Figure 7.
Inhibition of GDF9 + BMP15–induced AMH expression by FSH is mediated through HDAC enzymes. (A) Pretreatment of KGN cells with trichostatin A (TSA; 100 nM), a broad-spectrum HDAC inhibitor, reverses the inhibitory effects of FSH (5 ng/mL) on GDF9 + BMP15 (2.5 ng/mL)–induced AMH expression. (B) KGN cells were treated with siRNAs (100 nM) against different HDAC isoforms, and its effect on the FSH-mediated decrease on GDF9 + BMP15–induced AMH expression was determined. siRNA-mediated knockdown of HDAC2 rescues AMH/Amh mRNA levels in KGN cells and primary mGCs (C) stimulated with GDF9 + BMP15 (2.5 ng/mL) and treated with FSH (5 ng/mL). Nonspecific siRNA (Nsp) pool is used as control. AMH/Amh mRNA data are displayed as mean ± SE (n = 3 experiments) and normalized to GAPDH/Gapdh levels. *P ≤ 0.001 vs control.

Inhibition of GDF9 + BMP15–induced AMH expression by FSH is mediated through HDAC enzymes. (A) Pretreatment of KGN cells with trichostatin A (TSA; 100 nM), a broad-spectrum HDAC inhibitor, reverses the inhibitory effects of FSH (5 ng/mL) on GDF9 + BMP15 (2.5 ng/mL)–induced AMH expression. (B) KGN cells were treated with siRNAs (100 nM) against different HDAC isoforms, and its effect on the FSH-mediated decrease on GDF9 + BMP15–induced AMH expression was determined. siRNA-mediated knockdown of HDAC2 rescues AMH/Amh mRNA levels in KGN cells and primary mGCs (C) stimulated with GDF9 + BMP15 (2.5 ng/mL) and treated with FSH (5 ng/mL). Nonspecific siRNA (Nsp) pool is used as control. AMH/Amh mRNA data are displayed as mean ± SE (n = 3 experiments) and normalized to GAPDH/Gapdh levels. *P ≤ 0.001 vs control.

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