混合淋巴细胞培养中刺激细胞的（60）~Coγ射线照射量

混合淋巴细胞培养中刺激细胞的（６０）~Ｃｏγ射线照射量孙成文，张蕊芳，孔繁华（北京军事医学科学院附属医院１０００３９）混合淋巴细胞培养（ＭＬＣ）是骨髓移植前组织配型的重要方法，分单向和双向两种。在单向ＭＬＣ中，刺激细胞的６０Ｃｏγ射线照射量是试验的重?..     

硝基左旋精氨酸甲基酯对辐照小鼠小肠的保护作用

硝基左旋精氨酸甲基酯是一种一氧化氮合成酶的特异性抑制剂。本实验选用ＢＡＬＢ／ｃ小鼠，＾６０Ｃｏγ－射线全身一次性照射１２Ｇｙ后，再给予Ｌ－ＮＡＭＥ灌胃，于照后７２ｈ处死。应用ＮＤ组化，Ｈ－Ｅ染色及Ｆｅｕｌｇｅｎ后庆肠腺计数方法，对小肠壁的ＮＯＳ阳性结构。小肠的组织结构及肠腺存活率等进行观察。     

花生四烯酸产物对系膜细胞增殖作用的研究

用［３Ｈ］胸腺嘧啶核甙（［３Ｈ－ｔｈｙｍｉｄｉｎｅ，［３Ｈ］－ＴｄＲ）掺入法测定花生四烯酸产物对体外培养的大鼠肾小球系膜细胞的增殖作用。前列腺素Ｅ２（ｐｒｏｓｔａｇｌａｎｄｉｎ，ＰＧ）抑制血清所致的系膜细胞增殖。血栓素Ａ２（ｔｈｒｏｍｂｏｘａｎｅ，Ｔｘ）类似物Ｕ４６６１９、白三烯（ｌｅｕｋｏｔｕｉｅｎｅ，ＬＴ）Ｃ４、ＬＴＤ、１２－羟二十碳四烯酸（１２－ｈｙｄｒｏｘｙｅｉｃｏｓａｔｅｔｒａｅｎｏｉｃａｃｉｄ，１２－ＨＥＴＥ）、１５－ＨＥＴＥ促进静息的系膜细胞增殖，ＬＴＢ４及５－ＨＥＴＥ无此作用。用特异性蛋白激酶Ｃ（ｐｒｏｔｅｉｎｋｉｎａｓｅＣ，ＰＫｃ）抑制剂可抑制Ｕ４６６１９、ＬＴＣ４、ＬＴＤ４及１２－ＨＥＴＥ的促增殖作用。ＰＧＦ２α、Ｕ４６６１９、ＬＴＣ４、ＬＴＤ４促进系膜细胞合成二脂酰甘油（ｄｉａｃｙｌｇｌｙｃｅｒｏｌ，ＤＡＧ）。ＰＧＦ２α及ＬＴＤ４刺激系膜细胞合成三磷酸肌醇（ｉｎｏｓｉｔｏｌｔｒｉｐｈｏｓｐｈａｔｅ，ＩＰ３）。提示部分花生四烯酸产物活化ＰＫＣ而促进系膜细胞增殖。     

致敏豚鼠的气道高反应机理及药物干预作用

用卵蛋白致敏豚鼠（致敏组）后气道反应性显著升高。致敏组支气管肺泡灌洗液（ＢＡＬＦ）中的细胞总娄，分类和嗜酸细胞（Ｅｏｓ）绝对计数均与对照组无显著差异，但ＢＡＬＦ中低密度Ｅｏｓ（ＨＥ）和气道上皮细胞（ＢＥＣ）的百分却显著高于对照组，且与豚鼠对级胺的气道反应性ＰＣ２０值呈显著负相关，用雷公藤甲处理玩笑及鼠后，气道反应性显著降低，ＢＡＬＦ中ＨＥ和ＢＥＣ也显著减少，提示Ｅｏｓ活化及气道上皮损伤可能在致敏豚     

