Secretion of salusin-β from human monocyte-derived cells.

Salusin-β从人单核细胞/巨噬细胞中释放，表明在动脉粥样硬化的发生和发展中可能起自分泌/旁分泌作用。炎性细胞因子诱导的分泌不是preprosalusin基因诱导的结果，但可能是由增加的prosalusin的细胞内加工。我们的研究结果表明salusin-β可能是预防动脉粥样硬化的一个新的治疗靶点。由于放射免疫法无法准确测定血浆salusin-β水平，因此我们建立了一种特异性的酶联免疫吸附试验（ELISA），用于检测人血浆中salusin-β的浓度。正常人血浆salusin-β-like免疫反应性约为1 nmol/L。salusin-β的前瞻性研究通过ELISA检查了血浆salusin-β水平与动脉粥样硬化严重程度的关系以及salusin-β作为动脉粥样硬化生物标志物的有用性。

Salusin-β is released from human monocytes/macrophages suggest a possible autocrine/paracrine role in the development and progression of atherosclerosis. Inflammatory cytokines induced secretion was not the result of preprosalusin gene induction, but might have been caused by increased intracellular processing of prosalusin. Our results implicate that salusin-β could be a novel therapeutic target for the prevention of atherosclerosis. It has been impossible to accurately measure plasma salusin-β levels by radioimmunoassay, therefore, we have established a specific enzyme-linked immunosorbent assay(ELISA) suitable for detection of immunoreactive salusin-β in human plasma. The salusin-β-like immunoreactivity in normal human plasma was about 1 nmol/L. Prospective studies of salusin-βt hat examine relationships with plasma salusin-βlevels and severity of atherosclerosis by ELISA and the usefulness of salusin-β as a biomarker for atherosclerosis.