Fibrosis and regeneration are two very distinct responses to injury across a variety of species. For example, most human tissues develop a fibrotic scar when damaged. On the other hand, organisms like the newt are capable of regenerating a plethora of organs such as their limbs, heart, and parts of the eye including the retina and the lens. The mechanism behind how newts are able to avoid this scarring and instead regenerate an entirely new lens upon removal of this organ is not well-defined in previous literature. Our lab is investigating this mechanism and determining which cell populations, such as macrophages, play a role in this regeneration process. After developing several molecular tools that enabled us to begin studying macrophages in the newt, our results demonstrate that we have been able to detect and deplete these cells both in vitro and in vivo. Using this knowledge, we removed the lens of the newt and treated their eyes with a macrophage inhibitor to determine the effect this would have on lens regeneration. We found that depletion of macrophages prevented regeneration of the lens. We have now turned our attention to characterizing the macrophages as M1-activated or M2-activated, which will signify if these cells have pro-inflammatory or anti-inflammatory phenotypes respectively. This will give us insight into how the resident macrophages in human tissues differ from those in regeneration-competent tissues. Understanding the combined role of inflammation and macrophages in the process of lens regeneration will benefit our understanding of fibrosis, leading to better treatments for those who suffer from chronic health conditions. This work is especially pertinent to my future career as a physician who wants to improve the lives of those enduring debilitating diseases in their daily lives.
Author: Arielle Martinez
Graduate Student Advisors: George Tsissios and Anthony Sallese from the Department of Biology, Miami University and the Center for Visual Sciences at Miami University (CVSMU)
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