Exploring the Inflammatory Effects of Glioma-Derived Stem Cell Matrix on Astrocyte Phenotypes for Wound Healing

Presenter

Trisha Raman

Campus

UMass Amherst

Sponsor

Chase Cornelison, Department of Biomedical Engineering, UMass Amherst

Schedule

Session 3, 1:30 PM - 2:15 PM [Schedule by Time][Poster Grid for Time/Location]

Location

Poster Board A79, Campus Center Auditorium, Row 4 (A61-A80) [Poster Location Map]

Abstract

Trauma to the central and peripheral nervous systems such as traumatic brain injury, spinal cord injury and stroke leads to significant loss of function. This poses a considerable burden for patients as this loss of function often leads to lifelong disabilities due to the limited regenerative capacity of nervous tissue. Recent advancements have discovered the importance of astrocytes and their integral role in recovery following spinal cord injury. Manipulation of astrocyte pro- (A1) and anti- (A2) inflammatory phenotypes can provide valuable insights into astrocyte behavior, migration and wound healing potential, induced through cytokine activation. The combination of interleukin (IL)-1α, tumor necrosis factor (TNF) and complement component 1q (C1q) exhibits the strongest A1, or neurotoxic phenotype. Interleukin-10 has shown to induce the A2, or neuroprotective phenotype. Cell migration effects through tumor-derived matrices supports a novel approach in inducing astrocyte reactivity through matrix activation. Our research describes a methodology to discover and reprogram astrocyte behavior to promote neuroprotective phenotypes through cellular interaction with matrix glycoproteins. Through a migration scratch assay, we were able to explore the A1- and A2- inducing nature of glioblastoma stem cell (GSC) matrix on astrocytes. After quantifying results, cell migration was found to vary between each GSC line, leading us to infer that GSC glycoproteins promote astrocyte activation. Further quantification through qPCR will allow us to examine the markers within each GSC matrix and confirm which proteins specifically induce A1 and A2 activity. With this knowledge, we will be better able to understand and manipulate astrocyte responses to neural injury, and develop effective therapeutics to promote wound healing. 

Keywords

neuroregeneration, bioengineering, cancer matrix, medical therapeutics, traumatic brain injury

Research Area

Neuroscience and Cognitive Science

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