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1.
目的:探讨自噬抑制刺氯喹(cQ)在低氧(hypoxia)调节肺动脉平滑肌细胞(PASMCs)增殖中的作用。方法:将体外培养的大鼠PASMCs分为4组:正常对照组、1%低氧组、50μmol/L氯喹+1%低氧组、50ttmol/L氯喹组。MTF方法检测各组的PASMCs增殖率;MDC染色检测细胞自噬空泡的变化;Westernblot方法检测微管相关蛋白轻链3(LC3)蛋白的表达变化;划痕法检测细胞迁移的变化。结果:与对照组比较,氯喹组的PASMCs细胞增殖率无明显变化。与对照组比较,1%低氧组PASMCs增殖率明显增加,细胞内出现大量自噬空泡,细胞迁移速度明显增加。细胞LC3-Ⅱ蛋白表达增强。与1%低氧组比较,氯喹与低氧联合作用时细胞自噬空泡的积聚以及rE3.II蛋白表达增强,但细胞增殖率和迁移明显降低。结论:低氧激活自噬过程并促进了PASMCs增殖和迁移,而自噬抑制剂氯喹在一定程度上通过抑制自噬进程,达到抑制肺动脉平滑肌细胞增殖和迁移的作用。  相似文献   

2.
观察低氧对大鼠肺动脉平滑肌细胞(pulmonary artery smooth muscle cells,PASMCs)Periostin表达的影响及其相关信号转导机制。胶原酶I法原代培养PASMCs,经低氧(5%O2)分别处理PASMCs2,6,12,24h后,RT-PCR和Western blot法检测Periostin mRNA和蛋白表达。加入PI3K/Akt通路特异性抑制剂LY294002(10μmol/L)进行干预,Western blot分析比较不同条件下低氧处理24h后大鼠PASMCs中Periostin和Akt/P-Akt的蛋白表达。结果表日月,与常氧组比较,低氧处理6h组、12h组和24h纽Periostin mRNA和蛋白的表达均显著上升(P〈0.05,P〈0.01),低氧处理后的PASMCs中Periostin mRNA和蛋白的表达逐渐升高:低氧处理2h组无显著差异(P〉0.05)。用LY294002对PASMCs处理,并低氧24h后,Periostin的表达被显著抑制(P〈0.01),细胞P-Akt的表达下调(P〈0.05),总Akt的蛋白表达没有明显差异(P〉0.05)。推测低氧可诱导大鼠PASMCs中Periostin mRNA和蛋白的表达上调。低氧可能通过激活P13K/Akt通路促进Akt的磷酸化,进而使Periostin在PASMCs中过表达,提示Periostin在低氧性PASMCs增殖过程中可能起着重要作用。  相似文献   

3.
摘要 目的:研究浆细胞瘤多样异位基因1(PVT1)在肺动脉高压(PAH)大鼠中对于肺动脉平滑肌细胞(PASMCs)增殖和迁移的作用及其可能的机制。方法:将16只成年雄性SD大鼠随机分为肺动脉高压组(PAH组)和对照组,每组8只大鼠。PAH组大鼠通过单次项背部皮下注射MCT溶液造模,对照组大鼠给予单次项背部皮下注射等量生理盐水。通过胸右心室穿刺法测量右心室压力。取各组大鼠肺组织,并进行原代肺动脉平滑肌细胞分离培养。通过RT-qPCR和Western blot检测PVT1及Fxr1在PAH组织及PASMCs中的表达水平;通过HE染色评估PAH组织的血管壁形态;免疫荧光法检测HPASMC的纯度;CCK-8法和伤口愈合迁移实验检测PASMCs增殖和迁移情况。结果:与对照组相比,PAH组大鼠肺组织血管壁厚度偏厚、肺动脉压显著升高(P<0.05)。PVT1在PAH组大鼠的PAH组织和PASMCs中的表达水平显著上调(P<0.05),且其表达与肺动脉压呈正相关。与对照组相比,转染sh-PVT1的PASMCs显示出较低的细胞活力,同时转染sh-PVT1有效敲低了PASMCs中PVT1的表达水平(P<0.01)。与对照组相比,PVT1的敲低抑制了PASMCs迁移能力(P<0.01)。在转染pcDNA-PVT1的PASMCs中发现较高的增殖能力,PVT1的过表达促进了PASMCs迁移能力(P<0.01)。与对照组相比,Fxr1在PAH模型组的PAH组织和PASMCs中的表达水平显著上调(P<0.01)。结论:PVT1通过调节Fxr1的表达促进PASMCs的增殖和迁移,PVT1可能是PAH诊断和预测指标。  相似文献   

