Visfatin is released from 3T3-L1 adipocytes via a non-classical pathway
Visfatin is released from 3T3-L1 adipocytes via a non-classical pathway
复制标题
DOI：
10.1016/j.bbrc.2007.05.096
复制
发表时间：
2007-07-27
影响因子：
3.1
通讯作者：
Shimomura, Iichiro
中科院分区：
文献类型：
--
作者：
Tanaka, Masaki;Nozaki, Maiko;Shimomura, Iichiro
内脂素是一种分泌性蛋白质，具有胰岛素模拟和促炎作用，也作为细胞内酶产生NAD。肥胖者血浆内脂素水平和脂肪组织内脂素mRNA表达增加。内脂素不具有合适的可裂解信号序列，并且介导内脂素从脂肪细胞释放的机制仍然知之甚少。在这项研究中，我们证明，内脂素大量释放到培养基中的3 T3-L1脂肪细胞。亚细胞分级分析表明，visfatin定位于胞质溶胶中，而不是在细胞核，膜，囊泡，或线粒体组分。内脂素释放不减少Brefeldin A和莫能菌素，抑制内质网（ER）高尔基体依赖性分泌。此外，内脂素在微泡上不释放。这些结果表明，visfatin应通过ER-高尔基体或微泡非依赖性途径从3 T3-L1脂肪细胞释放。(c)2007年爱思唯尔公司All rights reserved.
Visfatin is a secretory protein which exerts insulin mimetic and proinflammatory effects, also functioning as an intracellular enzyme to produce NAD. Plasma visfatin levels and visfatin mRNA expression in adipose tissues are increased in obese subjects. Visfatin does not have a decent cleavable signal sequence, and the mechanism, that mediates release of visfatin from adipocytes, remains poorly understood. In this study, we demonstrate that visfatin is released abundantly into culture medium from 3T3-L1 adipocytes. Subcellular fractionation analysis showed that visfatin was localized in the cytosol, but not in nucleus, membrane, vesicles, or mitochondria fractions. Visfatin release was not reduced by Brefeldin A and Monensin, inhibitors of endoplasmic reticulum (ER)-Golgi-dependent secretion. In addition, visfatin was not released on microvesicles. These results suggest that visfatin should be released from 3T3-L1 adipocytes via an ER-Golgi or microvesicles independent pathway. (c) 2007 Elsevier Inc. All rights reserved.