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

Salusin-β从人单核细胞/巨噬细胞中释放，提示在动脉粥样硬化的发生和进展中可能具有自分泌/旁分泌作用。炎性细胞因子诱导的分泌不是prosalusin基因诱导的结果，而可能是prosalusin细胞内加工增加所致。我们的研究结果提示salusin-β可能是预防动脉粥样硬化的一种新的治疗靶点。由于放射免疫法无法准确测定血浆salusin-β水平，因此，我们建立了一种适用于检测人血浆中免疫反应性salusin-β的特异性酶联免疫吸附法（ELISA）。正常人血浆中salusin-β样免疫反应性约为1 nmol/L。salusin-βt的前瞻性研究，通过ELISA检测血浆salusin-β水平和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效性。

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.