2024 Undergraduate Research Showcase

EAE-Induced Blood-Brain Barrier Dysfunction and Aberrant Angiogenesis are Attenuated in Brain Endothelial-Specific Decorin Knockout Mice

Document Type

Student Presentation

Presentation Date

4-19-2024

Faculty Sponsor

Dr. Richard Beard

Abstract

The blood-brain barrier (BBB) consists of a network of microvessels containing an inner lining of endothelial cells which shields the CNS from harmful substances circulating in the blood. Neuroinflammation can disrupt BBB function and trigger angiogenesis, which contributes to CNS demyelinating disorders such as multiple sclerosis (MS). Decorin is an extracellular matrix proteoglycan that has recently garnered attention for its potential role in modulating BBB integrity and function.

We used the CreERT2–loxP genetic recombination system to achieve inducible BBB endothelial cell-specific decorin knockout in adult mice, aiming to investigate its impact on aberrant angiogenesis and barrier dysfunction during the progression of Experimental Autoimmune Encephalomyelitis (EAE), a murine demyelinating disease model for MS. Immunofluorescence confocal microscopy was conducted on brain slices of mice who underwent EAE to compare angiogenesis levels and barrier function between decorin knockout (Cre+) and control (Cre- littermate) mice.

Our preliminary findings suggest that mice lacking decorin exhibit reduced angiogenesis and increased barrier function during disease progression compared to their Cre- littermates. This implies that decorin upregulation during EAE can adversely affect the BBB. Our study highlights the potential implications of decorin modulation in maintaining BBB integrity and its therapeutic promise for treating CNS disorders like multiple sclerosis.

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