Conventional kinesin KIF5B mediates adiponectin secretion in 3T3-L1 adipocytes.

Conventional kinesin KIF5B mediates adiponectin secretion in 3T3-L1 adipocytes.
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传统驱动蛋白 KIF5B 介导 3T3-L1 脂肪细胞中脂联素的分泌。

DOI:
10.1016/j.bbrc.2016.06.008
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发表时间:
2016-08
期刊:
Biochem Biophys Res Commun
影响因子:
--
通讯作者:
Zhang Tie-Mei
Zhang Tie-Mei
中科院分区:
其他
文献类型:
--
作者:
Cui Ju;Pang Jing;Lin Ya-Jun;Jiang Ping;Gong Huan;Wang Zai;Li Jian;Cai Jian-Ping;Huang Jian-Dong;Zhang Tie-Mei

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胰岛素刺激脂肪细胞分泌脂联素和葡萄糖转运蛋白4(GLUT 4)转位,调节代谢稳态。与GLUT 4易位类似,脂联素在脂肪细胞中的细胞内运输和释放依赖于trans-Golgi网络和内体系统。最近的研究表明,传统驱动蛋白的重链(KIF 5 B)介导小鼠3 T3-L1脂肪细胞中的GLUT 4易位,然而,参与介导脂联素的细胞内运输和释放的运动机制尚不清楚。在这里,我们研究了KIF 5 B在脂联素分泌调节中的作用。KIF 5 B水平在3 T3-L1脂肪形成过程中上调。细胞质KIF 5 B的增加与脂联素的诱导同步。内源性KIF 5 B和脂联素部分共定位在核周和胞浆区域。此外,含脂联素的囊泡与KIF 5 B共免疫沉淀。KIF 5 B的敲低导致脂联素分泌的显著抑制,KIF 5 B的过表达增强脂联素的释放,而瘦素分泌不受KIF 5 B表达变化的影响。这些数据表明,脂联素的分泌,而不是瘦素,是依赖于功能KIF 5 B。
Insulin stimulates adiponectin secretion and glucose transporter type 4 (GLUT4) translocation in adipocyte to regulate metabolism homeostasis. Similar to GLUT4 translocation, intracellular trafficking and release of adiponectin in adipocytes relies on the trans-Golgi network and endosomal system. Recent studies show that the heavy chain of conventional kinesin (KIF5B) mediates GLUT4 translocation in murine 3T3-L1 adipocytes, however, the motor machinery involved in mediating intracellular trafficking and release of adiponectin is unknown. Here, we examined the role of KIF5B in the regulation of adiponectin secretion. The KIF5B level was up-regulated during 3T3-L1 adipogenesis. This increase in cytosolic KIF5B was synchronized with the induction of adiponectin. Endogenous KIF5B and adiponectin were partially colocalized at the peri-nuclear and cytosolic regions. In addition, adiponectin-containing vesicles were co-immunoprecipitated with KIF5B. Knockdown of KIF5B resulted in a marked inhibition of adiponectin secretion and overexpression of KIF5B enhanced adiponectin release, whereas leptin secretion was not affected by changes in KIF5B expression. These data suggest that the secretion of adiponectin, but not leptin, is dependent on functional KIF5B.
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