Poster Presentation The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2017

The potential role of VEGF111 and other VEGF isoforms in the development of endometriosis (#295)

Kevin Danastas 1 , Emily J Miller 2 , Alison J Hey-Cunningham 2 , Chris R Murphy 1 , Laura A Lindsay 1
  1. Discipline of Anatomy and Histology, School of Medical Sciences, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia
  2. Department of Obstetrics, Gynaecology and Neonatology, Central Clinical School, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia

Endometriosis is a benign gynaecological disorder characterised by the presence of endometrial glands and stroma outside of the uterus forming ectopic lesions, often on the ovaries or in the peritoneal cavity. The accepted theory for the development of endometriosis is dissemination of endometrial fragments during menstruation, which ectopically attach, rapidly develop a blood supply, and form a lesion. One major mediator of angiogenesis is vascular endothelial growth factor (VEGF), which exists as multiple isoforms. Recently, a rare isoform, VEGF111 was identified in DNA-damaged human cells and in the uteri of lizards and rats, where it is co-expressed with other VEGF isoforms for uterine angiogenesis.

The expression levels of VEGF111 and three other VEGF isoforms, along with total VEGF, were measured in endometrial biopsies from women with (n = 22) and without (n = 12) endometriosis, across different stages of the menstrual cycle by qPCR.   

For the first time, the natural expression of VEGF111 has been identified in human tissue, and its expression levels are significantly higher in women with endometriosis during menstruation, compared to women with endometriosis (p < 0.05) and other menstrual cycle phases. Similarly the expression levels of VEGF121 and VEGF189, and consequently, total VEGF, are also significantly higher during menstruation in endometriosis compared to all other groups (p < 0.05).

The results presented here are consistent with the theory that the endometrium of women with endometriosis differs from those without the disorder, promoting the development of ectopic lesions and the disease progression. The discovery of VEGF111 in the human endometrium, and its upregulation during menstruation in endometriosis along with other VEGF isoforms, improves our current understanding of the development of endometriosis, and paves the way for further research into the regulation of endometrial angiogenesis.