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17β-estradiol regulates the expression of apolipoprotein M through estrogen receptor α-specific binding motif in its promoter

Wei, Jiang; Yu, Yang; Luo, Guang-Hua; Feng, Yue hua; Shi, Yuan-ping; Zhang, Jun; Mu, Qin feng; Yu, Miao mei; Pan, Li li and Berggren-Söderlund, Maria LU , et al. (2017) In Lipids in Health and Disease 16(1). p.1-8
Abstract

Background: We have previously demonstrated that estrogen could significantly enhance expression of apolipoprotein M (apoM), whereas the molecular basis of its mechanism is not fully elucidated yet. To further investigate the mechanism behind the estrogen induced up-regulation of apoM expression. Results: Our results demonstrated either free 17β-estradiol (E2) or membrane-impermeable bovine serum albumin-conjugated E2 (E2-BSA) could modulate human apoM gene expression via the estrogen receptor alpha (ER-α) pathway in the HepG2 cells. Moreover, experiments with the luciferase activity analysis of truncated apoM promoters could demonstrate that a regulatory region (from-1580 to −1575 bp (−GGTCA-)) upstream of the transcriptional start... (More)

Background: We have previously demonstrated that estrogen could significantly enhance expression of apolipoprotein M (apoM), whereas the molecular basis of its mechanism is not fully elucidated yet. To further investigate the mechanism behind the estrogen induced up-regulation of apoM expression. Results: Our results demonstrated either free 17β-estradiol (E2) or membrane-impermeable bovine serum albumin-conjugated E2 (E2-BSA) could modulate human apoM gene expression via the estrogen receptor alpha (ER-α) pathway in the HepG2 cells. Moreover, experiments with the luciferase activity analysis of truncated apoM promoters could demonstrate that a regulatory region (from-1580 to −1575 bp (−GGTCA-)) upstream of the transcriptional start site of apoM gene was essential for the basal transcriptional activity that regulated by the ER-α. With the applications of an electrophoresis mobility shift assay and a chromatin immunoprecipitation assay, we could successfully identify a specific ER-α binding element in the apoM promoter region. Conculsion: In summary, the present study indicates that 17β-estradiol induced up-regulation of apoM in HepG2 cells is through an ER-α-dependent pathway involving ER-α binding element in the promoter of the apoM gene.

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publication status
published
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keywords
Apolipoprotein M, Chromatin Immunoprecipitation (ChIP) assay, Electrophoretic mobility shift assay (EMSA), Estrogen receptor alpha, Estrogen responsive element
in
Lipids in Health and Disease
volume
16
issue
1
pages
1 - 8
publisher
BioMed Central
external identifiers
  • scopus:85016504781
  • wos:000397886600001
ISSN
1476-511X
DOI
10.1186/s12944-017-0458-x
language
English
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yes
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dcf474b0-7a6f-4604-8252-817e57d2c3dc
date added to LUP
2017-04-26 14:49:10
date last changed
2017-09-18 13:33:21
@article{dcf474b0-7a6f-4604-8252-817e57d2c3dc,
  abstract     = {<p>Background: We have previously demonstrated that estrogen could significantly enhance expression of apolipoprotein M (apoM), whereas the molecular basis of its mechanism is not fully elucidated yet. To further investigate the mechanism behind the estrogen induced up-regulation of apoM expression. Results: Our results demonstrated either free 17β-estradiol (E2) or membrane-impermeable bovine serum albumin-conjugated E2 (E2-BSA) could modulate human apoM gene expression via the estrogen receptor alpha (ER-α) pathway in the HepG2 cells. Moreover, experiments with the luciferase activity analysis of truncated apoM promoters could demonstrate that a regulatory region (from-1580 to −1575 bp (−GGTCA-)) upstream of the transcriptional start site of apoM gene was essential for the basal transcriptional activity that regulated by the ER-α. With the applications of an electrophoresis mobility shift assay and a chromatin immunoprecipitation assay, we could successfully identify a specific ER-α binding element in the apoM promoter region. Conculsion: In summary, the present study indicates that 17β-estradiol induced up-regulation of apoM in HepG2 cells is through an ER-α-dependent pathway involving ER-α binding element in the promoter of the apoM gene.</p>},
  articleno    = {66},
  author       = {Wei, Jiang and Yu, Yang and Luo, Guang-Hua and Feng, Yue hua and Shi, Yuan-ping and Zhang, Jun and Mu, Qin feng and Yu, Miao mei and Pan, Li li and Berggren-Söderlund, Maria and Nilsson-Ehle, Peter and Zhang, Xiao-Ying and Xu, Ning},
  issn         = {1476-511X},
  keyword      = {Apolipoprotein M,Chromatin Immunoprecipitation (ChIP) assay,Electrophoretic mobility shift assay (EMSA),Estrogen receptor alpha,Estrogen responsive element},
  language     = {eng},
  month        = {03},
  number       = {1},
  pages        = {1--8},
  publisher    = {BioMed Central},
  series       = {Lipids in Health and Disease},
  title        = {17β-estradiol regulates the expression of apolipoprotein M through estrogen receptor α-specific binding motif in its promoter},
  url          = {http://dx.doi.org/10.1186/s12944-017-0458-x},
  volume       = {16},
  year         = {2017},
}