AGEs抑制内皮依赖的血管舒张

目的研究糖基化终产物（ＡＧＥｓ）对内皮依赖的血管舒张功能的影响及其可能机制。方法利用器官组织浴血管环法测定血管张力的变化,观察ＡＧＥｓ对乙酰胆碱（ＡＣｈ）产生的内皮依赖的和硝普销产生的内皮非依赖的血管舒张功能的影响以及Ｌ－精氨酸．细胞渗透型抗氧化剂ＭｎＴＭＰｙＰ,ＡＧＥｓ抗体及其Ｐ６０受体抗体对ＡＧＥｓ作用的影响。结果ＡＣｈ产生浓度依赖的血管舒张,ＡＧＥｓ能明显抑制ＡＣｈ的这种血管舒张作用,而且这种作用与ＡＧＥｓ浓度相关。ＡＧＥｓ的抗体及其Ｐ６０受体抗体可完全逆转ＡＧＥＳ的作用。Ｌ－精氨酸和细胞渗透性抗氧化剂不改变ＡＧＥｓ的作用。硝普销也呈现浓度依赖的血管舒张,但ＡＧＥｓ对硝普铜的作用无明显影响。结论 ＡＧＥｓ通过抑制内源性一氧化氮的产生抑制内皮依赖的血管舒张,这种作用是通过ＡＧＥｓ的Ｐ６０受体介导的,与激活氧自由基的产生无关。     

微丝重组对细胞增值作用的研究

用罗丹明－鬼笔环肽（ｒｈｏｄａｍｉｎｅ－ｐｈａｌｌｏｉｄｉｎ）显示微丝（ｍｉｃｒｏｆｉｌａｍｅｎｔｓ，ＭＦ）的荧光染色法对Ｇ期小鼠Ｃ３Ｈ１０Ｔ１／２成纤维细胞向Ｓ期过渡过程中，ＭＦ结构的变化及ＭＦ重组对ＤＮＡ合成的影响进行了研究，Ｇ期细胞在血清刺激１ｈ后ＭＦ解聚，３ｈ后重新组装，并恢复原来的分布。我们发现细胞松弛素Ｂ（ｃｙｔｏｃｈａｌａｓｉｎＢ，ＣＢ）使ＭＦ解聚并与蛋白激酶Ｃ（ｐｒｏｔｅｉｎｋｉｎａｓｅＣ，ＰＫＣ）激活剂──佛波酯（ｐｈｏｒｂｏｌｅｓｔｅｒ，ＴＰＡ）同样可促进Ｇ期细胞提前进入Ｓ期，促进ＤＮＡ合成，但ＴＰＡ和ＣＢ的刺激作用必需依赖于血清的存在，而ＰＫＣ抑制剂Ｈ７则阻断Ｇ期细胞进入Ｓ期，ＭＦ稳定剂ｐｈａｌｌｏｉｄｉｎ对ＤＮＡ合成具有一定的抑制作用，实验结果表明，Ｇ期细胞向Ｓ期过渡的早期阶段存在ＭＦ重组过程，ＣＢ促使Ｇ细胞ＭＦ解聚并可促进ＤＮＡ合成，提示ＭＦ重组是Ｇ期细胞向Ｓ期过渡的一个重要的早期事件。     

单向MLC中刺激细胞的照射剂量

本文讨论了混合淋巴培养中刺激细胞的＾６０Ｃｏγ射线照射剂量，６个人的淋巴细胞分成６份，分别用０、６、１０、１５、２０、２５Ｇｙ的＾６０Ｃｏγ射线照射，然后进行混合淋巴细胞培养。结果显示在混合淋巴细胞培养中，刺激细胞的＾６０Ｃｏγ射线照射量以２０Ｇｙ左右为宜。     

THE RELATIONSHIP BETWEEN THE VOLUMINA CHANGES OF LINK ATRIUM

ＴＨＥＲＥＬＡＴＩＯＮＳＨＩＰＢＥＴＷＥＥＮＴＨＥＶＯＬＵＭＩＮＡＣＨＡＮＧＥＳＯＦＬＩＮＫＡＴＲＩＵＭＰｅｎｇＢａｏ；ＬｉｎＺｈｏｎｇＷｅｎ（ＨｏｓｐｉｔａｌｏｆＳｈｅｎｇｚｈｅｎＣｉｔｙ，Ｓｈｅｎｇｚｈｅｎ，５１８０００，Ｃｈｉｎａ）Ａｂｓｔｒａ...     

