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


Imesch, P; Samartzis, E P; Schneider, M; Fink, D; Fedier, A (2011). Inhibition of transcription, expression, and secretion of the vascular epithelial growth factor in human epithelial endometriotic cells by romidepsin. Fertility and Sterility, 95(5):1579-1583.

Abstract

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-1a (HIF-1a), 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.

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-1a (HIF-1a), 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.

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11 citations in Web of Science®
16 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Gynecology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2011
Deposited On:17 Feb 2012 10:18
Last Modified:05 Apr 2016 15:37
Publisher:Elsevier
ISSN:0015-0282 (P) 1556-5653 (E)
Publisher DOI:10.1016/j.fertnstert.2010.12.058
PubMed ID:21295294
Permanent URL: http://doi.org/10.5167/uzh-59112

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