032,china Guang Cun Huang Jin Sheng Zhang Yue E Zhang Department of Pathology School of Basic Medical Sciences Fudan University Shanghai 200032 China Guang Cun Huang graduated from Medical Center of Fudan University (former Shanghai Medical University) in 1996 majoring in forensic medicine now assistant and master at the Department of Pathology School of Basic Medical Sciences Fudan University specialized in the study of hepatic pathology having 3 papers published.

AIM To study the molecular mechanisms ofretinoic acid(RA)on proliferation andexpression of cyclin-dependent kinase inhibitors(CKI),i.e.p16,p21 and p27 in cultured rathepatic stellate cells(HSC)stimulated withtransforming growth factor beta 1(TGF-β1).METHODS HSC were isolated from healthy ratlivers and *** stimulated with1 mg/L TGF-β1,subcultured HSC were treatedwith or without 1 nmol/L *** assay,immunocytochemistry(ICC)for p16,p21,p27and α-smooth muscle actin(α-SMA)protein,insitu hybridization(ISH)for retinoic acidreceptor beta 2(RAR-β2)and p16,p21 and p27mRNA and quantitative image analysis(partially)were *** RA inhibited HSC proliferation(41.50%,P2 *** addition,RAincreased the protein level of p16(218.75%,P21 protein expression;meanwhile,p27 was undetectable by ICC in bothcontrol and RA-treated ***,RA hadno influence on the mRNA levels of p16,p21 orp27 as determined by *** Up-regulation of p16 and p21 on post-transcriptional level may contribule, in part to RA inhibition of TGF-β1-initiated rat HSC activation in vitro.

关键词： retinoic acid cyclindependent kinase inhibitor hepatic stellate cell cell culture transforming growth factor beta 1 liver fibrosis

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Effects of adenosine agonist R-phenylisopropyl-adenosine on halothane anesthesia and antinociception in rats

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Acta Pharmacologica Sinica 2005年第2期26卷 181-185页

作者： Hai-chun MA~(2,4),Yan-fen WANG~3,Chun-sheng FENG~2,Hua ZHAO~(4,5),Shuji DOHI~6~2department of Anesthesiology,the First Hospital of jilin university,changchun 130021,china ~3department of Digestive Disease,the SecondHospital of jilin university,changchun 130041,china ~4department of physiology,basic medical school,jilin university,changchun 130021,china ~6department of Anesthesiology,school of Medicine,Gifu university,Gifu 5008705,Japan department of Anesthesiology the First Hospital of Jilin University Changchun 130021 China

Aim:To investigate the antinociceptive effect of adenosine agonist R-phenylisopropyl-adenosine（R-PIA）given to conscious rats by intracerebro-ventricular（ICV）and intrathecal（IT）,and identify the effect of R-PIA on minimumalveolar concentration（MAC）of halothane with pretreatment of A1receptor an-tagonist 8-cyclopentyl-1,3-dipropylxanthine（DPCPX）or K+channel blocker4-aminopyridine（4-AP）.Methods:Sprague-Dawley rats were implanted with 24-gauge stainless steel guide cannula using stereotaxic apparatus and ICV method,and an IT catheter（PE-10,8.5cm）was inserted into the lumbar subarachnoidspace,while the rats were under pentobarbital *** one week ofrecovery from surgery,rats were randomly assigned to one of the followingprotocols:MAC of halothane,or tail-flick *** measurements were per-formed after R-PIA（0.8-2.0μg）microinjection into ICV and IT with or withoutpretreatment of DPCPX or ***:Microinjection of adenosine agonist R-PIA in doses of 0.8-2.0μg into ICV and IT produced a significant dose-and time-dependent antinociceptive action as reflected by increasing latency times andICV administration of adenosine agonist R-PIA（0.8μg）reducing halothane anes-thetic requirements（by 29%）.The antinociception and reducing halothane re-quirements effected by adenosine agonist R-PIA was abolished by DPCPX ***:ICV and IT administration of adenosine agonist R-PIA pro-duced an antinociceptive effect in a dose-dependent manner and decreased hal-othane MAC with painful stimulation through activation of A1receptor subtype,and the underlying mechanism involves K+channel activation.

关键词： adenosine inhalation anesthesia analgesia potassium channels subarachnoid space cerebral ventricles

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