Dr Yutaka Matsubayashi has been named as a recipient of the Academy of Medical Sciences (AMS) Springboard Awards – the first time one has been awarded to a Bournemouth University researcher.
More than 40 Springboard Awards, totalling over £4 million, have been awarded to biomedical and health researchers in their first independent post to help launch their careers.
Dr Matsubayashi, a Lecturer in Systems Biology at BU, has received the grant to support his research investigating the mechanisms that orchestrate basement membrane formation – working towards the invention of future therapies.
The basement membrane is a scaffolding structure that supports almost all animal tissues, and the research has possible clinical applications for many medical conditions caused by basement membrane deficiency – such as kidney failure, skin fragility, and brain haemorrhage.
The grant will be used to employ a research assistant, and a network of collaborators inside and beyond Bournemouth University will also support the work.
The Springboard Awards provide up to £125,000 over two years and a personalised package of career support to help biomedical scientists to launch their research careers.
Dr Suzanne Candy, Director of Biomedical Grants & Policy at the Academy of Medical Sciences, said: “Together with our partners, we are fortunate to be able to support this talented group of researchers doing excellent science. Our strategic ambition is to help create an open and progressive research sector. By investing in these individuals and teams, we are broadening the range of people and disciplines engaged in biomedical and health research, across all regions of the UK, and globally.
“We look forward to supporting our award recipients and seeing how their research has a positive impact on the health of people everywhere.”
Every beat of the heart is finely tuned to eject a certain amount of blood. As we exercise, more blood flows into the heart, the cardiac muscle stretches and this leads to an increased force of contraction. Known as the Frank-Starling law, it is one of the most important aspects of human cardiac physiology but the molecular mechanisms are not entirely understood.
We do know that increases to the calcium levels in the heart cells (cardiomyocytes) support stronger contractions (anyone remember the ‘sliding ratchet model’ from GCSE biology!?) but how this calcium is regulated by stretch is not fully understood. What my colleagues and I have established (to be published in Frontiers of Physiology) is that a ‘mechanosensitive’ protein known as Piezo helps increase calcium when the cardiomyocytes are stretched. A lot of this work was done at BU’s Drosophila (fruit fly) genetics facility in Dorset House, using physiological tests of heart function in flies without the Piezo protein. When stretched, normal hearts respond by releasing more calcium and they continue to beat. In Piezo mutants, there’s no increase in calcium and the hearts often stop beating.
This is an important observation that contributes to our fundamental understanding of cardiac physiology and points to Piezo as a protein of considerable interest when considering the underlying causes of cardiac dysfunction in disease and ageing.
(The image shows the contractile protein ‘scaffold’ within an insect heart)
Research at BU has helped establish a cause of childhood kidney failure. The work, accepted for publication the journal Paediatric Nephrology, was a combined effort, including inputs from academic and clinical teams at the universities of Oxford, Bristol and Bournemouth. It focused on Steroid Resistant Nephrotic Syndrome (SRNS), a life-threatening form of kidney disease seen in young children, which may require dialysis and eventually a kidney transplant.
It is increasingly understood that genetic mutations play a critical role in SRNS but proving cause and effect is problematic. A patient’s family may have evidence of mutations in key ‘kidney genes’ but establishing if these actually combine in the patient to cause SRNS needs experimental evidence. Bournemouth’s contribution to this work involved disrupting a gene called Nucleoporin 93 (NUP93) in the kidney-like cells (nephrocytes) of fruit flies (Drosophila). When NUP93 function was lost in nephrocytes, failed to do their kidney filtration job and then died; providing strong evidence that mutations in the human gene do indeed lead to SRNS.
NUP93 is part of a protein complex that allows communication between a cell’s ‘head quarters’, the nucleus, and the rest of the cell. Perplexingly, NUP93 is found in all cells raising questions as to why mutations specifically affect the kidney. This work facilitates the search for a cure in the long term and, in the shorter term, allows for a definitive diagnosis when clinicians and families are confronted by this potentially devastating disease.
Paul Hartley (Life and Environmental Sciences).