Discipline: Biological Sciences
Subcategory: Physiology and Health
Kinnon Ward - Tuskegee University
Co-Author(s): Janice M. Diaz-Otero and Anne M. Dorrance, Michigan State University, East Lansing, MI
Stroke is a leading cause of disability worldwide. In patients, stroke can lead to cardiac complications increasing the risk of death. Studies suggest that ischemic stroke causes cardiac injury in response to elevated catecholamines released by the sympathetic nervous system (SNS). It is unclear if cardiac inflammation occurs as a result of injury after stroke. Macrophages are a key component in inflammatory processes. We hypothesized that an increase in M1 macrophage activity will cause cardiac inflammation in normotensive Sprague Dawley (SD) rats following ischemic stroke. Ischemic stroke was induced in 18-week-old male SD rats by middle cerebral artery (MCA) occlusion (MCAO). After 1 hour of ischemia, rats were reperfused and divided into two groups; one group of rats was euthanized at 24 hours and the other 7 days (d) post-stroke. Sham operated rats were used as control. Real time-PCR was performed to measure mRNA expression of the M1 pro-inflammatory marker interleukin-1 beta (IL-1β) along with general macrophage marker CD163. mRNA expression of the cell adhesion molecule monocyte chemoattractant protein-1 (MCP-1) that is released by damaged cardiac cells to signal macrophages was examined. We noticed a decrease in the mRNA expression of general macrophage marker CD163 and M1 specific macrophage marker IL-1β. Our results also showed a decrease in the mRNA expression of MCP-1 in stroke rats compared to sham. This study suggests that in normotensive rats there is reduced macrophage infiltration in the heart after an ischemic stroke. However, we still need to consider the effects of stroke in cardiac injury in the presence of comorbidities such as hypertension.
Funder Acknowledgement(s): National Institutes of Health grant R25HL103156
Faculty Advisor: Anne M. Dorrance, firstname.lastname@example.org
Role: For this project, I extracted RNA from the heart samples of stroke and sham operated Sprague Dawley rats. I homogenized the samples using Trizol as a reagent. After I extracted the RNA, I tested the nucleic acid concentration of the samples using NanoDrop technology. Following that, I used the RNA samples to perform qRT-PCR to examine the gene expression of both general and pro-inflammatory macrophage mediators along with cell adhesion molecules. Lastly, I compared and analyzed the data collected from stroke and sham operated rats using Prisms software.