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Experiments show that Ang Ⅱ activates JNK mediated by AT〓, and JNK increases transcription activity of c-Jun by phosphorylating c-Jun amido-terminal, and induces expression of c-Fos gene. c-Jun and c-Fos form transcriptional factor activated protein-1 complex. AP-1 may stimulates genes which correlate with cardiovascular remodeling expression, such as transforming growth factor, collagen type Ⅰ and Ⅲ, skeletal muscle α-actin,β-MHC, atrial natriuretic factor.
实验表明，在心肌和血管平滑肌细胞Ang Ⅱ通过AT〓介导激活JNK；JNK通过磷酸化c-Jun氨基末端增加c-Jun的转录活性并诱导c-Fos基因表达，c-Jun和c-Fos蛋白形成转录因子复合物激活蛋白-1(AP-1)，并刺激各种心血管重塑相关基因如转化生长因子-β1(TGF-β1)、Ⅰ，Ⅲ型胶原、骨骼肌α-actin、β-MHC(β-myosin heavy chain，β-肌球蛋白重链)、心钠素的表达。
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Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.
结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。
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Methods The nitroglycerin experimental migrainous animal model was reconstructed for the expression of c-fos and c-jun by means of immunohistochemical method Results The nitroglycerin experimental migrainous rats appeared reddish two ears, head shaking,scratching head with forepaws, activity increasing, both the number increasing and the area enlarging of the positive cells of the expression of c-...
免疫组化ABC法研究偏头痛大鼠脑组织即刻早期基因c -fos、c -jun的表达。结果硝酸甘油型实验性偏头痛大鼠出现双耳发红、甩头、前肢频繁搔头，活动增加等外在表现，脑组织c -fos、c -jun基因表达阳性细胞数增加，基因表达阳性细胞的面积扩大、灰度降低或变化不大。结论硝酸甘油型实验偏头痛大鼠模型复制方法简单、重复性较好、脑组织c -fos和c -jun基因异常表达明显，可以作为偏头痛治疗药物筛选、药效评价和发病机理研究的动物模型。
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JUN AVIGNON：(阿维农) STRASBOURG(斯特拉斯堡)
20 JUN NIMES(尼姆) AVIGNON(阿维农) | 21 JUN AVIGNON(阿维农) STRASBOURG(斯特拉斯堡) | 22 JUN STRASBOURG(斯特拉斯堡) ANNECY(安锡)
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Jun. 11：仁布--年木 (50公里)
Jun. 10 尼木--仁布 (45公里) | Jun. 11 仁布--年木 (50公里) | Jun. 12 年木--日喀则 (50公里)
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Jun. 17：山口--定日 (30公里)
Jun. 16 拉孜--山口 (45公里) | Jun. 17 山口--定日 (30公里) | Jun. 18 定日--扎西宗 (65公里)