4.
Zhao JP  Zhou ZG  Hu HL  Guo Z  Wang T  Zhen GH  Zhang ZX 《生理学报》2007,59(3):319-324
在低氧条件下,观察大鼠肺动脉平滑肌细胞(pulmonary arterial smooth muscle cells,PASMCs)中活性氧(reactive oxygen species,ROS)的变化,探讨ROS的变化是否通过调控低氧诱导因子-4α(hypoxia-inducible factor 1α, HIF-1α)的表达影响PASMCs的增殖。采用组织块法原代培养大鼠PASMCs,分成3组:常氧组(21%O2,24h),低氧组(5%O2,24h),低氧+Mn-TBAP组(5%O2,24h,Mn-TBAP是一种ROS清除剂)。用激光共聚焦显微镜荧光染色法检测细胞内ROS的变化;用RT-PCR和免疫组织化学方法分别测定HIF-1α mRNA和蛋白的表达;用MTT法检测细胞增殖程度。结果显示:(1)低氧组PASMCs内ROS水平明显高于常氧组(P〈0.05),低氧+Mn-TBAP组ROS水平明显低于低氧组(P〈0.05),但仍高于常氧组(P〈0.05);(2)低氧组及低氧+Mn-TBAP组的HIF-1α mRNA和蛋白表达均高于常氧组(P〈0.05),且低氧组表达高于低氧+Mn-TBAP组(P〈0.05);(3)低氧组细胞增殖明显高于常氧组和低氧+Mn-TBAP组(P〈0.05),低氧+Mn-TBAP组细胞增殖高于常氧组(P〈0.05)。结果表明:在低氧条件下大鼠PASMCs中ROS水平明显升高,RROS的变化能够调节HIF-1α的表达,进而影响平滑肌细胞的增殖,提示ROS可能在肺动脉高压的发病机制和低氧信号转导中具有重要作用。  相似文献   

5.
阿米洛利抑制NHE-1减轻低氧性肺动脉平滑肌细胞增殖   总被引:1,自引:0,他引:1  
目的:研究Na^+/H^+交换抑制剂阿米洛利对低氧刺激的大鼠肺动脉平滑肌细胞(PASMCs)增殖的影响,以及Na^+/H^+交挟体-l(NHE-1)活性和表达的变化.方法:常氧(21%O2)或低氧(2%O2)条件下培养PASMCs,并分别给予浓度为1.653、3.125、6.25、12.5、25和50μmol/L.等不同浓度的阿米洛利,培养24h,采用MTT比色实验和免疫组化检测PCNA阳性细胞率的方法反映细胞增殖情况,同时采用激光共聚焦检测细胞内pH以反映Na^+/H^+交换体-1活性,RT—PCR法检测Na^+/H^+交换体-1mRNA的表达量.结果:低氧培养的PASMCs细胞内pH升高,NHE—1mRNA的表达增多,而阿米洛利可以降低细胞内pH,减少NHE—1mRNA的表达量。同时低氧较常氧培养MTT光吸收值较常氧培养明显升高。PCNA阳性细胞率明显增高,而给予阿米洛利时上述两个指标随药物浓度增加而逐渐下降。结论:低氧可以激活PASMCs细胞膜上的E—1,增加其mRNA水平表达量,使细胞内碱化,促进细胞增殖,而Na^+/H^+交换抑制剂阿米洛利可以抑制其活性,减少mRNA水平的表达,导致细胞内酸化,从而抑制细胞增殖,并且此抑制作用在3.125~50μmol/L.浓度范围内呈现明显的浓度依赖性。  相似文献   

