Abstract:
:Uterine fibroids, also known as uterine leiomyomas, are a benign tumor of the human uterus and the commonest estrogen-dependent benign tumor found in women. Myocardin is an important transcriptional regulator in smooth and cardiac muscle development. The role of myocardin and its relationship with ERα in uterine fibroids have barely been addressed. We noticed that the expression of myocardin was markedly reduced in human uterine fibroid tissue compared with corresponding normal or adjacent myometrium tissue. Here we reported that myocardin induced the transcription and expression of differentiation markers SM22α and alpha smooth muscle actin (α-SMA) in rat primary uterine smooth muscle cells (USMCs) and this effect was inhibited by ERα. Notably, we showed that, ERα induced expression of proliferation markers PCNA and ki-67 in rat primary USMCs. We also found ERα interacted with myocardin and formed complex to bind to CArG box and inhibit the SM22α promoter activity. Furthermore, ERα inhibited the transcription and expression of myocardin, and reduced the levels of transcription and expression of downstream target SM22α, a SMC differentiation marker. Our data thus provided important and novel insights into how ERα and myocardin interact to control the cell differentiation and proliferation of USMCs. Thus, it may provide potential therapeutic target for uterine fibroids.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Liao XH,Li JY,Dong XM,Wang X,Xiang Y,Li H,Yu CX,Li JP,Yuan BY,Zhou J,Zhang TCdoi
10.1016/j.yexcr.2016.11.007subject
Has Abstractpub_date
2017-01-01 00:00:00pages
73-82issue
1eissn
0014-4827issn
1090-2422pii
S0014-4827(16)30380-9journal_volume
350pub_type
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