Research Spotlight
Understanding pulmonary artery changes A presentation about why pulmonary arteries change in pulmonary arterial hypertension was the winner of a PHA UK-sponsored prize at last year’s National PH Research Forum. Emphasis spoke to presenter Angelos Anastasakis about his work, his winnings, and the importance of medical research in rare disease areas.
First things first, how did your research project come about? I’m currently a fourth-year medical student at the University of Central London and during our third year of studies the medical school allows us to do a Bachelor of Science in a field that interests us. I chose cardiovascular sciences and during this course we carry out a research project. Initially I investigated the immune cell response in pulmonary arterial hypertension (PAH). The project was very successful and I established a good relationship with the lab I was working at - Royal Free Centre for Rheumatology and Connective Tissue Disease. They offered me the opportunity to carry on researching in the field of PAH over the summer holidays - this time looking at metabolism - and I was delighted to be able to do this.
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Can you tell us more about the research - what did it set out to do and what did it discover? The research I presented at the National PH Research Forum was from the above project and it was led by a final year PhD student called Jerry Abu-Hanna, who came up with the ideas which we investigated. We sought to understand why the pulmonary arteries in people with PAH become so thick and muscular. Hopefully by understanding these changes we can find a targeted drug to prevent them from occurring altogether. All cells take up oxygen and glucose and use this to make energy in the form of adenosine triphosphate (ATP). This is called mitochondrial respiration. We wanted to investigate mitochondrial respiration in the muscular part of pulmonary arteries, which is made up of smooth muscle cells.
We looked at smooth muscle cells taken from the pulmonary arteries of PAH patients and from patients without PAH. We found that mitochondrial respiration was increased in smooth muscle cells from PAH patients, as they were taking up more oxygen and producing more ATP. This increased energy can then be used to make more smooth muscle cells, explaining why the pulmonary arteries are so much more muscular in PAH. This energy or ATP is produced in mitochondria. Next, we wanted to see if mitochondria had an abnormal composition in smooth muscle cells from PAH patients to explain the increased energy production. We found that the mitochondria in PAH had an increased mass, which simply means they have more machinery which allows them to produce energy. Our next task was to see why this mass was increased. The process which adds