6.
Zhang W  Cao Y  Zhang Y  Ma QS  Ma L  Ge RL 《生理学报》2006,58(1):71-76
本研究应用基因克隆技术,将合成的发卡样特异性低氧诱导因子-1α(hypoxia inducible factor-1alpha,HIF-1α)干扰寡核苷酸(siRNA)序列插入真核表达载体中,构建出特异性HIF-1α基因RNA干扰(RNAi)真核表达载体。采用组织块种植法,原代培养大鼠肺动脉平滑肌细胞(pulmonary artery smooth muscle cells,PASMCs),将构建出的特异性HIF-1αRNAi真核表达载体转染到PASMCs;分别在常氧和低氧下进行细胞培养,采用RT-PCR检测PASMCsHIF-1αmRNA表达水平,用MTT和流式细胞仪检测细胞增殖水平,探讨低氧条件下HIF-1αRNAi真核表达载体对PASMCs增殖的影响。结果表明,低氧培养48h后,正常PASMCs和转染了HIF-1αsiRNA阴性表达载体的细胞增殖显著,HIF-1αmRNA表达水平也显著升高;而转染了HIF-1αsiRNA阳性表达质粒的细胞增殖不显著,HIF-1αmRNA表达水平较低。结果提示:HIF-1αRNAi真核表达载体能显著干扰培养的PASMCsHIF-1αmRNA表达,同时抑制低氧环境下PASMCs的增殖。  相似文献   

7.
低氧对培养的不同内径的肺动脉平滑肌细胞增殖的影响   总被引:4,自引:0,他引:4  
目的和方法:分离培养三种不同内径的肺动脉平滑肌细胞(PASMCs),用^3H-TdR掺入速率和细胞计数作为细胞增殖的指标,观察低氧对其增殖作用的影响。结果:低氧对三种不同内径的PASMCs(内径分别为>1000μm、500-800μm、300-400μm)增殖促进作用显著不同,其^3H-TdR掺入速率和细胞计数分别增加23.5%和11.1%、60.0%和33.8%、141.4%和52.0%,选择对低氧最敏感的PASMCs(内径为300-400μm),进一步探讨低氧促PASMCs增殖作用的细胞机制:钙拮抗剂verapail、蛋白激酶C抑制剂staurosporine(Stau)和细胞Na-H交换抑制剂amiloride可显著降低低氧情况下PASMCs^3H-TdR掺入速率和细胞计数。结论:低氧对三种不同内径的PASMCs增殖促进作用显著不同; Ca^2 、蛋白激酶C和Na^2 -H^ 交换的激活,可能是低氧促PASMCs增殖的重要胞内信息转导机制。  相似文献   

8.
目的:研究罗格列酮(rosiglitazone, RSG)对低氧性肺动脉高压大鼠过氧化物酶体增殖物激活受体-r(Peroxisome proliferator activated receptor gamma, PPAR-r)和10 号染色体缺失张力蛋白同源磷酸酶基因(Phosphatase and tensin homolog deleted on chromosome 10, PTEN)表达的影响。方法:SD 大鼠随机分为正常对照组、低氧组、低氧+ 罗格利酮组,建立低氧性肺动脉高压大鼠模 型,4 周后测定各组大鼠右心室压力、右心肥厚指标,同时检测各实验组PPAR-r、PTEN 的表达和组织病理学变化。培养原代大鼠 肺动脉平滑肌细胞,分别给与低氧、低氧+罗格列酮、低氧+GW9662 处理后观察细胞增殖及PPARr、PTEN 的表达变化。结果:① 与正常组相比,低氧组大鼠右心室压力、右心肥厚指标明显增加,肺小动脉管壁增厚,PPAR-r、PTEN 的表达明显减少。与低氧组相 比,低氧+罗格列酮组大鼠右心室压力下降,右心室及肺小动脉管壁的肥厚减轻,PTEN 的表达增加。②低氧下,PASMCs 中 PPARr、PTEN表达明显减低,细胞增殖较常氧明显增加,给与罗格列酮后,PTEN 表达增加,给与GW9662,PTEN表达减少。③罗 格列酮可以抑制PASMCs低氧下的增殖,而给与GW9662 后,这一抑制作用减轻。结论:早期应用罗格列酮可激活低氧性肺动脉 高压大鼠PPARr的活性,进而上调PTEN表达,改善低氧性肺动脉高压。  相似文献   

