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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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organization
publishing date
type
Contribution to journal
publication status
published
subject
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
article number
66
pages
1 - 8
publisher
BioMed Central (BMC)
external identifiers
  • scopus:85016504781
  • pmid:28359281
  • wos:000397886600001
ISSN
1476-511X
DOI
10.1186/s12944-017-0458-x
language
English
LU publication?
yes
id
dcf474b0-7a6f-4604-8252-817e57d2c3dc
date added to LUP
2017-04-26 14:49:10
date last changed
2025-01-07 12:06:09
@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>}},
  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}},
  keywords     = {{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 (BMC)}},
  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}},
  doi          = {{10.1186/s12944-017-0458-x}},
  volume       = {{16}},
  year         = {{2017}},
}