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Abstract
The purpose of this study was to elucidate signaling
pathways by which insulin like-growth factor 1 (IGF1)
promotes FSH-stimulated synthesis and retention of
hyaluronic acid (HA) in pig oocyte-cumulus complexes
(OCCs) cultured in serum-free medium. We found that IGF1
had no effect on FSH-stimulated production of cAMP and
activation of protein kinase A in the OCCs. Immunoblotting
with phospho-specific antibodies showed that FSH
moderately phosphorylated v-akt murine thymoma viral
oncogene homolog (AKT) and mitogen-activated kinase 3 and
1 (MAPK3/1) in cumulus cells. The exposure of OCCs to both
FSH and IGF1 resulted in a significant (P<0.05) increase
in AKT and MAPK3/1 phosphorylation. An inhibitor of
phosphoinositide-3-kinase (PIK3) LY 294002 significantly
(P<0.05) reduced the IGF1 enhanced phosphorylation of AKT
and inhibitors of AKT (SH6) and MAPK3/1 (U0126)
significantly (P<0.05) decreased synthesis and retention
of HA stimulated by parallel exposure of OCCs to both FSH
and IGF1. The IGF1-promoted synthesis of HA was not
accompanied by an increase in the relative abundance of
hyaluronan synthase 2 (HAS2) mRNA in the cumulus
cells. We conclude that IGF1 promotes the FSH-stimulated
synthesis and retention of HA in pig OCCs by PIK3/AKT and
MAPK3/1 dependent mechanisms.
Key words:
Gamete Biology •
Ovary •
Cumulus cells •
Follicle-stimulating hormone •
Signal transduction
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