9.
应用免疫细胞化学染色及Western印迹检测血管平滑肌细胞(vascular smooth muscle cells,VSMC)环加氧酶-2(cyclo—oxygenase-2,COX-2)表达、NF-kB抑制蛋白α(IkB-α)水平和NF—kB p65核转位的变化:电泳迁移率改变分析(electrophoretic mobility shift assay,EMSA)确定旋覆花内酯(1—o-acetylbritannilactone,ABL)对核内NF-kB p65与DNA调控元件的结合活性的影响。结果表明,脂多糖(lipopolysaccharide,LPS)处理的VSMC,p65核转位加快,细胞核内的NF-kB p65水平快速升高,同时伴有IkB3—α的减少;用ABL预处理VSMC后,LPS诱导的p65核转位增加及IkB3—α减少受到明显抑制,抑制作用呈剂量依赖性。EMSA结果显示,LPS处理VSMC,其核蛋白与含有NF—kB结合位点的探针的结合活性升高;而用ABL预处理的VSMC,LPS诱导的核蛋白与探针结合活性的升高受到明显抑制。进而,ABL对NF—kB活化启动的下游炎性基因COX-2表达也具有较强的抑制效果。因此,ABL是一种抗炎物质,通过抑制NF—kB活化和炎性基因COX-2的表达而减弱或消除LPS诱导的VSMC炎症应答反应。  相似文献   

10.
Zhao JP  Guo Z  Zhou ZG  Chen J  Hu HL  Wang T  Zhang ZX 《生理学报》2007,59(2):157-162
本文旨在探讨线粒体ATP敏感钾(mitochondrial ATP-sensitive K+,MitoKATP)通道对大鼠肺动脉平滑肌细胞低氧诱导因子-1α(hypoxia inducible factor-1α,HIF-1α)表达和细胞增殖的影响。原代培养大鼠肺动脉平滑肌细胞,分为常氧对照组、常氧+diazoxide(MitoKATP通道的选择性开放剂)组、常氧+5-hydroxydecanoate(5-HD,MitoKATP通道的选择性阻断剂)组、低氧对照组、低氧+diazoxide组、低氧+5-HD组,共6组,分别应用罗丹明123荧光技术检测各组大鼠肺动脉平滑肌细胞的线粒体膜电位,免疫组化检测HIF-1α的表达及酶联免疫检测仪检测细胞增殖的变化。结果显示,常氧+ diazoxide组与常氧对照组比较,罗丹明123荧光、HIF-1α表达及细胞增殖明显增强(P〈0.05);低氧+diazoxide组与低氧对照组比较,罗丹明123荧光、HIF-1α表达及细胞增殖明显增强(P〈0.05):常氧+5-HD组与常氧对照组比较,罗丹明123荧光、HIF-1α表达、细胞增殖没有明显变化(P〉0.05);但低氧+5-HD组与低氧对照组比较,罗丹明123荧光明显减弱、HIF-1α表达及细胞增殖有所减弱(P〈0.05)。结果提示:MitoKATP通道的开放能引起大鼠肺动脉平滑肌细胞线粒体膜去极化,并可以促进HIF-1α的表达及细胞增殖。  相似文献   

11.
Enhanced proliferation of pulmonary arterial vascular smooth muscle cells (PASMCs) is a key pathological component of vascular remodeling in hypoxia-induced pulmonary hypertension (HPH). Mammalian targeting of rapamycin (mTOR) signaling has been shown to play a role in protein translation and participate in the progression of pulmonary hypertension. Eukaryotic translation initiation factor-2α (eIF2α) is a key factor in regulation of cell growth and cell cycle, but its role in mTOR signaling and PASMCs proliferation remains unknown. Pulmonary hypertension (PH) rat model was established by hypoxia. Rapamycin was used to treat rats as an mTOR inhibitor. Proliferation of primarily cultured rat PASMCs was induced by hypoxia, rapamycin and siRNA of mTOR and eIF2α were used in loss-of-function studies. The expression and activation of eIF2α, mTOR and c-myc were analyzed. Results showed that mTOR/eIF2α signaling was significantly activated in pulmonary arteries from hypoxia exposed rats and PASMCs cultured under hypoxia condition. Treatment with mTOR inhibitor for 21 days attenuated vascular remodeling, suppressed mTOR and eIF2α activation, inhibited c-myc expression in HPH rats. In hypoxia-induced PASMCs, rapamycin and knockdown of mTOR and eIF2α by siRNA significantly abolished proliferation and increased c-myc expression. These results suggest a critical role of the mTOR/eIF2αpathway in hypoxic vascular remodeling and PASMCs proliferation of HPH.  相似文献   