CLONING AND SEQUENCE CHARACTERIZATION OF THE RE-ARRANDED VH GENE FROM HYBRIDOMA CELLS SECRETING ANTI-HUMAN C1-INHIBITOR McAb

由分泌抗人Ｃ１－ＩＮＨＭｃＡｂ的杂交瘤Ｆ７细胞株提取总ＲＮＡ，合成与ＶＨ基因ＦＲ１和ＦＲ４互补的通用引物，以ＲＮＡ反转录合成的第一链ｃＤＮＡ为模板，ＰＣＲ法克隆出Ｆ７ＶＨ基因的ＤＮＡ片段。将分离获得的目的ＤＮＡ片段亚克隆入ｐＵＣ１８／１９测序载体，从两头进行双脱氧核苷酸随机终止法的ＤＮＡ序列测定。结果显示：ＶＨ基因是由３３３个碱基组成，编码１１１个氨基酸残基。通过国际联机检索进行ＥＭＢＬ和Ｋａｂａｔ基因库扫描发现，Ｆ７ＶＨＤＮＡ仅与Ｉｇ同源，符合小鼠Ｉｇ的ＶＨ基因特征；同源性为６０％～８５％，应归属于Ｉｇ的ＶＨ基因。根据Ｋａｂａｔ分类方法，Ｆ７ＶＨ基因推导的氨基酸顺序属于小鼠Ｉｇ的ＶＨ基因的Ⅱ（Ａ）亚组，是由ＶＨ－Ｄ－ＪＨ３重排产生；其框架区的９和６７位点为脯氨酸（Ｐｒｏ）和赖氨酸（Ｌｙｓ）（非芳香族氨氨酸），符合Ⅱ（Ａ）亚组框架残基结构模式；其ＣＤＲ３区含有７个氨氨酸残基，表明Ｃ１－ＩＮＨ抗原表面结构并不复杂；ＦＲ２和ＦＲ３的２２和８９位点为半胱氨酸残基（Ｃｙｓ），与ＶＨ片段二硫键形成有关。成功获得Ｆ７ＶＨ基因为进一步构建和表达单链Ｆｖ（ｓｃＦｖ）抗体打下良好的基础。     

淋巴细胞培养上清诱导低密度嗜酸细胞作用

分离豚鼠外周血淋巴细胞加入ＣｏｎＡ在体外培养后，收集上清液。１０－５ｍｏｌ／Ｌ的组胺不能诱导正常密度嗜酸细胞（ＮＥｏ）转变为低密度嗜酸细胞（ＨＥｏ），但Ｅｏｓ经淋巴细胞培养上清预处理后，组胺能明显地刺激ＮＥｏ转变为ＨＥｏ（Ｐ＜０．０５），１０－６ｍｏｌ／ＬＰＡＦ能诱导１５．９％的ＮＥｏ转变为ＨＥｏ，而经淋巴细胞培养上清预处理能显著增强ＰＡＦ的作用。淋巴细胞培养上清与Ｅｏｓ悬液１：１比例温育３０ｍｉｎ，对Ｅｏｓ密度无显著影响，但温育４８ｈ能显著地诱导ＮＥｏ转变为ＨＥｏ（Ｐ＜０．０１）。同样，淋巴细胞培养上清与Ｅｏｓ作用３０ｍｉｎ，不能诱导Ｅｏｓ脱颗粒，作用４８ｈ能诱导Ｅｏｓ释放约２８％的Ｅｏｓ过氧化物酶（ＥＰｏ）。以上表明淋巴细胞产物能致敏Ｅｏｓ，增强炎性介质刺激ＨＥｏ产生的能力。淋巴细胞产物诱导ＨＥｏ产生的作用较ＰＡＦ等缓慢，这种作用可能是刺激Ｅｏｓ脱颗粒的结果。     

不同剂量60Co-γ射线对TM3细胞的损伤效应

目的：对不同剂量60Co-γ射线下TM3细胞的损伤进行细胞生物学行为、转录层面的分析。方法：TM3细胞分4组,包括3个60Co-γ射线照射组(3、6、9 Gy)及对照组(不照射)。于24、48、72 h观察各组细胞凋亡情况(流式细胞法)、氧化损伤(ELISA)、睾酮合成关键因子(StAR、P450scc、P450c17及3β-HSD)的mRNA表达(实时定量PCR法)。于24、48、72、96、120、144 h,观察细胞增殖情况(MTS法)。结果：第24、72 h,各照射组细胞凋亡率均高于对照组(P<0.008);MTS实验中,第144、120 h,各照射组OD490值均低于对照组(P<0.008);第24,48,72 h,3 Gy组8-OHdG浓度与对照组相比无差异(P>0.008),而9 Gy组高于对照组(P<0.008);在72 h,各照射组StAR、P450scc、3β-HSD mRNA表达均低于对照组(P<0.008),而P450c17的表达在3 Gy组中无显著改变,在6 Gy组中高于对照组,在9 Gy组中低于对照组。结论：60Co-γ射线使TM3细胞凋亡增加、细胞增殖能力下降。6 Gy、9 Gy照射可以导致TM3细胞DNA的氧化损伤。辐照导致TM3细胞中StAR、P450scc、3β-HSD mRNA表达下降。6 Gy的照射使P450c17 mRNA表达上升,9 Gy使之下降。     

