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Our Research Publications

Fibrin-polycaprolactone scaffolds for the differentiation of human neural progenitor cells into dopaminergic neurons. 

This work introduces a novel tissue-on-a-chip model using fibrin-coated polycaprolactone scaffolds to enhance differentiation and maturation of dopaminergic neurons from human-induced pluripotent stem cell-derived neural progenitor cells. The fibrin coating significantly improves neuronal adhesion, growth, and electrical activity, providing a promising platform for studying Parkinson's disease and other neurodegenerative disorders.

​Materials Characterization of Stereolithography 3D Printed Polymer to Develop a Self-Driven Microfluidic Device for Bioanalytical Applications

​This study characterizes the physical, chemical, and biological properties of a stereolithography (SLA) 3D-printed polymer, addressing gaps in knowledge about its stability and biocompatibility for bioanalytical applications. Findings reveal stable mechanical properties but time-sensitive changes in wettability, limiting postprinting usability for capillary-driven microfluidics. The insights support SLA’s feasibility as a high-throughput method for creating self-driven microfluidic devices.

Microcomputed Tomography for the Microstructure Evaluation of 3D Bioprinted Scaffolds

This study uses microcomputed tomography (micro-CT) to evaluate the microstructure of 3D bioprinted scaffolds incorporating gold nanoparticles (Au-NPs) coated with 2 kDa methoxy-PEG. Characterization confirmed spherical Au-NPs (66 nm core diameter) and showed non-toxicity to AC16 cardiomyocytes. Micro-CT imaging with Au-NPs enhanced scaffold visualization, while mechanical tests indicated Au-NP addition increased scaffold elasticity and viscosity. These findings support the use of Au-NP-enriched bioprinted hydrogels in tissue engineering, offering improved imaging and mechanical properties.

Inhibition of ERK 1/2 pathway downregulates YAP1/TAZ signaling in human cardiomyocytes exposed to hyperglycemic conditions

​This study investigates the impact of hyperglycemic conditions on cardiomyocytes, focusing on the ERK 1/2 and YAP1/TAZ signaling pathways. Cardiomyocytes were cultured under normoglycemic (5 or 25 mM D-glucose) and hyperglycemic (5 → 50 mM or 25 → 50 mM D-glucose) conditions, and RNA-sequencing identified significant changes in gene expression linked to inflammation and fibrosis, notably matrix metalloproteinases and inflammatory mediators. YAP1/TAZ protein levels were notably upregulated under hyperglycemic conditions (5 → 50 mM), and inhibiting ERK 1/2 signaling reduced YAP1/TAZ expression. This suggests that targeting ERK 1/2 may help mitigate hyperglycemia-associated cardiovascular inflammation and fibrosis

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