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Biology subjects

Machado, C. M. L.

Publications and source records attributed to Machado, C. M. L..

2 recordsLinked to original sources

Vascularized tumor on a microfluidic chip to study mechanisms promoting tumor neovascularization and vascular targeted therapies

The cascade of events leading to tumor formation includes induction of a tumor supporting neovasculature as a primary hallmark of cancer. Developing vasculature is difficult to evaluate in vivo but can be captured using microfluidic chip technology and patient derived cells. Herein, we established an on chip approach to investigate the mechanisms promoting tumor vascularization and vascular targeted therapies via co-culture of metastatic renal cell carcinoma spheroids and endothelial cells in a 3D environment. Our model permitted real-time, high-resolution observation and assessment of tumor-induced angiogenesis, where endothelial cells sprout towards the tumor and mimic a vascular network. Bevacizumab, an angiogenic inhibitor, disrupted interactions between vessels and tumors, destroying the vascular network. The on chip approach enabled assessment of endothelial cell biology, vessels functionality, drug delivery, and molecular expression of PSMA. Finally, observations in the vascularized tumor on chip permitted direct and conclusive quantification of this therapy in weeks as opposed to months in a comparable animal model. TeaserVascularized tumor on microfluidic chip provides opportunity to study targeted therapies and improves preclinical drug discovery.

cancer biology↗

Superoxide Dismutase 1 translocates to the nucleus in spinal cord mixed cells from newborn rats

Superoxide dismutase 1 (SOD1) catalyzes the superoxide conversion to oxygen and hydrogen peroxide in general. SOD1 can translocate to the cell nucleus in response to oxidative stress in yeast and human fibroblasts. Here, we report the translocation of sod1 to the cell nucleus in primary co-cultures of neurons and astrocytes derived from newborn rats explants even in the absence of oxidative stress stimuli. The successful tissue explants from rats allowed simplistic and clean modeling of Amyotrophic lateral sclerosis (ALS)-simile tissue microenvironment. This mixed-cells-population was responsive to H2O2 (100 M) oxidative stress with a progressive dying process up to 6 h after stimuli. However, no differences in SOD1 nucleus translocation were observed in rat amyotrophic lateral sclerosis (ALS)-simile tissue microenvironment up to 6 hours under oxidative stress. These results altogether point to a robust cellular collaboration between neurons and astrocytes so that the tissue can equilibrate this SOD1 translocation during the oxidative stress response and in the early animal development.

biochemistry↗