FAZLEABAS Asgi

  • Professor and Associate Chair, Obstetrics Gynaecology and Reproductive Biology, Mitchigan State University, USA
  • Director, Women’s Health Research, Mitchigan State University, USA
  • Co-Director, Reproductive and Developmental Sciences Programme, Mitchigan State University, USA

The laboratory of Professor Fazleabas utilises a baboon model for endometriosis in which the disease can be induced by inoculating the peritoneal cavity with autologous menstrual tissue. This permits us to study the etiology and pathophysiology of endometriosis from the onset of the disease and during its continued progression.

These studies have identified the progressive changes in gene expression in the eutopic endometrium which is a direct consequence of the presence of lesions. These changes are similar to that reported in women with disease and demonstrate that the development of progesterone resistance is a progressive process and may be related to epigenetic changes that are initiated during the initial establishment of the disease.

The kinetics of lesion development is also a progressive event following the induction of the disease and is governed by the up regulation genes that are involved in the process of angiogenesis and cell adhesion. The latter stages of lesion development are also associated with the presence of nerve fibers. Current studies are focused on the mechanisms by which microRNAs and their respective target genes regulate cell proliferation, apoptosis and inflammation which may contribute to the development of the disease and epigenetic changes in the eutopic endometrium that contributes to endometriosis associated infertility.

The unique nature of the primate model to study endometriosis and the strong multi-disciplinary collaborative group which we have established has led to important and fundamental findings regarding the causative effects of endometriosis and the mechanisms by which aberrant gene expression in the eutopic endometrium may contribute to infertility.