12.
We have previously demonstrated that expression of the atrial natriuretic peptide (ANP) clearance receptor (NPR-C) is reduced selectively in the lung of rats and mice exposed to hypoxia but not in pulmonary arterial smooth muscle cells (PASMCs) cultured under hypoxic conditions. The current study tested the hypothesis that hypoxia-responsive growth factors, fibroblast growth factors (FGF-1 and FGF-2) and platelet-derived growth factor-BB (PDGF-BB), that activate tyrosine kinase receptors can reduce expression of NPR-C in PASMCs independent of environmental oxygen tension. Growth-arrested rat PASMCs were incubated under hypoxic conditions (1% O2) for 24 h; with FGF-1, FGF-2, or PDGF-BB (0.1-20 ng/ml for 1-24 h); or with ANG II (1-100 nM), endothelin-1 (ET-1, 0.1 microM), ANP (0.1 microM), sodium nitroprusside (SNP, 0.1 microM), or 8-bromo-cGMP (0.1 mM) for 24 h under normoxic conditions. Steady-state NPR-C mRNA levels were assessed by Northern blot analysis. FGF-1, FGF-2, and PDGF-BB induced dose- and time-dependent reduction of NPR-C mRNA expression within 1 h at a threshold concentration of 1 ng/ml; hypoxia, ANG II, ET-1, ANP, SNP, or cGMP did not decrease NPR-C mRNA levels in PASMCs under the above conditions. Downregulation of NPR-C expression by FGF-1, FGF-2, and PDGF-BB was inhibited by the selective FGF-1 receptor tyrosine kinase inhibitor PD-166866 and mitogen-activated protein/extracellular signal-regulated kinase inhibitors U-0126 and PD-98059. These results indicate that activation of tyrosine kinase receptors by hypoxia-responsive growth factors, but neither hypoxia per se nor activation of G protein-coupled receptors, inhibits NPR-C gene expression in PASMCs. These results suggest that FGF-1, FGF-2, and PDGF-BB play a role in the signal transduction pathway linking hypoxia to altered NPR-C expression in lung.  相似文献   

13.
14.
The biological activity of TNF-related apoptosis inducing ligand (TRAIL) was analyzed in primary human erythroblasts derived from mononuclear cells of blood donors, kept in culture in the presence of 20 percent foetal calf serum, growth factors (EPO, SCF, IL-3) and glucocorticoids (10-6 M dexamethasone, 10-6 M oestradiol) or under growth factor and serum starvation. In the presence of growth factors and serum, primary erythroblasts showed a differential expression of TRAIL-Receptors (Rs) at various degrees of maturation and responded to TRAIL treatment with a mild cytotoxicity. On the other hand, in the absence of serum and growth factors, TRAIL treatment unexpectedly up-regulated TRAIL-R4 decoy receptor and promoted erythroblast survival. The concomitant activation of NF-kB/IkB survival pathway was detected with Western blotting and immunofluorescence procedures and confirmed by experiments performed with SN50, a pharmacological inhibitor of the NF-kB/IkB pathway. Our study indicates that TRAIL has a twofold activity on erythroid lineages: it induces a mild erythroid cell cytotoxicity in the presence of serum and growth factors, while it promotes erythroid cell survival through the activation of the NF-kB/IkB pathway under starvation conditions.  相似文献   

15.
目的: 观察过氧化物酶体增殖物激活受体δ(PPARδ)激动剂GW501516对低氧原代大鼠肺动脉平滑肌细胞(PASMCs)增殖的影响,并探讨其可能机制,为低氧肺血管重构的防治寻找新靶点。方法: 对照组PASMCs采用21%氧气培养,低氧组采用 3%氧气诱导PASMCs增殖,通过不同浓度的GW501516(10、30、100 nmol/L)低氧条件下孵育PASMCs 12、24、48 h筛选GW501516抑制低氧PASMCs增殖的最适浓度;选择100 nmol/L GW501516和(或)蛋白激酶B(AKT)激动剂SC79在低氧条件下孵育PASMCs 24 h,探讨GW501516抑制PASMCs增殖可能机制,通过CCK-8与BrdU试剂盒检测细胞增殖与DNA的合成,流式细胞仪分析细胞周期,实时定量PCR(RT-PCR)检测细胞周期蛋白(Cyclin)D1,细胞周期蛋白激酶抑制蛋白p27(p27)mRNA的表达,Western blot检测PPARδ、总的和磷酸化蛋白激酶B(AKT)与糖原合酶激酶3β(GSK3β)的表达。结果: 与低氧组相比,不同浓度的GW501516(10、30、100 nmol/L)干预12、24、48 h后能够抑制低氧条件下PASMCs增殖与DNA的合成,且100 nmol/L GW501516抑制作用最强(P<0.05或P<0.01);与对照组相比,100 nmol/L GW501516干预PASMCs 24 h能够显著上调PPARδ的表达,而低氧可显著下调PPARδ的表达(P<0.01);与低氧组相比,100 nmol/L GW501516干预24 h后能够显著抑制PASMCs增殖与DNA的合成(P<0.01),增加处于G0/G1期的PASMCs比例,明显减少S期和G2/M期的PASMCs比例(P<0.05 或P<0.01),显著抑制Cyclin D1 mRNA的表达并促进p27 mRNA的表达(P< 0.01),显著抑制AKT与GSK3β磷酸化(P<0.01),而与100 nmol/L GW501516低氧组相比,AKT激动剂SC79能够逆转100 nmol/L GW501516 上述作用(P<0.05或P<0.01)。结论: GW501516通过抑制AKT/GSK3β信号通路抑制低氧条件下PASMCs增殖。  相似文献   

