Antiproliferative effect of adiponectin on rat uterine leiomyoma ELT-3 cells

Atsuko Wakabayashi, Takashi Takeda, Kenji Tsuiji, Bin Li, Masahiro Sakata, Ken‐ichirou Morishige, Nobuo Yaegashi, Tadashi Kimura
In: Gynecological Endocrinology · 2010 · vol. 27(1) , pp. 33–38 · doi:10.3109/09513590.2010.487605 · PMID:20504099 · W2033901026
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Adiponectin repressed rat uterine leiomyoma ELT-3 cell proliferation without inducing apoptosis, mediated by adiponectin receptor 1 and 2 expression.

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Abstract

OBJECTIVE: Although fibroids greatly affect reproductive health, the pathophysiology and epidemiology are not well known. Recently, we have reported the relationship between uterine leiomyoma and metabolic syndrome. Many studies have indicated that reductions in plasma adiponectin levels play major roles in the development of metabolic syndrome. In this study, we investigated the significant repressive effect of adiponectin on rat uterine leiomyoma ELT-3 cells proliferation. STUDY DESIGN: Expression of adiponectin receptor 1 and receptor 2 was evaluated by RT-PCR and Western blot analysis. Cell proliferation was assessed by the MTS assay and cell counting. Apoptosis was evaluated by Hoechst staining and cleaved poly (ADP-ribose) polymerase (PARP). RESULTS: Adiponectin receptor 1 and receptor 2 were expressed in ELT-3 cells. Adiponectin repressed rat uterine leiomyoma ELT-3 cells cell proliferation without inducing apoptosis. CONCLUSION: The repression of adiponectin on leiomyoma cell proliferation in the rat may explain a crucial role of adiponectin in the association of metabolic syndrome with uterine leiomyoma.

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