Felicia Rodriguez

MIT Department: Biological Engineering
Undergraduate Institution: New Mexico State University, Las Cruces
Faculty Mentor: Forest White
Research Supervisor: Nader Morshed
Website: LinkedIn

Biography

I am Felicia Rodriguez from Las Cruces, NM. I am studying chemical engineering and minoring in biochemistry and biomedical engineering at New Mexico State University. I am most interested in interdisciplinary, translational research that seeks to address issues with declined neurological function and neurodegenerative diseases. I intend to obtain my doctoral degree in biomedical engineering focusing on neurological issues. In my free time I like to rock climb, explore the Organ Mountains with my dogs, and play games with my friends.

2019 Research Abstract

Examining Siglec Signaling in Alzheimer’s Disease

Felicia Rodriguez1, Nader Morshed2, Forest White2
1Department of Chemical and Materials Engineering, New Mexico State University
2Department of Biological Engineering, Massachusetts Institute of Technology

Alzheimer’s Disease (AD) is a form of accelerated neurodegeneration and the most common form of dementia. There are currently few therapeutic options for AD patients, but the immune inflammatory response presents a potential therapeutic target once there is understanding of the underlying cellular signaling networks. We aimed to see if we could identify new targets in the immune system using an untargeted approach to signaling analysis. Using mass spectrometry to evaluate changes in protein phosphorylation of multiple mouse models of AD compared to aged matched controls, we have identified a Siglec signaling receptor that is activated on disease-associated microglial cells. We developed an expression system in BV2 cells with the wild type Siglec-F receptor, as well as inactive receptors where one or both cytoplasmic tyrosine residues have been mutated to phenylalanine. We assayed apoptosis to determine if altering functional tyrosine residues of these receptors will impact cell death and found that cells expressing wild type Siglec-F undergo significantly more apoptosis compared to those with mutated sites. We then treated BV2 cells with SHP099, an inhibitor of inflammatory transcription changes, to identify SHP-2-dependent and -independent signaling networks. This analysis identified other signaling proteins that could potentially be targeted to inhibit apoptosis. From these results, we see a potential to dissect signaling pathways activated by Siglec-F and target distinct phenotypic responses for inhibition. This approach could create a new avenue of therapeutic development for neuroinflammatory diseases.