Lipoxin A4 regulates expression of the estrogen receptor and inhibits 17ß-estradiol induced p38 mitogen-activated protein kinase phosphorylation in human endometriotic stromal cells  

Oleh:

Shuo, Chen ; Rong-Feng, Wu ; Lin, Sui ; Wei-Dong, Zhou ; Mao-Bi, Zhu ; Qiong-Hua, Chen

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 102 no. 01 (Jul. 2014), page 264–271.
Topik: Endometriosis; estrogen receptor; LXA4; p38 MAPK

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2014.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective To study the role of lipoxin A4 (LXA4) in endometriosis. Design Molecular analysis in human samples and primary human endometriotic stromal cells (ESCs). Setting University hospital. Patient(s) Forty-nine premenopausal women (30 patients with endometriosis and 19 controls). Intervention(s) Normal and ectopic endometrial biopsies obtained during surgery performed during the proliferative phase of the menstrual cycle; ESCs used for in vitro studies. Main Outcome Measure(s) Levels of LXA4 measured by enzyme-linked immunosorbent assay (ELISA); mRNA levels of the estrogen receptor (ER), progestogen receptor (PR), tumor necrosis factor a (TNF-a), and interleukin 6 (IL-6) quantified by quantitative reverse-transcription polymerase chain reaction (qRT-PCR); and p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation evaluated by Western blotting. Result(s) The LXA4 expression level decreased in ectopic tissue as well as ERa and PR, although the expression of ERß increased in ectopic endometrium compared with the controls. Investigations with correlation analysis revealed the expression of LXA4 was positively correlated with ERa and negatively correlated with ERß in vivo. Moreover, administering LXA4 could augment ERß expression in ESCs and inhibit the 17ß-estradiol-induced phosphorylation of p38 MAPK very likely through ERß. Conclusion(s) Our findings indicate that LXA4 regulates ERß expression and inhibits 17ß-estradiol-induced phosphorylation of p38 MAPK, very likely through ERß in ESCs.

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