Maddie Cramer, a doctoral student in the Bioengineering Department at the University of Pittsburgh and a team member in the laboratory of Stephen Badylak, DVM, PhD, MD, will receive the Outstanding Student Award from TERMIS-AA. Dr. Badylak is a deputy director of the McGowan Institute for Regenerative Medicine, professor in the Department of Surgery, and director of the Center for Pre-Clinical Tissue Engineering within the Institute.

This honor includes publication of her paper in Tissue Engineering Part A, a $500 honorarium, and an oral presentation of her work at their December Webinar Series. She will receive $1000 travel toward the annual meeting in Toronto next July and be recognized on stage in person for her award.

The title of Ms. Cramer’s paper is “The Influence of Matrix Bound Nanovesicle Associated Interleukin-33 on Macrophage Phenotype.” The abstract follows:

The innate immune response, particularly the phenotype of responding macrophages, has significant clinical implications in the remodeling outcome following implantation of biomaterials and engineered tissues. In general, facilitation of an anti-inflammatory (M2-like) phenotype is associated with tissue repair and favorable outcomes, while pro-inflammatory (M1-like) activation can contribute to chronic inflammation and a classic foreign body response. Biologic scaffolds composed of extracellular matrix (ECM) and, more recently, matrix bound nanovesicles (MBV) embedded within the ECM are known to direct macrophages toward an anti-inflammatory phenotype and stimulate a constructive remodeling outcome. The mechanisms of MBV-mediated macrophage activation are not fully understood, but interleukin-33 (IL-33) cargo within the MBV is required for M2-like activation. Previous work has shown that IL-33 is encapsulated within the lumen of MBV and stimulates phenotypical changes in macrophages independent of its canonical surface receptor ST2. In the present study we used next generation RNA-sequencing to determine the gene signature of macrophages following exposure to MBV with and without IL-33 cargo. MBV-associated IL-33 instructed an anti-inflammatory phenotype in both wildtype and st2-/- macrophages by downregulating M2-like and upregulating M1-like genes. The repertoire of genes regulated by ST2-independent IL-33 signaling were broadly related to the inflammatory response and crosstalk between cells of both the innate and adaptive immune systems. These results signify the importance of the MBV cargo protein IL-33 in stimulating a pro-remodeling M2-like phenotype in macrophages and provides guidance for the designing of next generation biomaterials and tissue engineering strategies.

Congratulations, Ms. Cramer!

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University of Pittsburgh Swanson School of Engineering News Release