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Biology subjects

Vessella, T.

Publications and source records attributed to Vessella, T..

3 recordsLinked to original sources

Independent Tuning of Stiffness and Pore Size in 3D Rat Tail Collagen I Matrices

The interplay between extracellular matrix (ECM) mechanics and the tumor microenvironment is increasingly recognized as a key driver of cancer progression. Three-dimensional (3D) collagen I culture systems provide more physiologically relevant environments than traditional 2D cultures, yet seperately controlling the structural and mechanical features of 3D matrices remains challenging due to their inherent interdependence. Here, we present a collagen-based approach to decouple bulk stiffness and pore size by varying collagen concentration and polymerization temperature. Collagen concentration was varied to modulate bulk storage modulus, while polymerization temperature was adjusted to alter pore dimensons at comparable collagen concentrations. Using this approach, we generated 3D Collagen I matrices with bulk storage moduli of approximately 80, 228, and 360 Pa while maintaining a similar median pore sizes near 2.5 m. Conversely, 1.5 mg/mL collagen, median pore size varied from approximately 2.5 to 3.1 m while bulk storage modulus remained near 80 Pa, whereas at 3.5 mg/mL collagen, pore size varied from approximately 2.0 to 2.4 m while bulk storage modulus remained near 350 Pa. We further evaluated the responses of MCF-10A epithelial cells and MDA-MB-231 metastatic breast cancer cells to matrices spanning these sturactual and mechanical conditions. Although the changes in pore size within each stiffness range were modest, they were associated with measurable and statistical differences in cell morphology. These findings demonstrate that even modest changes in collagen network architecture can produce measurable differences in cellular behvarior under comparable bulk mechanical conditions, highlighitng the importance of considering matrix structure in addition to stiffness when investigating cell-matrix interactions.

biophysics↗

Investigation of cell mechanics and migration on DDR2-expressing neuroblastoma cell line

Neuroblastoma is a devastating disease accounting for ~15% of all childhood cancer deaths. Collagen content and fiber association within the tumor stroma influence tumor progression and metastasis. High expression levels of collagen receptor kinase, Discoidin domain receptor II (DDR2), are associated with poor survival of neuroblastoma patients. Additionally, cancer cells generate and sustain mechanical forces within their enviroment as a part of their normal physiology. Despite this, whether collagen activated DDR2 signaling dysregulate these migration forces is still elusive. To address these questions, a shRNA DDR2 knockdown neuroblastoma cell line (SH-SY5Y) was engineered to evaluate the consequence of DDR2 on cellular mechanics. Atomic force microscopy and traction force microscopy were utlizing to unveil the biophysical altercations. DDR2 down-regulation was found to significantly reduce proliferation, cell stiffness, and cellular elongation. Aditionally, DDR2 down-regulated cells had decreased traction forces when plated on collagen coated elastic substrates. Together, these results highlight the important role that DDR2 has in reducing migration mechanics in neuroblastoma and might be a promising target for future therapies.

cell biology↗

The roles of DDR2 and substrate stiffness on cancer cell transcriptome and proliferation

The interactions between cancer cells and the ECM regulate carcinogenesis. The collagen receptor kinase DDR2 is dysregulated in certain cancer cells, but its precise role in these malignancies remains unclear. In this study, we perform RNA-seq to determine how DDR2 and the biomechanical environment regulate cancer cell behaviors. We show that DDR2 knockdown in SH-SY5Y neuroblastoma cells inhibits proliferation and promotes senescence by regulating relevant genes. Increasing substrate stiffness reduces proliferation and promotes cell spreading but does not change senescence or transcriptome. Furthermore, DDR2 knockdown modulates cellular responses to substrate stiffness changes, unraveling a crosstalk between DDR2 and mechanosensing. These findings indicate DDR2 and ECM biomechanics regulate cancer cell behavior through distinct mechanisms, providing new mechanistic insights of cancer progression.

biochemistry↗