Increased expression of endothelial lipase in rat models of hypertension

Increased expression of endothelial lipase in rat models of hypertension
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DOI:
10.1016/j.cardiores.2005.01.013
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发表时间:
2005-06-01
影响因子:
10.8
通讯作者:
Yokoyama, M
Yokoyama, M
中科院分区:
医学1区
文献类型:
--
作者:
Shimokawa, Y;Hirata, K;Yokoyama, M

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目的:为了更好地了解参与血管疾病的内皮脂肪酶(EL),我们研究是否EL的表达调节高血压动物models of hypertension.Methods:EL的大鼠cDNA同源物被确定使用逆转录聚合酶链反应。用血管紧张素II(Ang II)和佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)刺激培养的大鼠主动脉平滑肌细胞,北方印迹法分析EL mRNA表达。结果:大鼠EL cDNA编码含信号肽的493个氨基酸残基的蛋白质,与小鼠和人EL的同源性分别为91.9%和80.9%。北方杂交结果显示,EL在大鼠多种组织中均有表达。在培养的大鼠主动脉平滑肌细胞,血管紧张素II和PMA增加EL mRNA水平的2.9和3.3倍,分别。在血管紧张素II诱导的高血压大鼠,EL表达上调,在主动脉,心脏和肺。结论:高血压大鼠主动脉和心脏的EL表达增加。因此,EL可能在血管疾病的局部病理生理学中发挥作用。(c)2005年欧洲心脏病学会。出版社:Elsevier B.V版权所有。
Objective: To gain a better understanding of the involvement of endothelial lipase (EL) in vascular disease, we examined whether the EL expression is regulated in animal models of hypertension.Methods: The rat cDNA homologue of EL was identified using reverse transcription-polymerase chain reaction. Cultured rat aortic smooth muscle cells were stimulated with angiotensin II (Ang II) and phorbol 12-myristate 13-acetate (PMA), and EL mRNA expression was analyzed by Northern blotting. EL mRNA levels in tissues from stroke-prone spontaneously hypertensive rats (SHR-SP) and Ang II-induced hypertensive rats were evaluated using RNase protection assays.Results: Rat EL cDNA encoded a protein containing 493 amino acid residues including a signal peptide, and shares 91.9% and 80.9% sequence homology with murine and human EL, respectively. Northern blotting revealed that EL was expressed in a wide range of rat tissues. In cultured rat aortic smooth muscle cells, Ang II and PMA increased EL mRNA levels by 2.9- and 3.3-fold, respectively. In Ang II-induced hypertensive rats, EL expression was upregulated in the aorta, heart, and lung. In SHR-SP, EL expression was upregulated in the aorta and heart.Conclusion: EL expression is increased in rat models of hypertension. Thus, EL might have a role in the local pathophysiology of vascular diseases. (c) 2005 European Society of Cardiology. Published by Elsevier B.V All rights reserved.