jurisicova
Andrea JurisicovaPhD
Associate Professor
Reproduction and Development Platform

Contact Info

T. (416) 586-4800 Ext. 2052
F. (416) 586-8588

Location

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 871-600 University Avenue
Toronto
ON, M5X 1X5

Research Interests

Ovarian biology; Early embryo development.

Accepting

None

Research/Teaching

Research Synopsis:

Keywords: Reproductive physiology, oogenesis, cell death, mitochondria, autophagy, preimplantation embryo development, trophoblast stem cells, placentation.

Detailed Description:

Establishment of female germline and ovarian follicle life span.
Menopause is generally thought to result from follicular depletion. While the incidence of premature ovarian failure (POF) in the human population is low, it increases (up to 30%) for females with a previous family history of this condition, indicating existance of gene defects, only a few of which have been characterized. For non-familial POF, factors such as smoking, environmental pollution and exposure to radiation or chemotherapy are a major cause of oocyte destruction. The overall goal of our research is to identify molecular pathways responsible for regulation of early oocyte survival.

Preimplantation embryo development.
One of the major abnormalities observed during human embryo development is excessive early embryo loss contributing to low success rates after assisted reproduction. Oocyte quality is one of the determining factors of developmental competence, affecting preimplantation embryo survival. The overall goal of our research is to identify molecular pathways responsible for regulation of embryo survival. The underlying molecular reasons for failed preimplantation development are frequently attributed to poor oocyte quality of unknown etiology. As there is currently no screening or medical treatment available to patients with this diagnosis, oocyte donation is the only suggested option. We are currently developing strategies for restoration of missing maternal component(s) that could be used to rescue embryos of low developmental competence, based on pathways identified in various genetic murine models of female infertility.

Regulation of trophoblast fate and cell death.
Fetal development depends upon a co-ordinated series of events in both embryo and supporting placenta. Cell death is a critical driving force behind organ sculpturing and eliminating abnormal, misplaced, non-functional or harmful cells in the embryo proper, although very little is known about its physiological function in placental development. We are studying importance of activation of cell death pathways during placental development in both human and mouse models of preeclampsia, intrauterine growth retardation or spontaneous abortions.

METHODS USED

Cell and tissue culture: Oocytes, trophoblast stem cells.

Procedures: Immunohistochemistry, immunocytochemistry, qRT-PCR, Western Blot, live cell imaging.

EQUIPMENT USED

Benchtop centrifuge, blotting apparatus, confocal microscope, culture hood, culture incubators, dissecting microscope, fluorescence microscope, gel apparatus, low- and high-speed centrifuge, low and ultralow freezers, microwave oven, plate reader, real-time/thermocycler, stirrer/hot plate, water baths.

PRESENT TRAINEES

Tania Yavorska
Taline Naranian
Shakib Omari

PRESENT COLLABORATIONS

Within the Department of Physiology:
Robert Casper
Lee Adamson
Isabella Caniggia
Steve Lye
Sue Quaggin

Outside of the Department of Physiology
Razq Hakem - Medical Biophysics University of Toronto and OCI/PMH
Zhenyu Hao - Ontario Cancer Institute
Igor Jurisica - Medical Biophysics and OCI/PMH
Kelle Moley - Washington University School of Medicine, St.Lois
Mellisa Mann - University of Western Ontario

Publications and Awards

Recent Publications

http://www.ncbi.nlm.nih.gov/pubmed/26111777

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