Endothelin-1 and angiotensin-II stimulate delayed mitogenesis in cultured rat aortic smooth muscle cells: evidence for common signaling mechanisms.
Endothelin-1 and angiotensin-II stimulate delayed mitogenesis in cultured rat aortic smooth muscle cells: evidence for common signaling mechanisms.
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内皮素-1 和血管紧张素-II 刺激培养的大鼠主动脉平滑肌细胞的有丝分裂发生延迟：常见信号传导机制的证据。
作者：
H. Weber;M. Webb;R. Serafino;D. Taylor;S. Moreland;J. Norman;C. Molloy
血管活性肽内皮素-1 （ET-1）和血管紧张素- ii （AII）与慢性高血压有关，并可能在相关血管疾病如再狭窄和动脉粥样硬化中发挥重要作用。在大鼠主动脉平滑肌（RASM）细胞模型中，ET-1和AII均诱导DNA合成浓度依赖性延迟增加，相对于无血清对照组。每个肽段的DNA合成刺激在100 nM处最大。RASM细胞的所有处理均比ET-1（3倍）产生更大的有丝分裂作用（4- 7倍）。当添加AII时，ET-1对DNA合成有补充作用（比对照高5- 10倍）。虽然RASM细胞同时表达ETA和AT1受体，但放射配体结合实验表明，AT1受体的数量是ETA受体的10倍左右。在信号转导研究中，ET-1和AII各自引起细胞内Ca2+浓度的浓度依赖性增加。ET-1和AII也刺激磷酸肌醇代谢和蛋白激酶c的特定底物磷酸化。总肌醇磷酸对ET-1和AII的释放呈浓度依赖性，分别被ETA受体选择性拮抗剂BQ-123和AT1受体选择性拮抗剂氯沙坦抑制。此外，在加入ET-1或AII后的5分钟内，观察到120千道尔顿蛋白和75千道尔顿蛋白以及丝裂原活化蛋白激酶p44mapk和p42mapk的酪氨酸磷酸化。综上所述，这些数据表明ET-1和AII可能通过共同的细胞内信号传导机制促进平滑肌细胞生长。
The vasoactive peptides endothelin-1 (ET-1) and angiotensin-II (AII) have been implicated in chronic hypertension and may play important roles in related vascular diseases such as restenosis and atherosclerosis. Using a rat aortic smooth muscle (RASM) cell model, both ET-1 and AII induced concentration-dependent delayed increases in DNA synthesis relative to that in the serum-deprived controls. Stimulation of DNA synthesis was maximal at 100 nM for each peptide. All treatment of RASM cells resulted in a greater mitogenic effect (4- to 7-fold) than that observed for ET-1 (3-fold). When added in the presence of AII, ET-1 had a supplemental effect on DNA synthesis (5- to 10-fold above control). Although RASM cells expressed both ETA and AT1 receptors, radioligand binding experiments indicated that approximately 10-fold as many AT1 receptors as ETA receptors were present. In signal transduction studies, ET-1 and AII each elicited concentration-dependent increases in the intracellular Ca2+ concentration. ET-1 and AII also stimulated phosphoinositide metabolism and phosphorylation of a specific substrate for protein kinase-C. The release of total inositol phosphates in response to ET-1 and AII was concentration dependent and inhibited by the ETA receptor-selective antagonist BQ-123 and the AT1 receptor-selective antagonist losartan, respectively. In addition, tyrosine phosphorylation of 120- and 75-kilodalton proteins as well as the mitogen-activated protein kinases p44mapk and p42mapk was observed within 5 min of the addition of either ET-1 or AII. Taken together, these data indicate that ET-1 and AII may promote smooth muscle cell growth through common intracellular signaling mechanisms.
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收缩激动剂在血管平滑肌细胞生长调节中的作用。
影响因子：
--
作者：
Owens,GK
通讯作者：
Owens,GK
Endothelin-1 增加兔血管平滑肌细胞的细胞内钙动员，但不增加钙摄取。
DOI：
10.1016/0006-291x(89)91744-0
发表时间：
1989
影响因子：
3.1
作者：
Bialecki,RA;IzzoJr,NJ;Colucci,WS
通讯作者：
Colucci,WS
影响因子：
3
作者：
T. Scott‐Burden;T. Resink;A. Hahn;P. Vanhoutte
通讯作者：
T. Scott‐Burden;T. Resink;A. Hahn;P. Vanhoutte
内皮素异肽对 fos 和 jun 基因表达以及 AP-1 顺式元件活性的差异调节。
DOI：
--
发表时间：
1992
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Simonson,MS;Jones,JM;Dunn,MJ
通讯作者：
Dunn,MJ
影响因子：
15.9
作者：
NAFTILAN, AJ;PRATT, RE;DZAU, VJ
通讯作者：
DZAU, VJ