Johnson Digital Bioengineering LAb
Our lab is located in the Institute for Quantitative Health Science and Engineering at Michigan State University in East Lansing, MI. We are affiliated with the Departments of Pharmacology & Toxicology and Biomedical Engineering.
What we DO
We leverage the versitility of digital manufacturing to construct models of human development and disease.
Why we do IT
Our goal is to develop strategies and technologies that lead to the prevention of birth defects and disease in vulnerable populations.
Biology driven design.
Intercellular signaling drives early development. Early organization of the embryo is orchestrated by just a few pathways including the Wnt, Tgf-B, SHH, FGF, and Notch pathways which often act as a means of cell/matrix or cell to cell communication. We engineered a device to phenocopy the developing facial processes (epithelial cells overlayed onto 3D mesenchymal cells) since these are sensitive to both genetic and environmental insults during development leading to facial clefting (cleft lip/palate). The resulting microtissues show critical similarities to tissue sections from the developing palate. More importantly, they support the spatial signaling interactions that are sensitive to teratogenic insults. We hope to use these microtissues to identity genetic risk-factors and chemical exposure combinations that may cause this birth defect in every 700 live births.
Digital manufacturing fuels innovation.
We developed a novel digital manufacturing process dubbed “microplate micromilling” that integrates microfluidic channels and features directly into standard commercially available polystyrene cell culture plates (48, 96, 384, 1536 etc.). This platform is used to generate tractable, adaptable, high content and throughput compatible intercellular signaling models.
See a full list of publications on Pubmed using the link below or check out a couple recent articles on the right.
Engineered Perineural Vascular Plexus for Modeling Developmental Toxicity
By quantifying 3D cell migration, metabolic activity, vascular network disruption, and cytotoxicity, the PNVP model may be a useful tool to make physiologically relevant predictions of developmental toxicity.By quantifying 3D cell migration, metabolic activity, vascular network disruption, and cytotoxicity, the PNVP model may be a useful tool to make physiologically relevant predictions of developmental toxicity.
Mammary adipose stromal cells derived from obese women reduce sensitivity to the aromatase inhibitor anastrazole in an organotypic breast model.
MCF7-derived ducts co-cultured with pre-adipocytes derived from obese individuals help elucidate mechanism of clinical findings.
Brian P. Johnson PhD firstname.lastname@example.org
775 Woodlot Dr Rm 3315 IQ Bioengineering Building East Lansing, MI 48824