Abstract
To investigate the changes in the expression of specific genes that occur during the acute-to-chronic post-stroke phase, we identified differentially expressed genes (DEGs) between naive cortical tissues and peri-infarct tissues at 1, 4, and 8 weeks after photothrombotic stroke. The profiles of DEGs were subjected to the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and gene ontology analyses, followed by string analysis of the protein–protein interactions (PPI) of the products of these genes. We found 3771, 536, and 533 DEGs at 1, 4, and 8 weeks after stroke, respectively. A marked decrease in biological–process categories, such as brain development and memory, and a decrease in neurotransmitter synaptic and signaling pathways were observed 1 week after stroke. The PPI analysis showed the downregulation of Dlg4, Bdnf, Gria1, Rhoa, Mapk8, and glutamatergic receptors. An increase in biological–process categories, including cell population proliferation, cell adhesion, and inflammatory responses, was detected at 4 and 8 weeks post-stroke. The KEGG pathways of complement and coagulation cascades, phagosomes, antigen processing, and antigen presentation were also altered. CD44, C1, Fcgr2b, Spp1, and Cd74 occupied a prominent position in network analyses. These time-dependent changes in gene profiles reveal the unique pathophysiological characteristics of stroke and suggest new therapeutic targets for this disease.
Highlights
Stroke is the second leading global cause of death and contributes to years lived with disability worldwide [1]
The motor outcome was evaluated in rats using the modified neurological severity score. mNSS scores ranged from 0 up to 14
To understand the differences in gene expression that occur over time after stroke
Summary
Stroke is the second leading global cause of death and contributes to years lived with disability worldwide [1]. The majority of patients with stroke survive the acute phase and live with disability for many years [2] The only drug that is currently available to treat stroke is tissue plasminogen activator, which has a very limited time window (4.5 h) [3]; rehabilitation is the only therapeutic option for patients with stroke who suffer from disability. Neural repair arises spontaneously after stroke, continues through the semi-acute phase and slowly diminishes with time [2]. Most research efforts aimed at promoting recovery focus on the early phase: recovery from chronic stroke is not in the spotlight. Because the long-term disability is much longer than the intensive recovery time, understanding the residual processes and finding therapeutic targets over the critical recovery period would be helpful for these patients
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
