A Penn State University researcher will use a $65,000 grant from the Lysosomal and Rare Disorders Research and Treatment Center (LDRTC) to create a 3-D bone tissue model for the study of Gaucher disease.
Ozbolat’s grant is one of four totaling about $1.5 million to investigate ways to bioprint biological tissues such as bones, lungs, and other organs for use as models in several studies. His awards include a $75,000 grant from the Osteology Foundation to focus on bioprinting bone with the aim of developing technology transference to clinical and surgical settings.
Three-dimensional bioprinting is a process in which biomaterials such as cells and growth factors are combined to create tissue-like structures that mimic natural tissues. The technology uses bioink — the material used to produce artificial live tissue — to create the structures in layers.
Another $450,000 grant from the National Science Foundation is meant to explore new 3-D bioprinting processes for creating implantable tissues and organs. Ozbolat will address questions regarding 3-D bioprinting, including the optimal size and density of cell spheroids, as well as their mechanics and ability to survive.
A $900,000 grant from the National Institutes of Health Cooperative Center on Human Immunology will support the development of 3-D models of lungs and the respiratory tract to understand how the immune system interacts with the lung environment and fights virus or metabolic agents.
By applying bioprinting in medicines’ discovery and development, for example, scientists can identify ineffective or harmful medicines early in the process, and shift resources to more promising treatment candidates. Current approved treatments for Gaucher include enzyme replacement and substrate reduction therapies.
Affecting about one in 100,000 individuals in the United States, Gaucher is a lysosomal storage disorder in which a fat molecule called glucocerebroside accumulates in various organs and tissues, affecting organs and bones. According to the National Gaucher Foundation, as many as 62 percent of Gaucher patients have some kind of detectable bone disease.
Clinically divided into three types, the condition is mostly caused by mutations in the GBA gene that impair the protein from acquiring its normal 3-D conformation (a process called folding), causing premature degradation.
The nonprofit LDRTC is dedicated to best practices in the management and treatment of lysosomal disorders.
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