16.
We detected the expression of IL-12 p40/p35 mRNA by semi-quantitative RT-PCR and silver staining, and studied the molecular interaction between the IL-12 expression and the NF-kB activation induced by LPS and IFN-γ/LPS in murine peritoneal suppressor macrophages (MPSMs). It was found that IFN-γ strongly enhanced the LPS-induced IL-12 p40 and p35 mRNA expression. Both p40 and p35 mRNA levels were approximately equal. IFN-γ also greatly promoted the LPS-induced secretion of IL-12 p70 in MPSMs. The Proteasome Inhibitor I (PSI) could block the expres-sion of IL-12 p40 and p35 mRNA, and the degradation of IkBα induced by LPS or LPS/IFN-γ. EM-SA showed that LPS could augment the NF-kB binding activity to p40 promoter DNA. However, IFN-γ could neither enhance the LPS-induced NF-kB activity nor promote the degradation of IkBα. Taken together, the data suggest: (i) IFN-γ/LPS could strongly induce the expression of IL-12 p40 and p35 mRNA; both the expression levels were equal; this phenomenon coincided with the high-level secretion of IL-12 p70 induced by IFN-γ/LPS; (ii) NF-kB signal pathway is essential for IFN-γ/LPS to induce IL-12 mRNA expression; (iii) by blocking the degradation of IkB, the PSI sup-presses the IL-12 p40/p35 mRNA expression induced by LPS and IFN-γ/LPS; (iv) NF-kB signal may not be involved in the mechanism by which IFN-γ enhanced the expression of the LPS-induced IL-12 p40/p35 mRNA.  相似文献   

17.
It has been shown that the sympathetic nervous system is activated in pulmonary arterial hypertension (PAH). Norepinephrine (NE) levels are increased by chemoreflex-dependent sympathetic overactivation and involved in pulmonary vascular remodeling. However, the underlying mechanisms of the remodeling induced by NE are poorly understood. In this study, we found that, in vivo, the expression of tyrosine hydroxylase and the concentration of plasma NE were increased in PAH rats compared with normal rats. Increases in ventricular hypertrophy and medial width of the pulmonary arteries were reversed by prazosin, α1-adrenoceptor (α1-AR) antagonists, in PAH rats. Elevated expression of α1D-AR was detected in PAH rats. In addition, prazosin reduced the increasing expression of PCNA, CyclinA and CyclinE induced by hypoxia. In vitro, MTT assay, flow cytometry, Western blotting and immunofluorescence were performed to investigate the effects of NE on proliferation of pulmonary artery smooth muscle cells (PASMCs). We revealed that NE promoted PASMCs viability, increased the expression of PCNA, CyclinA and CyclinE, made more cells from G0/G1 phase to G2/M + S phase and enhanced the microtubule formation. Above NE-induced changes could be suppressed by BMY 7378, an inhibitor of α1D-AR. Furthermore, ERK-1/2 pathway was activated by NE. U0126, a specific inhibitor for ERK-1/2, attenuated the NE-induced proliferation of PASMCs under normoxia and hypoxia. Taken together, our results suggest that NE which stimulates α1D-AR promotes proliferation of PASMCs and the effect is, at least in part, mediated via the ERK-1/2 pathway.  相似文献   

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