Regulation of macrophage foam cell formation and atherosclerosis by novel regulatory peptides for cardiovascular system

持续皮下输注尿紧张素II（一种强血管收缩肽），使脂肪喂养的apoe基因敲除小鼠的动脉粥样硬化病变增强了8倍。对尿紧张素ii处理小鼠腹腔巨噬细胞的分析显示，氧化LDL诱导的泡沫细胞形成增加了7倍。Salusins是一种源自相同前体的新型血管调节肽。连续皮下输注salusin-α可抑制apoE-KO小鼠动脉粥样硬化的发展68%，而salusin-β可使其增强2.6倍。腹腔巨噬细胞来自salusin？α-处理小鼠氧化LDL诱导的泡沫细胞形成减少68%，而salusin-β处理小鼠巨噬细胞泡沫细胞形成增加2.6倍。因此，尿紧张素II和salusins可被视为动脉粥样硬化的新治疗靶点。

Continuous subcutaneous infusion of urotensin II, a strong vasoconstrictor peptide, enhanced atherosclerotic lesions by 8-fold in fat-fed apoE-knockout mice. Analyses of peritoneal macrophages from urotensin II-treated mice revealed 7-fold increase in foam cell formation induced by oxidized LDL. Salusins are novel vasoregulatory peptides that derive from the same precursor. Development of atherosclerosis in apoE-KO mice was suppressed by 68% by continuous subcutaneous infusion of salusin-α but was 2.6-fold enhanced by salusin-β. Peritoneal macrophages from salusin?α-treated mice revealed 68% reduction in foam cell formation induced by oxidized LDL whereas macrophages from salusin-β-treated mice showed 2.6-fold increase in foam cell formation. Thus, urotensin II and salusins can be regarded as novel therapeutic targets for atherosclerosis.