188铼辐射抑制血管平滑肌细胞增殖研究

目的：探讨放射性核素¹⁸⁸铼（¹⁸⁸Re）对培养平滑肌细胞增殖的作用及其机制。方法：应用¹⁸⁸Re β射线进行培养平滑肌细胞的内辐射。通过细胞计数、再增殖试验、[³H]-TdR掺入试验、流式细胞术细胞周期分析、免疫细胞化学及细胞存活率检测等方法,观察辐射抑制平滑肌细胞增殖的有效及最佳剂量、有效抑制时间、细胞增殖率变化、细胞周期分布、细胞存活率及其相关基因表达。结果：5.2 Gy剂量辐射,50%以上平滑肌细胞增殖受抑,细胞增殖率为46%;20.6 Gy剂量辐射,DNA合成抑制率达92%,增殖期细胞占3%;辐射后2周未见细胞再增殖,<20.6 Gy辐射未见细胞存活力下降;辐射后P53表达升高,PCNA表达降低。结论：¹⁸⁸Re β辐射对平滑肌细胞增殖抑制有效且持久半数有效剂量为5 Gy最佳辐射剂量为20 Gy。低剂量辐射抑制平滑肌细胞增殖的主要机制为损伤细胞分裂增殖能力。P53及PCNA调控辐射抑制细胞增殖过程。     

^60Coγ射线照射对肺泡Ⅱ型细胞和肺泡隔间质细胞的生物效应

目的：探讨^60Coγ射线照射对肺泡Ⅱ型细胞和肺泡隔间质细胞的生物效应。方法：原代分离肺内Ⅱ型上皮细胞（AT-Ⅱ）和间质细胞包括巨噬细胞和成纤维细胞，分别进行0、3、5、7Gy的γ射线照射，用细胞核嗜银染色观察照射对AT-Ⅱ增殖的影响；用酶谱分析检测照射后AT-Ⅱ和间质细胞培养上清中基质金属蛋白酶-2、-9（MMP-2，-9）的活性；用ELISA检测间质细胞培养上清中TGF-β1和Ⅳ型胶原含量。结果：AT-Ⅱ的核仁数量随照射剂量增加而增多，其中7Gy组最高；AT-Ⅱ培养上清中MMP-2、-9活性随照射剂量增加呈先增高后降低趋势，间质细胞上清中MMP-2、-9活性和TGF-β1水平逐渐升高，Ⅳ型胶原分泌水平呈先降低后升高趋势。结论：放射性肺损伤早期，AT-Ⅱ、巨噬细胞和成纤维细胞均参与肺组织无效性重建过程，与晚期肺纤维化启动有一定的内在联系。     

Role of MAPK7 in cell proliferation and metastasis in ovarian cancer

Aim: To investigate the effect of mitogen-activated protein kinase 7 (MAPK7) in ovarian cancer metastasis and to explore its potential mechanism. Methods: pcDNA-MAPK7 and siRNA-MAPK7 vectors were transfected into the human ovarian cell line OVCAR-3 based on gene silencing and overexpression methods. Effects of MAPK7 overexpression and silencing on OVCAR-3 cells proliferation, cell invasion, and migration were analyzed using the MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) assay, Matrigel methods, and Markered methods respectively. In addition, effect of MAPK7 expression on extracellular matrix (ECM) associated protein was detected using Western blot. Results: Compared with the controls, MAPK7 was up-regulated when cells were transfected with pcDNA-MAPK7 plasma, as well as MAPK7 was sliced when cells were transfected with siRNA-MAPK7 plasma (P<0.05). Besides, biological function analysis performed that overexpression of MAPK7 significantly increased OVCAR-3 cell proliferation, invasion, and migration (P<0.05), while these effects were inhibited by MAPK7 silencing (P<0.05). Additionally, MAPK7 overexpression increased type II collagen expression (P<0.05). However, there was no significant difference between MAPK7 expression and type I collagen expression (P>0.05). Conclusion: Our data implied the up-regulated MAPK7 might contribute to ovarian cancer metastasis through up-regulating type II collagen expression and then were involved in cell biological processes such as cell proliferation, invasion, and migration. MAPK7 may be a potential therapeutic target in the clinical treatment for ovarian cancer.     

