Search Results
You are looking at 1 - 2 of 2 items for
- Author: Tong Sun x
- Refine by access: All content x
Search for other papers by Hong-Zhi Sun in
Google Scholar
PubMed
Search for other papers by Tong-Wei Yang in
Google Scholar
PubMed
Search for other papers by Wei-Jin Zang in
Google Scholar
PubMed
Search for other papers by Shu-Fang Wu in
Google Scholar
PubMed
Dehydroepiandrosterone (DHEA) is an endogenous steroid that is metabolized to androgens and/or estrogens in the human prostate. DHEA levels decline with age, and use of DHEA supplements to retard the aging process is of unproved effectiveness and safety. In this study, rat ventral prostatic epithelial cells were used to determine whether DHEA-modulated proliferation and prostate-specific antigen (PSA listed as KLKB1 in the MGI Database) production were mediated via the androgen receptor (AR) and its potential mechanism. We demonstrated that proliferation of prostatic epithelial cells and increase of PSA expression induced by DHEA were neutralized by Casodex or Ar siRNA, two specific AR blockers. DHEA stimulated Nfkb DNA binding activity, with this effect being blunted by Casodex or Ar siRNA. Moreover, the inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT nullified the effects of DHEA on NFKB activation. These findings suggested that DHEA stimulated normal prostatic epithelial cell proliferation, and AR is involved in DHEA-induced PSA expression in normal prostatic epithelial cells. This stimulation effect induced by DHEA is mediated by the activation of NFKB via PI3K/AKT pathway.
Search for other papers by Tong Sun in
Google Scholar
PubMed
Search for other papers by Wen-Bo Deng in
Google Scholar
PubMed
Search for other papers by Hong-Lu Diao in
Google Scholar
PubMed
Search for other papers by Hua Ni in
Google Scholar
PubMed
Search for other papers by Yu-Yan Bai in
Google Scholar
PubMed
Search for other papers by Xing-Hong Ma in
Google Scholar
PubMed
Search for other papers by Li-Bin Xu in
Google Scholar
PubMed
Search for other papers by Zeng-Ming Yang in
Google Scholar
PubMed
Prostaglandin (PGE) 2 is the most common prostanoid and plays an important role in female reproduction. The aim of this study was to examine the expression and regulation of microsomal (m) PGE synthase (PGES)-1 and cytosolic (c) PGES in the mouse ovary during sexual maturation, gonadotropin treatment and luteal development by in situ hybridization and immunohistochemistry. Both mPGES-1 mRNA signals and immunostaining were localized in the granulosa cells, but not in the thecal cells and oocytes. cPGES mRNA signals were localized in both granulosa cells and oocytes, whereas cPGES immunostaining was exclusively localized in the oocytes. In our superovulated model of immature mice, there was a basal level of mPGES-1 mRNA signals in the granulosa cells at 48 h after equine chorionic gonadotropin (eCG) treatment. mPGES-1 mRNA level was induced by human chorionic gonadotropin (hCG) treatment for 0.5 h, whereas mPGES-1 immunostaining was slightly induced at 0.5 h after hCG treatment and reached a maximal level at 3 h after hCG treatment. eCG treatment had no obvious effects on either cPGES mRNA signals or immunostaining. A strong level of cPGES immunostaining was present in both unstimulated and eCG-treated groups. Both mPGES-1 mRNA signals and immunostaining were highly detected in the corpus luteum 2 days post-hCG injection and declined from days 3 to 7 post-hCG injection. cPGES immunostaining was at a basal level or not detectable from days 1 to 7 after hCG injection and was highly expressed in the corpus luteum from days 9 to 15 post-hCG injection. PGE2 biosynthesized through the mPGES-1 pathway may be important for follicular development, ovulation and luteal formation.
