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

Abstract

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. - Highlights: • The KIF5B level was up regulated during 3T3-L1 adipogenesis. • Endogenous KIF5B and adiponectin were partially colicalized. • Adiponectin-containing vesicles were co-immunoprecipitated with KIF5B. • The secretion ofmore » adiponectin, but not leptin, is dependent on functional KIF5B.« less

Authors:
 [1]; ; ; ;  [1];  [2]; ;  [1];  [3];  [4];  [1]
  1. The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing (China)
  2. Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing (China)
  3. School of Biomedical Sciences and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Pokfulam (Hong Kong)
  4. (China)
Publication Date:
OSTI Identifier:
22606142
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 476; Journal Issue: 4; Other Information: Copyright (c) 2016 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; GLUCOSE; HOMEOSTASIS; INHIBITION; INSULIN; LEPTIN; METABOLISM; SECRETION; TRANSLOCATION

Citation Formats

Cui, Ju, E-mail: juzi.cui@gmail.com, Pang, Jing, Lin, Ya-Jun, Jiang, Ping, Gong, Huan, Wang, Zai, Li, Jian, Cai, Jian-Ping, Huang, Jian-Dong, E-mail: jdhuang@hku.hk, The Centre for Synthetic Biology Engineering Research, Shenzhen Institutes of Advanced Technology, Shenzhen, and Zhang, Tie-Mei, E-mail: tmzhang126@126.com. Conventional kinesin KIF5B mediates adiponectin secretion in 3T3-L1 adipocytes. United States: N. p., 2016. Web. doi:10.1016/J.BBRC.2016.06.008.
Cui, Ju, E-mail: juzi.cui@gmail.com, Pang, Jing, Lin, Ya-Jun, Jiang, Ping, Gong, Huan, Wang, Zai, Li, Jian, Cai, Jian-Ping, Huang, Jian-Dong, E-mail: jdhuang@hku.hk, The Centre for Synthetic Biology Engineering Research, Shenzhen Institutes of Advanced Technology, Shenzhen, & Zhang, Tie-Mei, E-mail: tmzhang126@126.com. Conventional kinesin KIF5B mediates adiponectin secretion in 3T3-L1 adipocytes. United States. doi:10.1016/J.BBRC.2016.06.008.
Cui, Ju, E-mail: juzi.cui@gmail.com, Pang, Jing, Lin, Ya-Jun, Jiang, Ping, Gong, Huan, Wang, Zai, Li, Jian, Cai, Jian-Ping, Huang, Jian-Dong, E-mail: jdhuang@hku.hk, The Centre for Synthetic Biology Engineering Research, Shenzhen Institutes of Advanced Technology, Shenzhen, and Zhang, Tie-Mei, E-mail: tmzhang126@126.com. 2016. "Conventional kinesin KIF5B mediates adiponectin secretion in 3T3-L1 adipocytes". United States. doi:10.1016/J.BBRC.2016.06.008.
@article{osti_22606142,
title = {Conventional kinesin KIF5B mediates adiponectin secretion in 3T3-L1 adipocytes},
author = {Cui, Ju, E-mail: juzi.cui@gmail.com and Pang, Jing and Lin, Ya-Jun and Jiang, Ping and Gong, Huan and Wang, Zai and Li, Jian and Cai, Jian-Ping and Huang, Jian-Dong, E-mail: jdhuang@hku.hk and The Centre for Synthetic Biology Engineering Research, Shenzhen Institutes of Advanced Technology, Shenzhen and Zhang, Tie-Mei, E-mail: tmzhang126@126.com},
abstractNote = {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. - Highlights: • The KIF5B level was up regulated during 3T3-L1 adipogenesis. • Endogenous KIF5B and adiponectin were partially colicalized. • Adiponectin-containing vesicles were co-immunoprecipitated with KIF5B. • The secretion of adiponectin, but not leptin, is dependent on functional KIF5B.},
doi = {10.1016/J.BBRC.2016.06.008},
journal = {Biochemical and Biophysical Research Communications},
number = 4,
volume = 476,
place = {United States},
year = 2016,
month = 8
}
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