Expression and regulation of cholesterol sulfotransferase (SULT2B1b) in human endometrium  

Oleh:

Koizumi, Minako ; Momoeda, Mikio ; Hiroi, Hisahiko ; Hosokawa, Yumi ; Tsutsumi, Ryo

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 93 no. 05 (Mar. 2010), page 1538-1544.
Topik: Endometrium; progesterone; relaxin; cholesterol sulfate

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2010.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Objective To investigate the hormonal regulation of SULT2B1b in human endometrium. Design In vitro study with human endometrial tissues and cultured human endometrial cells. Setting University hospital. Patient(s) Thirty-seven women undergoing hysterectomy for benign disease. Intervention(s) Human endometrial tissues were collected for in situ hybridization. Culture medium of human endometrial epithelial cells (EECs) was collected for determination of secretion of cholesterol sulfate (CS). Total RNAs were extracted from human endometrial tissues and cultured cells for real-time reverse transcriptase–polymerase chain reaction (RT-PCR). Main Outcome Measure(s) The expression of SULT2B1b mRNA in human endometrial tissues and cultured cells. Result(s) In situ hybridization studies and real-time RT-PCR showed that the amount of SULT2B1b mRNA in human endometrial tissues was significantly higher during the midluteal phase than during other phases of the menstrual cycle. The secretion of CS from EECs was confirmed using [35S]-phosphoadenosine phosphosulfate. The expression of SULT2B1b mRNA was induced by cAMP or P in human endometrial stromal cells (ESCs), whereas it was induced by cAMP or relaxin in EECs. The induction of SULT2B1b mRNA by P or relaxin was abolished by the specific protein kinase A (PKA) inhibitor, Rp-adenosine 3',5' cyclic monophosphothioate (Rp-cAMPS). Conclusion(s) The expression of SULT2B1b mRNA in ESCs is induced by P and that in EECs is induced by relaxin via the cAMP pathway.

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