Modulation of ovine SBD-1 expression by 17beta-estradiol in ovine oviduct epithelial cells
1 College of veterinary, Inner Mongolia Agricultural University, Huhhot, 010018, People’s Republic of China
2 Key Laboratory of Clinical Diagnosis and Treatment Technology in Animal Disease, Ministry of Agriculture, Hohhot, 010018, People’s Republic of China
3 School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, 010059, People’s Republic of China
4 Vocational and Technical College, Inner Mongolia Agricultural University, Baotou, 014109, People’s Republic of China
5 Keshiketeng Banner Animal Disease Control Center, Chifeng, 025350, People’s Republic of China
6 Pathogenic Organisms and Immunology Lab, basic medical college, Inner Mongolia Medical University, Hohhot, 010059, People’s Republic of China
7 College of animal science, Inner Mongolia Agricultural University, Huhhot, 010018, People’s Republic of China
BMC Veterinary Research 2012, 8:143 doi:10.1186/1746-6148-8-143Published: 25 August 2012
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.
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.
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.