國家衛生研究院 NHRI:Item 3990099045/10741
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    题名: Caveolin-1 secreted from adipose tissues and adipocytes functions as an adipogenesis enhancer
    作者: Chang, CC;Chen, CY;Wen, HC;Huang, CY;Hung, MS;Lu, HC;Chen, WL;Chang, CH
    贡献者: Institute of Cellular and Systems Medicine;Institute of Biotechnology and Pharmaceutical Research
    摘要: 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.
    日期: 2017-11
    關聯: Obesity. 2017 Nov;25(11):1932-1940.
    Link to: http://dx.doi.org/10.1002/oby.21970
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1930-7381&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000414031800017
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85030147979
    显示于类别:[張中和] 期刊論文
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