Abstract: Stress is one of the commonest and underappreciated causes of reproductive frailty in women. The stress system leads to adaptive responses via mobilization of hormonal systems. Adaptability and resistance to stress are fundamental to life. The response to stressors depends on the type of stressor, the timing and duration of stress, the genetic predisposition, personality characteristics, and the way of coping with stress. In pregnancy, maternal stress is known to disturb fetal glucocorticoid environment. In utero stress exposure is a significant predictor of subsequent adult telomere length. In humans, maternal exposure to prenatal psychosocial stress could be associated with decreased insulin sensitivity in the offspring assessed during young adulthood as well as in animals in intrauterine growth restriction (IUGR) cases. Some of the metabolic consequences of IUGR can be mitigated by ensuring early appropriate catchup growth, while avoiding excessive weight gain if relative hypercortisolism is not installed. The effect of maternal stress on fetuses regarding fetal HPA axis responsiveness (increased or decreased) remains under investigation. Animal studies confirmed that increase in stress hormones and pro-inflammatory cytokines in the fetal compartment during sensitive or critical developmental windows can impact the structure and function of the brain and peripheral targets which are related to body composition, energy balance homeostasis, and metabolic function (i.e. adipose tissue, pancreas, and liver). Maternal stress and depression are associated with structural and functional changes of brain parts such as hippocampus. In utero stress modifies epigenetically components of the HPA axis which can be transmitted transgenerationally. Epigenetic changes result in altered gene expression, ultimately affecting the risk for mental disorders.

Abstract: While the mature heart is a highly morphologically complex structure, it originates during early embryonic development from a relatively simple linear tube. This linear heart tube undergoes a series of morphogenetic events, including cardiac looping and chamber ballooning, to give shape to the maturing heart. At tube stage, the heart consists of two nested tubes – an outer myocardial layer, and an inner layer composed of specialised endothelial cells, the endocardium. These two tissue layers are separated by a layer of cardiac extracellular matrix (ECM), and our lab is interested in how this cardiac ECM could promote heart morphogenesis.
Here, I will first describe how by using live in vivo imaging we have identified a regionalised expansion of the cardiac ECM at early stages of heart tube morphogenesis. I will present our investigations into how ECM asymmetry is regulated, and its functional role in cardiac development. Later, I will also discuss how the major ECM component laminin regulates specific stages of cardiac morphogenesis.
Altogether, our overarching goal is to understand how the cells of the heart interact with each other, and their environment, to allow a simple tissue to undergo the highly regionalised morphological changes that shape the heart.

This new partnership will invest in translational fellowships and seed awards to drive the development of new preventative and therapeutic strategies to treat disease around the world. The partnership will also enable the provision of supporting expertise in impact delivery, and strengthen links with partner institutions in both industry and our local hospital network.

Come and find out how to apply and get involved.
Tea/coffee and cakes supplied.