Abstract
Nitric oxide (NO) regulation of ovarian function in mammals has been studied extensively. However, relatively less information is available on NO action on meiotic G2-M1 transition in teleost oocytes. In the present study using follicle-enclosed oocytes of Anabas testudineus, NO regulation of intra-oocyte signaling events during meiotic G2-M1 transition were examined. Priming with NO donor, sodium nitroprusside (SNP) prevented 17α,20β-dihydroxy-4-pregenen-3-one (17,20β-P)-induced germinal vesicle break down (GVBD) in dose- and duration-dependent manner. Impaired GVBD response in SNP-treated groups corroborated well with reduced p34Cdc2 (Thr161) phosphorylation. Immunoblot analysis revealed that congruent with elevated cAMP-dependent protein kinase (PKA) phosphorylation (activation), NO inhibition of meiotic maturation involves down regulation of Cdc25 activation, Mos synthesis and MAPK3/1 (ERK1/2) phosphorylation. However, priming with PKA inhibitor (H89) could reverse SNP attenuation of oocyte GVBD significantly. Collectively our results indicate that negative influence of NO on meiotic G2-M1 transition in perch oocytes might involve PKA activation.
Original language | English (US) |
---|---|
Pages (from-to) | 162-169 |
Number of pages | 8 |
Journal | Molecular and cellular endocrinology |
Volume | 460 |
DOIs | |
State | Published - Jan 15 2018 |
Externally published | Yes |
Keywords
- Anabas testudineus
- Cdc25
- Nitric oxide
- Oocyte maturation
- PKA
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Endocrinology