title: Modulation of ovine SBD-1 expression by 17beta-estradiol in ovine oviduct epithelial cells.
abstract: BACKGROUND
  Mucosal epithelia, including those of the oviduct, secrete antimicrobial innate immune molecules (AIIMS). These have bactericidal/bacteriostatic functions against a variety of pathogens. Among the AIIMs, sheep β-defensin-1 (SBD-1) is one of the most potent. Even though the SBD-1 is an important AIIM and it is regulated closely by estrogenic hormone, the regulation mechanism of 17β-estradiol has not been clearly established. We investigated the effects of E2 and agonist or inhibitor on ovine oviduct epithelial cells in regard to SBD-1 expression using reverse transcription quantitative PCR (RT-qPCR). In addition, three different pathways were inhibited separately or simultaneously to confirm the effect of different inhibitors in the regulation mechanism.
  
  
  RESULTS
  17beta-estradiol (E2) induced release of SBD-1 in ovine oviduct epithelial cells. SBD-1 expression was mediated through G-protein-coupled receptor 30 (GPR30) and Estrogen Receptors (ERs) activation in ovine oviduct epithelial cell. Inhibition of gene expression of protein kinase A (PKA), protein kinase C (PKC), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) led to a decreased SBD-1 expression.
  
  
  CONCLUSIONS
  Taken together, E2-induced up-regulation of SBD-1 expressions were GPR30-dependent during prophase and ERs-dependent during later-stage in ovine oviduct epithelial cells, and we assume that the effect was completed by the PKA, PKC, and NF-κB pathways simultaneous.
authors.affiliation: College of Veterinary, Inner Mongolia Agricultural University, Huhhot, 010018, People's Republic of China.
authors.forename: Shiyong
authors.initials: S
authors.lastname: Wen
authors.forename: Guifang
authors.initials: G
authors.lastname: Cao
authors.forename: Tuya
authors.initials: T
authors.lastname: Bao
authors.forename: Lanling
authors.initials: L
authors.lastname: Cheng
authors.forename: Haijun
authors.initials: H
authors.lastname: Li
authors.forename: Chenguang
authors.initials: C
authors.lastname: Du
authors.forename: Yong
authors.initials: Y
authors.lastname: Tu
authors.forename: Qi
authors.initials: Q
authors.lastname: Li
authors.forename: Ruizhen
authors.initials: R
authors.lastname: Jian
authors.forename: Pengwei
authors.initials: P
authors.lastname: Zhao
authors.lastname: Wuriliga
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004847:Epithelial Cells / Q000378:metabolism*; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects*; D010057:Oviducts / Q000166:cytology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011960:Receptors, Estrogen / Q000235:genetics / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism; D012756:Sheep; D015854:Up-Regulation; D023083:beta-Defensins / Q000235:genetics / Q000378:metabolism*
chemical_list: D012333:RNA, Messenger; D011960:Receptors, Estrogen; D043562:Receptors, G-Protein-Coupled; D023083:beta-Defensins; D004958:Estradiol