Our Research

Mission: Engineering biomaterial models to leverage the regenerative potential of the immune system across health inequities

We execute on our mission by developing compassionate innovators equipped to transform biomedical research.

Find updates on our recent publications in Google Scholar. If you cannot access any of our publications, please email emt[at]umd.edu and we will provide a copy!

Immune vascular interactions in lupus

Systemic lupus erythematosus (SLE) is a medical condition in which the immune system attacks healthy cells and tissues in the body. It affects approximately 1.5 million people in the United States, with women of color being 2-3 times more likely to develop and die from SLE than other groups. One complication of SLE is vasculitis, inflammation of the blood vessels, which progresses more rapidly due to interactions between the immune system and blood vessel lining.  Detecting vasculitis in the early stages can be challenging because the symptoms are often subtle and nonspecific. To improve early detection, we are using biomaterial models to study how immune cells interact with blood vessels in SLE patients. By studying these interactions, we hope to identify new ways to detect and treat vasculitis in its early stages. Because SLE is a health disparity, we are also studying how a patient's background, such as lived experiences, can influence their immune cell function and the development of vascular inflammation. By better understanding these factors, we hope to develop more targeted and effective models for SLE and its heterogeneity.

Reviving Macrophages for Effective Tissue Regeneration in Aging - Insights from Biomaterial Models

Over 700 million people worldwide are 65 years or older, and as we age, our ability to heal decreases. Macrophages, immune cells that play a crucial role in tissue regeneration, also become less effective with age. To better understand this process, we are designing a biomaterial model system to investigate how the age of macrophages affects macrophages' ability to support tissue healing. We are also interested in using our model system to explore potential therapeutic interventions that can improve macrophage function. By focusing on tissue regeneration in aging, we hope to gain insights into how macrophages change over time and identify ways to rescue their function using targeted therapies.  Our work will shed light on this critical aspect of the aging process and pave the way for more effective treatments in the future.

Overlooking Ancestry in Regenerative Medicine - Addressing Health Inequities through Biomaterial Models

Everyone's health is influenced by their background, both genetics and lived experiences. However, most regenerative medicine research focuses on people of European descent, which overlooks the impact of ancestry on disease development and wound healing. To fill this gap, we use biomaterial models to understand how ancestry affects innate immune cellular responses in wound healing. By studying these interactions, we aim to identify wound healing risks and outcomes for people from systemically excluded backgrounds. Our research introduces a new perspective on health inequities, bringing attention to the systemic exclusion of oppressed and excluded communities in biomedical science. Ultimately, we hope to use our findings to develop more personalized and effective treatments for all individuals.

Decoding the Signals - How the Extracellular Matrix Directs Macrophage Behavior for Tissue Regeneration

Macrophage immune cells play a vital role in tissue homeostasis, wound healing, and tissue regeneration, but we still have much to learn about how they function. Specifically, we are interested in understanding how the extracellular matrix (ECM) influences macrophage behavior. To do this, we design biomaterial tools to study how different ECM components, known as ECM ligands, direct macrophage function. By investigating how the composition of the ECM affects macrophage activation and homeostasis, we hope to better understand the signals that control tissue regeneration. Ultimately, our work could lead to new strategies for promoting tissue repair and healing. 

Unraveling Uterine Fibroids- Designing Biomaterials to Modulate Fibroblast and Macrophage Responses

Uterine fibroids, which affect up to 70-80% of women by the age of 50, are characterized by excessive growth of fibrous tissue, driven in part by the complex interplay between hormones, fibroblasts, and immune cells like macrophages.  Fibroids disproportionately affect Black women, who tend to develop them at younger ages and experience more severe symptoms compared to women of other racial and ethnic backgrounds. We aim to understand fibroblast activity and macrophage behavior in uterine fibroids. By designing biomaterial systems that mimic the fibroid ECM, we can study how specific ECM components guide the responses of these cells. This knowledge could pave the way for fundamental understanding  in the regulation of fibroid development and improve treatment outcomes for women’s health.

Enroll in our research study

Blood Donors Needed for Research  in Biomaterial Models of Ancestral Contributions to Wound Healing Study

PAPERS PUBLISHED:

A complete list of all our publications can be found on  Google Scholar













PDF: https://www.karger.com/Article/Pdf/523859 




PDF: https://link.springer.com/content/pdf/10.1557/s43578-021-00423-y.pdf 




PDF: https://link.springer.com/content/pdf/10.1007/s40883-021-00237-8.pdf 


PDF: https://www.nature.com/articles/s41526-021-00141-z.pdf 


PDF: https://www.nature.com/articles/s41526-021-00141-z.pdf 


PDF: https://link.springer.com/content/pdf/10.1007/s13346-021-00970-1.pdf


PDF: https://www.science.org/doi/epdf/10.1126/sciadv.abj5830


PDF: https://science.sciencemag.org/content/sci/371/6536/1398.full.pdf


PDF: https://link.springer.com/content/pdf/10.1007/s10439-018-02170-4.pdf


PDF: https://link.springer.com/content/pdf/10.1007/s40883-018-0074-y.pdf 


PDF: https://link.springer.com/content/pdf/10.1007/s40883-018-0048-0.pdf


PDF: https://onlinelibrary.wiley.com/doi/pdf/10.1002/adbi.201600021



PDF: https://www.liebertpub.com/doi/pdfplus/10.1089/biores.2014.0029