Dr Tony Michael
Director of Taught Programmes, Reader in Reproductive Biology
Email: email@example.comTelephone: +44 (0)20 7882 6983Room Number: Room 3.14, Fogg Building
- Cell Biology (BIO111)
- The Human Cell (BMD115)
- Biomedical Physiology I – Exchange, Movement and Integration (BMD121)
- Reproductive and Developmental Biology (SBC328)
- Endocrine Physiology and Biochemistry (SBS517)
Environmental change impacts on various physiological systems in a range of vertebrate species from fish and amphibians to humans. The link between components of the external environment (e.g. the availability of food or shelter) and internal physiological systems is often mediated via the hypothalamo-pituitary-adrenal (HPA) axis, activity of which increases at times of chronic stress, culminating in increased output of the potent adrenal steroid hormone, cortisol.
My research as a reproductive biologist (and specifically as a steroid biochemist) focusses on the mechanisms by which stress levels of cortisol can influence reproductive physiology and fertility in mammals. I have investigated and published on the effects of cortisol on pituitary gonadotropes, testis Leydig cells, spermatozoa, reproductive tracts (both male and female) and placental physiology, but my major interest lies in the hormonal control of ovarian follicles and oocytes.
In all potential target cells, the access of cortisol to intracellular steroid hormone receptors is locally modulated by the 11β-hydroxysteroid dehydrogenase (11βHSD) isoenzymes. These members of the short-chain alcohol dehydrogenase (SCAD) enzyme superfamily catalyse the reversible inter-conversion of cortisol with its inert 11-keto metabolite, cortisone. Within reproductive structures, the metabolism and actions of cortisol appear to be tightly regulated by both protein and lipid hormones, as well as by the redox state of NADP+/NADPH. This intricate regulation of cortisol metabolism indicates a requirement to limit any adverse actions of cortisol in order to safeguard reproduction and fertility under conditions of chronic stress.
Most of my research into the reproductive significance of cortisol and the 11βHSD enzymes has had a biomedical focus. Working with collaborators in Obstetrics & Gynaecology, I have established links between 11βHSD activities and (1) anovulatory infertility (specifically polycystic ovary syndrome), (2) the clinical outcome of assisted conception programmes, and (3) early events in the pathogenesis of pre-eclampsia. In collaborations with colleagues at the Royal Veterinary College (RVC) in London, I have also conducted studies in domestic livestock, specifically in sheep, cows and pigs. These studies have linked changes in cortisol metabolism to fetal development, ovarian follicle growth and formation of anovulatory ovarian cysts, oocyte maturation and developmental potential, sperm survival and ejaculate viability, and to male fertility.
Other ongoing reproductive biology projects include collaborative research into the ovarian actions of prostaglandins (specifically PGF2α). In terms of applying my knowledge of steroid biochemistry outside of reproduction, I collaborate with Prof. Mike Philpott and Dr. Ros Hannen at the Blizard Institute (QMUL) to investigate the potential for local synthesis and metabolism of cortisol in skin.