Elsevier

Fertility and Sterility

Volume 95, Issue 5, April 2011, Pages 1579-1583
Fertility and Sterility

Endometriosis
Inhibition of transcription, expression, and secretion of the vascular epithelial growth factor in human epithelial endometriotic cells by romidepsin

https://doi.org/10.1016/j.fertnstert.2010.12.058Get rights and content
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Objective

To investigate whether the histone deacetylase (HDAC) inhibitor romidepsin down-regulates VEGF (vascular endothelial growth factor) gene expression and abrogates VEGF protein secretion in human epithelial endometriotic cells.

Design

In vitro study with human immortalized epithelial endometriotic cells.

Setting

University hospital.

Patient(s)

Not applicable.

Intervention(s)

None.

Main Outcome Measure(s)

Real-time reverse-transcriptase polymerase chain reaction to evaluate VEGF gene expression, immunoblot analysis to evaluate protein expression, and enzyme-linked immunosorbent assay to evaluate VEGF protein secretion into the culture medium.

Result(s)

Treatment of 11z human endometriotic cells with romidepsin statistically significantly inhibited VEGF gene transcription and down-regulated VEGF protein expression. Moreover, romidepsin abrogated the secretion of VEGF protein into the culture medium. Romidepsin also reduced the expression of hypoxia-inducible factor-1α (HIF-1α), which is implicated in the transcription of the VEGF gene, in cobalt chloride-pretreated (to mimic hypoxic conditions) 11z cultures.

Conclusion(s)

Romidepsin targets VEGF at the transcriptional level, which subsequently leads to the reduction of secreted VEGF (the “active” form of VEGF). Therefore, romidepsin may be a potential therapeutic candidate against angiogenesis in endometriosis.

Key Words

Endometriosis
HIF-1α
human epithelial endometriotic cells
romidepsin
VEGF expression and secretion

Cited by (0)

P.I. has nothing to disclose. E.P.S. has nothing to disclose. M.S. has nothing to disclose. D.F. has nothing to disclose. A.F. has nothing to disclose.

Supported by the EMDO Foundation Zurich and the Hartmann Muller Foundation.