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author:("Zhao, pengi")
1.  Porcine Epidemic Diarrhea Virus Variants with High Pathogenicity, China 
Emerging Infectious Diseases  2013;19(12):2048-2049.
doi:10.3201/eid1912.121088
PMCID: PMC3840889  PMID: 24274832
Porcine epidemic diarrhea virus; variants; animal infection experiment; viruses; China; pigs
2.  Modulation of ovine SBD-1 expression by 17beta-estradiol in ovine oviduct epithelial cells 
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.
doi:10.1186/1746-6148-8-143
PMCID: PMC3487956  PMID: 22920556
Sheep; Oviduct epithelial; SBD-1; Modulation; Signaling pathway

Results 1-2 (2)