[Selective ERβ action of dehydroepiandrosterone for osteoblast cell line]

To investigate the selective mechanism of dehydroepiandrosterone (DHEA) for osteoblast via ERβ.

High expression of ERβ in hMG63-ERβ group (infected with pWPT-ERβ), gene silencing of ERβ in hMG63-shERβ group (infected with pLVTHM-GFP/ERβ-shRNA) and hMG63 group (control) were cultured and treated with 1×10(-7) mol/L DHEA, with or without U0126 and etoposide. The proliferation and apoptosis of hMG63 were evaluated by flow cytometry. The mRNA level of estrogen receptor subtype was detected by reverse transcription-PCR.

The expression of ERβ in hMG63-ERβ group and hMG63-shERβ group were increased 7.39 times and decreased 17% compared with that in hMG63 group (control). DHEA could increase ERβ expression in hMG63 in each group, however, it did not influence the expression of ERα mRNA. When the level of ERβ was high, DHEA could accelerate the proliferation [proliferation index were (81.6 ± 7.6)% in hMG63-ERβ, (75.0 ± 5.3)% in hMG63, P < 0.05] and inhibit the apoptosis [apoptosis rate were (12.2 ± 1.6)% in hMG63-ERβ, (14.6 ± 1.5)% in hMG63, P < 0.01], which was blocked by U0126 [proliferation index were (33.2 ± 2.0)% in hMG63-ERβ, (41.2 ± 2.4)% in hMG63, apoptosis rate were (40.5 ± 4.3)% in hMG63-ERβ, (43.3 ± 4.1)% in hMG63, all P < 0.05]. When the expression of ERβ was silenced, DHEA could not inhibit the apoptosis of hMG63 anymore.

DHEA selectively act on osteoblasts via the dominant expression of ERβ.