Murray State University
Quantification of Genetic Variances in Functionally Reactive Astrocytes
Institution
Murray State University
Faculty Advisor/ Mentor
David Canning
Abstract
Gliosis is the term used to describe the response of the Central Nervous System to trauma (such as Alzheimer’s and blunt trauma to the Central Nervous System). One class of cells in the gliotic response are astrocytes which produce local inflammation and, more importantly, produce molecular inhibitors that negate neural regeneration. The deposition of chondroitin sulfate is believed to be the main neural inhibitor produced by astrocytes. The presence of chondroitin sulfate inhibits cells of the nervous system from forming new neural connections leading to permanent neurological damage. The changes that occur in functionally reactive astrocytes are genetic in origin and quantification of these changes at the transcriptive level of genetic expression would be advantageous to seeking a reversal of trauma induced paralysis. Our goal in this project is to identify, and quantify, the genetic expression profiles that lead to the induction of the reactive astrocyte phenotype. To date, we have identified a small cluster of genes whose expression profiles closely mimic the induction of reactive astrogliosis.
Quantification of Genetic Variances in Functionally Reactive Astrocytes
Gliosis is the term used to describe the response of the Central Nervous System to trauma (such as Alzheimer’s and blunt trauma to the Central Nervous System). One class of cells in the gliotic response are astrocytes which produce local inflammation and, more importantly, produce molecular inhibitors that negate neural regeneration. The deposition of chondroitin sulfate is believed to be the main neural inhibitor produced by astrocytes. The presence of chondroitin sulfate inhibits cells of the nervous system from forming new neural connections leading to permanent neurological damage. The changes that occur in functionally reactive astrocytes are genetic in origin and quantification of these changes at the transcriptive level of genetic expression would be advantageous to seeking a reversal of trauma induced paralysis. Our goal in this project is to identify, and quantify, the genetic expression profiles that lead to the induction of the reactive astrocyte phenotype. To date, we have identified a small cluster of genes whose expression profiles closely mimic the induction of reactive astrogliosis.