Assistant Professor, Anatomy and Cell Biology
Dr. Stephen J. Renaud is a reproductive biologist investigating cellular and molecular mechanisms of placenta development and function as well as the causes of various pregnancy complications, including preeclampsia, intrauterine growth restriction, and preterm birth.
Research Profile: via Google Scholar
Also in the Department of Anatomy and Cell Biology (including cross-appointed): Nathalie Bérubé, Arthur Brown, Sandrine de Ribaupierre, Lauren Flynn, Victor Han, David Hess, Lisa Hoffman, Peeyush Lala, Michelle Mottola, and Katherine Willmore
Through cell and animal models Dr. Renaud is investigating the genetic and environmental determinants of those diseases, to ultimately impact public health and global health policies.
My research interests encompass the cellular and molecular mechanisms of placental development and function. There are two reasons I am interested in studying the placenta. First, the placenta is an exceptionally unique organ, one with evolutionary adaptations not observed in any other tissue. The second reason is from a public health perspective. The placenta intimately connects a mother with her developing baby, and it performs vital functions required for pregnancy such as regulating nutrient exchange between maternal and fetal blood, and producing hormones necessary for fetal development. Placental maldevelopment or dysfunction is linked with a variety of pregnancy complications (e.g. pre-eclampsia, fetal growth restriction, pre-term birth, placenta accreta, spontaneous abortion) that cause significant maternal and fetal illness or death. Despite its importance for the health of mothers and their babies, we really don’t have a good grasp on how the placenta develops or functions.
Our research interests can be broadly divided into two themes:
- Development of the trophoblast: the epithelial component of the placenta is comprised of trophoblast cells. These cells originate from a multilineage differentiation pathway that progressively differentiate into specialized trophoblast lineages, each with distinct morphologies and functions. We are particularly interested in how transcription factors and epigenetic regulators coordinate the progressive differentiation of trophoblast cells into defined lineages. Active projects in the laboratory include i) determining how conserved “OVO-like” transcription factors coordinate the transition of trophoblast cells from progenitor to differentiated states; and ii) transcriptional control of endogenous retroviral genes, which are genes that encode cellular fusogens necessary for generation of the placental epithelial barrier.
- Defining interactions between maternal immune cells and trophoblast cells: we are interested in how trophoblast cells interact with maternal immune cells. Trophoblast cells express paternal antigens and should be recognized as foreign by maternal immune cells. Why trophoblast cells are tolerated during normal pregnancies is not clear, but it is hypothesized that aberrant interactions between maternal immune cells and trophoblast cells may play a role in the development of various obstetric complications. We use both in vitro and in vivo models to provide insight on how the immune environment can shape trophoblast behaviour, placental development, and fetal health.
Why is placenta development important?
Even in developed countries like Canada, the development of the placenta – the organ that connects a mother to her child – can cause life-threatening pregnancy complications.
Dr. Stephen J. Renaud studies how placental development can cause common pregnancy complications like preeclampsia. Preeclampsia, identified as a multifactorial disease, has been linked to race, obesity, and age, as well as a host of other variables.
Alternate pregnancy complications include intrauterine growth restriction (IUGR) and spontaneous abortion. In each case the placenta malfunctions in some way, putting the life of the baby or mother at risk.
How is placenta development studied?
One way to study placental development is by analyzing “trophoblast” cells, linked to both IUGR and preeclampsia. Trophoblast cells act like a filter, facilitating the transfer of food and oxygen from the mother to the baby. Preeclampsia often occurs when those trophoblasts are compromised.
Renaud started his research with trophoblast cells. He determined the mother’s immune cells could be the cause, negatively affecting trophoblast cells and causing the placenta to develop incorrectly.
“That subject was the focus of my graduate work,” Renaud said. “My postdoctoral work more directly focused on how the placenta develops under normal circumstances.”
Renaud now studies trophoblast cell development and how they interact with their environment, including the mother’s immune cells, to determine the root of placenta-related complications.
Where is the research now?
Renaud works primarily on two complications: preeclampsia, which targets the mother, and IUGR, which limits the growth and development of the child. His goal is to anticipate and manage symptoms of these complications.
Currently, there is no reliable way to determine which pregnancies are “high risk.”
Many mothers, including Renaud’s wife, have overcome serious complications to have healthy, successful pregnancies. With more research, doctors could fully prevent the serious, life-threatening side effects of those complications.
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About Stephen Renaud
Dr. Stephen J. Renaud is a reproductive biologist investigating cellular and molecular mechanisms of placenta development and function as well as the causes of various pregnancy complications, including preeclampsia, intrauterine growth restriction, and preterm birth.
