UMDF will once again host “The Big Pitch” where three post-doc researchers who are selected out of 50+ applicants, compete for a $50,000 accelerators prize. Each finalist gives a five-minute pitch on their research project live at the conference.
UMDF accelerators have the exclusive opportunity to vote for their favorite pitch. Visit the UMDF accelerators page or drop by a UMDF booth to find out how to become an accelerator today.
IRB Barcelona
Implications and Novel Therapeutic Insights on Mitochondrial Integrity in Hematopoiesis and Immune Balance in the Context of Mitochondrial Diseases
This research investigates how important cells called multipotent progenitor cells, which play a crucial role in creating different blood cells in our body, stay healthy. These cells exhibit an efficient energy management system, but mutations in the mitochondrial DNA can impact on the organelle quality control mechanisms, resulting in issues with the maintenance and differentiation processes of these cells. Additionally, mutations in the mitochondrial genome of mature blood cells and the resulting inflammation can harm the health of the different organs. Such concerns are particularly significant in individuals with mitochondrial diseases. By studying different mouse models that mimic these health conditions and blood cells obtained from healthy donors and patients, our goal is to gain a deeper understanding of these complexities. This project aims to help individuals with similar health challenges by developing new ways to diagnose and treat them effectively.
University of Cambridge
Implications and Novel Therapeutic Insights on Mitochondrial Integrity in Hematopoiesis and Immune Balance in the Context of Mitochondrial Diseases
Mitochondrial diseases manifest with a wide range of symptoms, affecting various organs and tissues in our bodies. Thanks to technology, scientists have identified most of the DNA mutations responsible for these diseases, yet we still do not fully comprehend what determines this diversity. One cellular adaptation mechanism to cope with the accumulation of defective material inside cells is the secretion of this damaged content in the form of vesicles. These vesicles can be taken up by neighbouring cells or cells located at distant sites enabling a broader effect. Furthermore, it has been observed that these vesicles can carry mitochondria, which may have negative effects on the recipient cells. The objective of my project is to study these vesicles by characterizing their number, content, and effects on neighbouring cells, focusing on cell types typically most affected in mitochondrial diseases, such as muscle cells and neurons. The results of the experiments in cellular models will be confirmed and validated in blood samples of patients with mitochondrial diseases. I believe that the proposed research will reveal new ways how mitochondria can participate in communication between different cells in the body, potentially improving cell survival and future therapy development in mitochondrial diseases.
Children’s Hospital of Philadelphia
‘Dysregulation of MTORC1 in Human Cell Models of Mitochondrial Complex V Deficiency
Cells must adapt to their environment to grow and survive. The process of the cell learning about its external environment, for example nutrient availability, health of surrounding, etc. is called cell signaling. Cell signaling is usually conducted inside the cell by a series of specific proteins that talk to each other in a set order, to relay information from outside the cell to the cell itself to allow the cell to make decision about how to adapt. One recipient of this information in the cell may be the mitochondria. Mitochondria are responsible for energy production and are intimately involved in cell signaling pathways. To make energy, proteins in the mitochondria called Mitochondrial Complex proteins use a type of cellular electricity known as electrons to pass electrical energy to their neighbors in a line back and forth. At the very end of the line, a protein called ATP Synthase (also called Mitochondrial Complex V – CV) produces energy. In mitochondrial disease when mitochondria do not work properly, cell signaling, and the ability of the Mitochondrial Complex proteins are disrupted. Signals that were designed to be temporary ‘mitochondrial overwhelm’ signals may stay on permanently. Since mitochondrial diseases can be caused by multiple different abnormalities in the mitochondria, developing universal treatments is difficult. This proposal aims to study a specific mitochondrial disease called ATP Synthase (Complex V deficiency) and how it interacts with the mTOR pathway, one of the main cell signaling pathways to communicate nutrient availability. This work builds on the discovery that the mTOR pathway is abnormal in animal models of Complex V deficiency and that mTOR directly inhibits complex V in healthy animals. This work could help future researchers to develop and direct precision treatments for mitochondrial disease that manipulate cell signaling pathways.