Spike conduction properties of T-shaped C neurons in the rabbit nodose ganglion

Noradrenaline (NA) and angiotensin II (A II) were infused intravenously in conscious dogs without (series I) and with (series II) additional infusions of sodium nitroprusside at doses re-establishing normal levels of mean arterial pressure (MAP). In series I, NA infusion (1.6 g/min per kg for 30 min) initially elevated MAP by some 25 mm Hg and lowered heart rate by some 30 beats/min. Plasma concentrations of arginine vasopressin (AVP) remained constant, while those of A II and atrial natriuretic factor were slightly, but significantly, increased. Infusion of A II (10 or 20 ng/min per kg for 30 min) induced similar rises in MAP and slight reductions of heart rate and increased plasma AVP by 70% and atrial natriuretic factor by 60%. In series II, sodium nitroprusside (1–4 g/min per kg) was added for 30 min to infusions of NE (1.6 g/min per kg) and A II (20 ng/min per kg) in order to maintain MAP at its control level. This resulted in an 11-fold increase in plasma AVP during NA infusion and a 19-fold increase during A II infusion. Infusing sodium nitroprusside (4 g/min per kg) alone lowered MAP to clearly hypotensive levels, but the resulting rises in plasma AVP were less than, rather than equal to, those seen at normotensive MAP levels during the combined infusions of sodium nitroprusside with A II or NA, respectively. It is concluded that both NA and A II exert strong stimulatory actions on AVP release which are, however, counteracted by inhibitory influences arising from the hypertensive effects of NA and A II.     

Effect of dose rate on the radiation-induced bystander response

Radiation-induced biological bystander effects have become a well-established phenomenon associated with the interaction of radiation with cells. These so-called bystander effects have been seen across a variety of end points for both high and low linear energy transfer (LET) radiations, utilizing a variety of dose rates and radiation sources. In this study, the effect of dose rate and different low LET sources on the bystander cell survival fraction (SF) was examined. The cell line investigated was the human keratinocyte HPV-G. The bystander response was measured via clonogenic assay after medium transfer protocol. Cells were irradiated using (60)Co gamma-rays and 20 MeV electrons at doses of 0.5, 5 and 10 Gy with varying dose rates. Both gamma and electron irradiation decreased recipient SF at 0.5 Gy and 5 Gy, respectively. Subsequent recovery of the SF to control levels for 10 Gy was observed. There was no dose rate dependence for (60)Co irradiation. A significant difference in the survival fraction was observed for electron irradiation at 10 Gy and a high dose rate. Furthermore, survival fractions were compared between (60)Co and 20 MeV electron irradiations. This showed a significant increase in the survival fraction 'recovery' at 10 Gy for a (60)Co dose rate of 1.1 Gy min(-1) compared to 20 MeV electrons at 1.0 Gy min(-1). No such difference was observed when comparing at higher dose rates. Lastly, increases in survival fraction at 10 Gy were abolished and the SF decreased by the plating of increased numbers of recipient cells. Such evidence may help gain insight into the nature and mechanism(s) surrounding bystander signal production, how these phenomena are tested and their eventual application in a clinical setting.     

PLGF参与Ang II诱导的心脏成纤维细胞激活

 目的：探讨胎盘生长因子（PLGF）在血管紧张素II（Ang II）激活心脏成纤维细胞(CFs)中的表达及其作用。方法：原代分离培养并鉴定新生SD大鼠CFs。蛋白免疫印迹检测α-平滑肌肌动蛋白（α-SMA）、PLGF和磷酸化ERK1/2(p-ERK1/2),免疫荧光观察α-SMA的表达,WST-1法检测细胞增殖,RT-PCR检测PLGF、I型和III型胶原蛋白的mRNA表达水平。结果：(1)Ang II组PLGF mRNA 表达明显高于对照组（P<0．01),联用替米沙坦后,PLGF mRNA表达水平下降;Ang  II组PLGF蛋白表达水平高于对照组（P<0.05); (2)PLGF诱导CFs增殖及α-SMA蛋白表达增加（P<0.05）;PLGF干预CFs 60 min后,p-ERK1/2蛋白水平表达明显高于对照组（P<0.01);(3)Ang II+anti-PLGF组与Ang II组比较,细胞增殖和α-SMA蛋白表达水平下降（P<0.05）,I型和III型胶原蛋白mRNA表达水平亦下调（P<0.05）。结论：PLGF可能参与Ang II诱导的CFs增殖和纤维化过程。     

