Chia-Chu Chang1,2,3, Chen-Yu Chen4, Hui-Chin Wen4, Chih-Yang Huang1, Ming-Shiu Hung5, Hsi-Chi Lu6, Woan-Ling Chen3,6, Chung-Ho Chang1,3,4. 1. PhD Program for Aging, China Medical University, Taichung, Taiwan, Republic of China. 2. School of Medicine, Chung Shan Medical University, Taichung, Taiwan, Republic of China. 3. Environmental and Precision Medicine Laboratory, Department of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan, Republic of China. 4. Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Miaoli, Taiwan, Republic of China. 5. Institute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan, Miaoli, Taiwan, Republic of China. 6. Department of Food Science, Tunghai University, Taichung, Taiwan, Republic of China.
Abstract
OBJECTIVE: Caveolin-1 (Cav-1) is expressed abundantly in adipose tissue and involved in many physiological processes. While Cav-1 has been reported to be secreted in pancreatic acinar cells and LNCaP prostate cancer cells, its secretion from adipose tissue awaits investigation. METHODS: Cav-1 secretion from 3T3-L1 adipocytes and fat tissues from normal chow diet- and high-fat diet (HFD)-fed mice was measured. Functions and uptake of secreted Cav-1 proteins were assessed by adding Cav-1 back to preadipocytes and LNCaP cells. RESULTS: Cav-1 secretion was evident in adipose tissues and were substantially promoted in HFD-fed mice. Cav-1 was detectable in the conditioned media of 3T3-L1 adipocytes but not preadipocytes. Hypertrophied adipocytes induced by glucose and fatty acids secreted more Cav-1, suggesting that hypertrophied adipocytes were responsible for enhanced Cav-1 secretion in obese mice. Secreted Cav-1 was taken up by preadipocytes and LNCaP cells. 3T3-L1 preadipocytes overexpressing Cav-1 were better differentiated, suggesting that secreted Cav-1 may promote adipogenesis. Hypertrophied 3T3-L1 adipocytes enhanced ERK1/2 activation, and the attenuation of ERK1/2 activity by PD98059 inhibited Cav-1 secretion. CONCLUSIONS: Cav-1 is actively secreted from adipocytes as a putative adipogenesis enhancer. Hypertrophied adipocytes secrete Cav-1 via ERK1/2-dependent mechanisms to promote adipogenesis, thus establishing a vicious cycle.
OBJECTIVE:Caveolin-1 (Cav-1) is expressed abundantly in adipose tissue and involved in many physiological processes. While Cav-1 has been reported to be secreted in pancreatic acinar cells and LNCaP prostate cancer cells, its secretion from adipose tissue awaits investigation. METHODS:Cav-1 secretion from 3T3-L1 adipocytes and fat tissues from normal chow diet- and high-fat diet (HFD)-fed mice was measured. Functions and uptake of secreted Cav-1 proteins were assessed by adding Cav-1 back to preadipocytes and LNCaP cells. RESULTS:Cav-1 secretion was evident in adipose tissues and were substantially promoted in HFD-fed mice. Cav-1 was detectable in the conditioned media of 3T3-L1 adipocytes but not preadipocytes. Hypertrophied adipocytes induced by glucose and fatty acids secreted more Cav-1, suggesting that hypertrophied adipocytes were responsible for enhanced Cav-1 secretion in obesemice. Secreted Cav-1 was taken up by preadipocytes and LNCaP cells. 3T3-L1 preadipocytes overexpressing Cav-1 were better differentiated, suggesting that secreted Cav-1 may promote adipogenesis. Hypertrophied 3T3-L1 adipocytes enhanced ERK1/2 activation, and the attenuation of ERK1/2 activity by PD98059 inhibited Cav-1 secretion. CONCLUSIONS:Cav-1 is actively secreted from adipocytes as a putative adipogenesis enhancer. Hypertrophied adipocytes secrete Cav-1 via ERK1/2-dependent mechanisms to promote adipogenesis, thus establishing a vicious cycle.
Authors: Clair Crewe; Nolwenn Joffin; Joseph M Rutkowski; Min Kim; Fang Zhang; Dwight A Towler; Ruth Gordillo; Philipp E Scherer Journal: Cell Date: 2018-10-04 Impact factor: 41.582
Authors: Xiaofei Guo; Yan Bai; Li Zhang; Bo Zhang; Naufal Zagidullin; Katherine Carvalho; Zhimin Du; Benzhi Cai Journal: Stem Cell Res Ther Date: 2018-02-26 Impact factor: 6.832