Research Profile: via Google Scholar
Also in the Department of Anatomy and Cell Biology (including cross-appointed): Nathalie Bérubé, Arthur Brown, Sandrine de Ribaupierre, Lauren Flynn, Victor Han, David Hess, Lisa Hoffman, Peeyush Lala, Michelle Mottola, and Katherine Willmore
Through cell and animal models Dr. Renaud is investigating the genetic and environmental determinants of those diseases, to ultimately impact public health and global health policies.
My research interests encompass the cellular and molecular mechanisms of placental development and function. There are two reasons I am interested in studying the placenta. First, the placenta is an exceptionally unique organ, one with evolutionary adaptations not observed in any other tissue. The second reason is from a public health perspective. The placenta intimately connects a mother with her developing baby, and it performs vital functions required for pregnancy such as regulating nutrient exchange between maternal and fetal blood, and producing hormones necessary for fetal development. Placental maldevelopment or dysfunction is linked with a variety of pregnancy complications (e.g. pre-eclampsia, fetal growth restriction, pre-term birth, placenta accreta, spontaneous abortion) that cause significant maternal and fetal illness or death. Despite its importance for the health of mothers and their babies, we really don’t have a good grasp on how the placenta develops or functions.
Our research interests can be broadly divided into two themes:
- Development of the trophoblast: the epithelial component of the placenta is comprised of trophoblast cells. These cells originate from a multilineage differentiation pathway that progressively differentiate into specialized trophoblast lineages, each with distinct morphologies and functions. We are particularly interested in how transcription factors and epigenetic regulators coordinate the progressive differentiation of trophoblast cells into defined lineages. Active projects in the laboratory include i) determining how conserved “OVO-like” transcription factors coordinate the transition of trophoblast cells from progenitor to differentiated states; and ii) transcriptional control of endogenous retroviral genes, which are genes that encode cellular fusogens necessary for generation of the placental epithelial barrier.
- Defining interactions between maternal immune cells and trophoblast cells: we are interested in how trophoblast cells interact with maternal immune cells. Trophoblast cells express paternal antigens and should be recognized as foreign by maternal immune cells. Why trophoblast cells are tolerated during normal pregnancies is not clear, but it is hypothesized that aberrant interactions between maternal immune cells and trophoblast cells may play a role in the development of various obstetric complications. We use both in vitro and in vivo models to provide insight on how the immune environment can shape trophoblast behaviour, placental development, and fetal health.
Why is placenta development important?
Even in developed countries like Canada, the development of the placenta – the organ that connects a mother to her child – can cause life-threatening pregnancy complications.
Dr. Stephen J. Renaud studies how placental development can cause common pregnancy complications like preeclampsia. Preeclampsia, identified as a multifactorial disease, has been linked to race, obesity, and age, as well as a host of other variables.
Alternate pregnancy complications include intrauterine growth restriction (IUGR) and spontaneous abortion. In each case the placenta malfunctions in some way, putting the life of the baby or mother at risk.
How is placenta development studied?
One way to study placental development is by analyzing “trophoblast” cells, linked to both IUGR and preeclampsia. Trophoblast cells act like a filter, facilitating the transfer of food and oxygen from the mother to the baby. Preeclampsia often occurs when those trophoblasts are compromised.
Renaud started his research with trophoblast cells. He determined the mother’s immune cells could be the cause, negatively affecting trophoblast cells and causing the placenta to develop incorrectly.
“That subject was the focus of my graduate work,” Renaud said. “My postdoctoral work more directly focused on how the placenta develops under normal circumstances.”
Renaud now studies trophoblast cell development and how they interact with their environment, including the mother’s immune cells, to determine the root of placenta-related complications.
Where is the research now?
Renaud works primarily on two complications: preeclampsia, which targets the mother, and IUGR, which limits the growth and development of the child. His goal is to anticipate and manage symptoms of these complications.
Currently, there is no reliable way to determine which pregnancies are “high risk.”
Many mothers, including Renaud’s wife, have overcome serious complications to have healthy, successful pregnancies. With more research, doctors could fully prevent the serious, life-threatening side effects of those complications.
| Present | Assistant Professor, Western University ‐ Department of Anatomy and Cell Biology | |
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| Present | Associate Scientist, Lawson Health Research Institute ‐ Children's Health Research Institute (CHRI) | |
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Disciplines
Cell Biology and Anatomy
Research Interests
Placental Development and Function, Preeclampsia, IUGR, Fetal Health, Maternal Health, Pregnancy, Trophoblast Cells, Immune Cells, Pregnancy Complications, Children's Health, Preterm Birth, Biomedical Research, Developmental Biology, Cell and Molecular Biology, Cell Models, Animal Models, Genetic Determinants, and Environmental Determinants