Effects of radiation and latent virus on immune responses in a space flight model

BACKGROUND: The immunosuppressive effects of space flight radiation and reactivation of latent virus infections in human beings are largely unknown. OBJECTIVE: To develop a murine model that can predict the adverse effects of space flight radiation and reactivation of latent virus infection for human beings. METHODS: In experiment I, some BALB/c mice received whole-body gamma-irradiation (3 Gy) on day 0 and murine polyoma virus (PyV) on day 1. In experiment II, mice received irradiation (3 Gy) or none on days 0 and/or 49, and PyV or none on day 1: A1, 3 Gy/PyV/3 Gy; A2, 3 Gy/ PyV/0 Gy; B1, 0 Gy/PyV/3 Gy; B2, 0 Gy/ PyV/0 Gy; C, 3 Gy/0 PyV/0 Gy; and D, 0 Gy/0 PyV/0 Gy. RESULTS: In experiment I, PyV was detected by PCR more frequently in several host organs tested and for a longer period of time in irradiated than in control animals. In experiment II, PyV replication in the spleen was detected in A1>B1 mice on days 10 and 20; both groups cleared PyV by day 49. After irradiation on day 49, reactivated PyV was detected in more B1 than A1 mice. A1 mice had lower spleen weights and cell counts than other groups at all time points. From 0 to 49 days, irradiation suppressed spleen cell proliferation to concanavalin A in all irradiated groups except in B1 when the virus was cleared at day 20. PyV enhanced IFN-gamma production in all groups: B1>A1>C, D (0-49 days; all differences, P < .05). CONCLUSION: This small animal model of space flight suggests that the combined effects of radiation and virus replication will significantly affect T-lymphocyte-mediated immunity that may lead to chronic viral infection and malignancy.     

Microvascular reactivity in experimental diabetes: responses of male and female rats

OBJECTIVE: To study the influence of sex on the responses of microvessels to vasoactive agents in experimental diabetes. MATERIALS: Diabetes was induced by alloxan (40 mg/kg, iv) in male and female Wistar rats (8-10-week-old). METHODS: Using an image splitter television microscope, mesenteric arteriolar and venular diameter changes induced by topically applied vasoactive agents (histamine, bradykinin, platelet activating factor-PAF, acetylcholine, sodium nitroprusside, noradrenaline and angiotensin II) were examined. RESULTS: Whereas the vasoconstrictor response to noradrenaline was equivalent in normal and diabetic animals, either female or male rats, an increased vasoconstrictor response to angiotensin II was observed in male but not in female diabetic rats in comparison with respective controls. Similarly to that observed in males, the dilator response of microvessels to topically applied bradykinin, histamine and PAF was impaired in female diabetic rats. Whereas reversal of the impaired responses to these agents was obtained by acute treatment of diabetic animals with insulin the altered responses to angiotensin II observed in male diabetic rats were not corrected. Differently from that observed in males, impaired response of microvessels to acetylcholine but not to sodium nitroprusside was observed in female diestrous diabetic rats; acute insulin treatment corrected it. CONCLUSIONS: We conclude that not all the alterations of the microvascular reactivity and the correction by insulin are gender dependent in diabetes.     

Effect of angiotensin-(1-7) and angiotensin II on the proliferation and activation of human endometrial stromal cells in vitro

Recent studies have shown that angiotensin II (Ang II) or angiotensin-(1-7) [Ang-(1-7)] has effect on the proliferation and activation of a variety of cells, however, the exact mechanisms that the role of Ang II or Ang-(1-7) in human endometrial stromal cell (ESCs) remains elusive. Here we demonstrated that Ang II could promote proliferation and activation of ESCs, up-regulated the expression of a-SMA, TGF-β1 and IGF-I, increased the secretion of extracellular matrix [Type I collagen (Col I) and fibronectin (FN)] of ESCs; Ang-(1-7) could inhibit Ang II induced the proliferation and activation of ESCs, down-regulated the expression of a-SMA, TGF-β1 and IGF-I, decreased the secretion of extracellular matrix (Col I and FN) of ESCs. These findings suggest that Ang-(1-7) can inhibits Ang II induced the proliferation of ESCs, Ang-(1-7) can inhibits the Ang II induced activation of ESCs and decreases secretion of Col I and FN by suppressing TGF-β1 and IGF-I expression.