The conference took place during the last days of October 2013 at the Genome Campus in Hinxton, near Cambridge. The title of the conference “Regenerative Medicine: From Biology to therapy” could also have been the title of the opening lecture by Sir John Gurdon. He outlined and commented on different reprogramming strategies of somatic cells into a pluri- or totipotent state. He started with his own work on SCNT which is the transfer a somatic nucleus into an Oocyte. Factors in the oocyte can remodel the epigenetic landscape of the somatic nucleus in a way that it acquires totipotency once again. This work, together with the approach that Yamanaka identified in 2006 to reprogram somatic cells to pluripotency by transduction of 4 specific transcription factors now forms a strong basis for basic biomedical research and therapeutic strategies. It was a really nice talk, in which he demonstrated with a variety of examples how this technique can be used to model human disease by in vitro models derived from patient iPSC lines.
The first session focused on regeneration models that can be found throughout the animal kingdom. It showed how we can learn the basic mechanisms of tissue regeneration in non-mammalian species. For instance, Enrique Amaya from the University of Manchester started with an interesting talk about the role of Reactive Oxygen Species (ROS) in tadpole tail regeneration. ROS are normally present in the earliest phase of wound healing and released by innate immune cells to fight infections. Surprisingly, he showed that the regenerating tissue stays in an oxidised state until late stages in regeneration. A similar oxidised environment was also found during early development. Thus there seems to be a connection between the redox state of the cells and their developmental program. In this framework a more oxidised state seems to be closely linked to more embryonic or regenerative cell programs. This opens new exciting questions about how metabolism is linked to regeneration and development. Planaria also took centre stage in this session. Kerstin Bartscherer from the MPI for Molecular Biomedicine introduced planaria as a model organism for regeneration. The talk attracted a lot of interest, since some of the audience didn’t know much about their regenerative ability.
The next session focused on non-IPS cell methods of regeneration biology. One of my personal highlights of the conference was the talk given by Giovanna Malluci, from the MCR Toxicology Unit. In neurodegenerative diseases the first thing which is normally lost or degenerates is the synapse. All other degenerative processes including the ultimate loss of the neurons themselves take place after this process. Her research group is therefore asking if there are ways to reestablish synapses and preserve them. This research was inspired by the hibernation of squirrels. During hibernation the synapses in the squirrel brains are disconnected and after hibernation they are reassembled again. This occurs almost perfectly and with no loss of memory. She investigated if lowering the body temperature in mice would have a similar effect. Interestingly, this mimicking of hibernation had similar effects in mice and could even preserve synapse integrity in a familial Alzheimer’s Disease model. She also found genes associated with the hibernation response which recapitulate the same protective effect without the cooling procedure when over expressed in these mice. This resulted in an overall alleviated clinical score in the disease model and in a significantly higher life expectancy. Strikingly, loss of this component decreased synapse stability and led to premature death.
I also gave a talk in this session. I spoke about some of the work that I have performed as part of my PhD, explaining the role of JNK signalling in posterior polarity specification in planarians. Although throughout my PhD I’ve given many talks, including some for my department, this was the first time that I had given a talk to such a large and renowned audience. It was a great experience, both for the interest it generated and for the feedback that I got.
On the last day the talks focused on the therapeutical end of regeneration biology. This was great for me, since it reminded us what can be achieved with the basic science that we are studying, but also how much we still need to understand. I was especially impressed by Amy Wagers’s talk (Harvard). She elaborated how tissue specific stem cells undergo ageing and in turn experience a functional decline. This might be a cause for the loss of homeostasis and a hallmark of what we call ageing. An exciting question is “Can we reverse ageing effects at the cellular level?”. She showed that cells in an old body can restore their function when they are exposed to a young environment. This was achieved by connecting old and young mice in a way that they share their circulatory system. This experimental setup is called heterochronic parabiosis. But what are the factors in the young blood that make the cells younger again? In a screen for proteins in the serum she actually found a factor called GDF11. When this growth factor was injected into old mice suffering from heart hypertrophy the phenotype could be reversed. Similarly, this factor also seems to rejuvenate satellite cells which are the tissue specific stem cells in the skeletal muscle.
All in all it was a great, intense three days, with lots of inspiring talks in a very nice venue. I would therefore like to thank the organisers for arranging the conference, as well as the BSCB for awarding me the Honor Fell Travel award, which allowed me to attend. I would highly recommend to my colleagues that they attend this conference in the future and I certainly will.