In the United States, over 750,000 people will experience a heart attack annually. A heart attack occurs when blood flow is blocked from reaching a certain region of the heart.  This leads to cell death due to the lack of nutrients and oxygen, resulting in permanent damage to the heart. The heart is unable to efficiently generate new cells to replace ones that have died; therefore, further damage and degeneration can result, which contributes to heart disease.  To address these regeneration issues, researchers are studying ways to try and increase the regenerative properties of heart cells in hopes of generating new therapeutic treatments. Recently, a team from the Harvard School of Engineering investigated the influence of extracellular vesicles (EV’s) in promoting heart regeneration following a heart attack. 

Extracellular vesicles are particles exported from cells that can carry various components such as proteins and RNA. In order to study the role of EV’s, the researchers used heart-on-a-chip technology in which heart cells are plated on an engineered plastic chip containing sensors that can then monitor the plated cells. Using this chip technology, scientists can expose heart cells to a variety of conditions to mimic a heart attack. The researchers were able to determine that vascular endothelial cells, which are responsible for moving blood through the heart, secrete EV’s while the heart cells are deprived of oxygen. This is significant because it shows how the different cell types in the heart can respond to stress and influence how the surrounding cells respond to that stress.

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A heart attack causes the death of surrounding heart cells, which, over time, can lead to the development of heart disease. 

Image Source: PM Images

These EV’s secreted from vascular endothelial cells contain a high density of protective proteins that are involved in various cellular processes that can enable the surrounding heart cells to respond better to oxygen deprivation. Further analysis of the proteins found in secreted EV’s identified their involvement in metabolic and energy processing. These proteins essentially enable heart cells to continue to conduct the cellular processes used in normal oxygen conditions, providing a safety net against the spread of damage. 

These findings are significant in helping researchers better understand how the heart responds during and after a heart attack. By working to better understand the mechanisms used by heart cells to respond to damage, new research developments can lead to the development of therapeutics and treatments that can enhance the EV response and work to limit the damage. Investigating new treatments can hopefully work to limit the development of heart disease and increase peoples’ quality of life in the future.  

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Jennifer Thompson

Author Jennifer Thompson

Jennifer is a UCLA graduate that majored in Molecular, Cell and Developmental Biology and minored in Biomedical Research. She is currently attending the University of Michigan to obtain her Masters in Genetic Counseling. Her interests include cardiac development and maturation research, running, reading, and watching movies.

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