BME Student Seminar (Zoom): Richard Tran and Joseph Hsu

Wednesday, February 3, 2021 - 1:00 p.m. to Thursday, February 4, 2021 - 1:55 p.m.
Zoom (link below)
Richard Tran and Joseph Hsu

Richard Tran: The Effect of Cyclic Strain on Human Fibroblasts with Lamin A/C Mutations and its Relation to Heart Disease

Abstract: Although mutations in the Lamin A/C gene (LMNA) cause a variety of devastating diseases, the pathological mechanism is often unknown. Lamin A/C proteins play a crucial role in forming a meshwork under the nuclear membrane, providing the nucleus with mechanical integrity and interacting with other proteins for gene regulation. Most LMNA mutations result in heart diseases, including some types that primarily have heart disease as the main pathology. In this study, we used cells from patients with different LMNA mutations that primarily lead to heart disease. Indeed, it is a mystery why a mutation to the protein in every nucleus of the body manifests as a disease of primarily the heart in these patients. Here, we aimed to investigate if mechanics mimicking the myocardial environment is sufficient to cause differences in cells with and without the LMNA mutation. To test this, a stretcher device was used to induce cyclic strain upon cells; and viability/proliferation, cytoskeleton and extracellular matrix organization, and nuclear morphology were quantified.

Joseph Hsu: Investigating the Role of Homotypic Interactions in Macrophage Activation

Abstract: Macrophages play a key role in the innate immune system, and their activation is tightly regulated to avoid excess and harmful inflammation. Studies have revealed the roles of soluble and adhesive cues in the regulation of macrophage polarization. Furthermore, recent studies also show that macrophage signaling within a population is critical for coordinating a collective response. Nevertheless, more works are needed to understand how such coordination modulates the resultant response. In this study, we characterized the roles of intercellular communication within macrophage populations by stimulating cells in bulk, in small groups and in isolation. We found that macrophage activation depends on the communication among the cell population, and both seeding density and absolute cell number contribute to the resultant responses. Overall, our study helps provide a better understanding of this emerging area of research. We believe that further works in this field could provide new strategies to modulate inflammatory responses for different needs in clinical settings.

Please contact Julianne Vu jevu@uci.edu with any questions.