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Published on: September 11, 2017
Altered expression of novel genes in the cerebral cortex following experimental brain injury
Nobuhide Kobori1, Guy L Clifton, Pramod Dash
1The Vivian L. Smith Center for Neurological Research, Department of Neurobiology and Anatomy, The University of Texas Medical School, PO Box 20708, Houston, TX 77255, USA.
Abstract:
Damage to the cerebral cortex results in neurological impairments such as motor, attention, memory and executive dysfunctions. To examine the molecular mechanisms contributing to these deficits, mRNA expression was profiled using high-density cDNA microarray hybridization after experimental cortical impact injury in mice. The mRNA levels at 2 h, 6 h, 24 h, 3 days and 14 days after injury were compared with those of control animals. This revealed 86 annotated genes and 24 expression sequence tags (ESTs) as being differentially expressed with a 1.5-fold or greater change. Quantitative real-time PCR analysis was used to independently verify these results for selected genes. Seven functional classes of genes were found to be altered following injury, including transcription factors, signal transduction genes and inflammatory proteins. While a few of these genes have been previously reported to be differentially regulated following injury, the most of the genes have not been previously implicated in traumatic brain injury (TBI) pathophysiology. For example, consistent with previous reports, the transcription factor c-jun and the neurotrophic factor bdnf mRNA levels were altered as a result of TBI. Among the novel genes, the mRNA levels for the high mobility group protein 1 (hmg-1), the regulator of G-protein signaling 2 (rgs-2), the transforming growth factor beta inducible early growth response (tieg), the inhibitor of DNA binding 3 (id3), and the heterogeneous nuclear ribonucleoprotein H (hnrnp h) were changed following injury. The functional significance of these genes in neurite outgrowth, neuronal regeneration, and plasticity following injury are discussed.
Insights
This study investigated gene expression changes after experimental traumatic brain injury (TBI) in mice. Researchers identified novel genes involved in brain repair, offering new insights into TBI pathophysiology and potential therapeutic targets.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Cerebral cortex damage leads to motor, attention, memory, and executive function deficits.
- Understanding the molecular mechanisms underlying these neurological impairments is crucial for developing effective treatments.
Purpose of the Study:
- To identify genes differentially expressed following experimental cortical impact injury in mice.
- To elucidate the molecular pathways involved in traumatic brain injury (TBI) pathophysiology.
Main Methods:
- High-density cDNA microarray hybridization was used to profile mRNA expression at multiple time points post-injury.
- Quantitative real-time PCR was employed for independent verification of gene expression changes.
Main Results:
- 86 annotated genes and 24 expression sequence tags (ESTs) showed differential expression (≥1.5-fold change) after TBI.
- Seven functional classes of genes, including transcription factors, signal transduction genes, and inflammatory proteins, were altered.
- Novel genes such as high mobility group protein 1 (hmg-1) and regulator of G-protein signaling 2 (rgs-2) were identified as potentially involved in TBI.
Conclusions:
- The study identified numerous genes, many previously unlinked to TBI, that are altered following cortical injury.
- These findings provide new molecular targets for understanding and potentially treating neurological deficits associated with TBI.
- The identified genes may play significant roles in neurite outgrowth, neuronal regeneration, and plasticity post-injury.
