Hexachlorobenzene exposure induces pro-angiogenic microenvironment in an in vitro model of endometriosis

CEBALLOS L; MIRET N; PONTILLO CA; ZÁRATE L; NUÑEZ M; ÁLVAREZ L; RANDI AS; CHIAPPINI FA

Congreso; Reunión Anual de Sociedades de Biociencias; 2019

Endometriosis, characterized by ectopic growth of endometrial tissue, is a common gynecological disease. The symptoms are pelvic pain and infertility, affecting women quality of life. Angiogenesis is critical in the development and maintenance of endometriotic lesions. It is a multistep process of new blood vessel formation that involves secretion of growth factors and extracellular matrix degradation, as well as migration, proliferation, and tube formation by endothelial cells. Vascular endothelial growth factor (VEGF) is an angiogenic factor that plays an important role in endometriosis progression. Exposure to endocrine-disrupting environmental pollutants is associated with the disease etiology. Hexachlorobenzene (HCB) is a pesticide that induces toxic reproductive effects in laboratory animals. Previous results showed that HCB increases the volume of endometriotic like-lesions, microvessel density and VEGF levels in a rat endometriosis model. The present study examined the effect of HCB on endometriosis angiogenesis in vitro. Human Endometrial Stromal cells (T-HESCs) were exposed to HCB (0.005, 0.05, 0.5 and 5 μM) or vehicle for 48 h, and the conditioned media were then used to stimulate EA.hy926 endothelial cells to evaluate cell proliferation (MTT assay and PCNA expression), migration (scratch motility assay) and tube-like structure formation in a Matrigel assay. The results showed that HCB (0.005-0.05 μM) induced VEGF secretion (p