Characterizing the Effect of Mitochondria Uptake on Macrophages

Abstract

As central hubs for many cellular processes, mitochondria are crucial for cellmetabolism and survival. For a long time, it was widely assumed that mitochondria are constrained within the cytoplasm of the cell. However, a decade of research has revealed the possibility of intercellular mitochondria migration, involving the movement of mitochondria from one cell type to unrelated cell types. Energy-intensive cells such as cardiomyocytes and brown adipocytes are subjected to a high rate of ROS (reactive oxygen species) generation. Mitochondria quality control pathways are critical in preserving mitochondrial health and homeostasis to maintain cellular functions. Cardiomyocytes export dysfunctional mitochondria as an alternative method of quality control. Resident macrophages in the environment actively capture and degrade cardiac mitochondria. While this process benefits cardiomyocytes by preserving their mitochondrial function, the biological consequences of acquiring cardiac mitochondria have not been fully characterized in macrophages. Here, we used an in vitro system combining primary macrophages and the artificial transfer of cardiac mitochondria to investigate macrophage respiration, proliferation, as well as the morphology and turnover of their endogenous mitochondria after mitochondria uptake.