5.00
Hdl Handle:
http://hdl.handle.net/10755/158947
Type:
Presentation
Title:
Long Term Epigenetic Modification after Mild Traumatic Brain Injury
Abstract:
Long Term Epigenetic Modification after Mild Traumatic Brain Injury
Conference Sponsor:Midwest Nursing Research Society
Conference Year:2009
Author:Darwish, Hala, Ph.D
P.I. Institution Name:Univ.of Illinois at Chicago
Title:Medical-Surgical Nursing
Contact Address:845 S Damen (MC/802) Rm 229, Chicago, IL, 60612, USA
Contact Telephone:312-355-0282
Co-Authors:H. Darwish, T. Briones, Medical Surgical Nursing, Univ.of Illinois at Chicago, Chicago, IL;
Studies show that epigenetic modifications such as DNA methylation and histone acetylation play a role in normal and pathological brain functioning. Although DNA methyltransferases (DNMT, enzymes that facilitate DNA methylation) are highly expressed in neurons, there is a dearth of information on epigenetic changes following traumatic brain injury (TBI). In the present study, we examined changes in DNA methylation and histone modifications following recovery from mild TBI. Adult male Wistar rats [n = 7 mild tbi and n = 6 shams] weighing approximately 300-350 grams were included in the study. Mild TBI was induced in anesthetized animals through controlled cortical impact injury (1.5 mm compression) while sham rats received the same anesthesia and surgical incision without cortical injury. Following surgery, rats were allowed to recover for 35 days with free access to food and water. Rats were sacrificed after the predetermined recovery period, brains were removed and the hippocampus, brain region involved in learning and memory and emotional processing, was prepared for immunohistochemistry. Our results showed that DNMT3b (marker for de novo methylation) is significantly increased in the hippocampus of mild TBI rats when compared to the sham animals. In contrast, DNMT1 (marker for development and maintenance methylation) is significantly reduced in mild TBI rats in comparison to the sham animals. In addition, we found that Sir2 (sirtuin, a histone deacetylase) expression was significantly decreased in the mild TBI animals compared to the sham rats. These results suggest that epigenetic changes following mild TBI can persist for weeks after injury. Since both DNA methylation and histone acetylation are involved in regulating gene expression, the clinical relevance of our data lies in understanding the changes in gene expression associated with neuroprotection and neurodegeneration. Supported by NR007666 and NINR T32 NR007075-14
Repository Posting Date:
26-Oct-2011
Date of Publication:
17-Oct-2011
Sponsors:
Midwest Nursing Research Society

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleLong Term Epigenetic Modification after Mild Traumatic Brain Injuryen_GB
dc.identifier.urihttp://hdl.handle.net/10755/158947-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Long Term Epigenetic Modification after Mild Traumatic Brain Injury</td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Midwest Nursing Research Society</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2009</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Darwish, Hala, Ph.D</td></tr><tr class="item-institute"><td class="label">P.I. Institution Name:</td><td class="value">Univ.of Illinois at Chicago</td></tr><tr class="item-author-title"><td class="label">Title:</td><td class="value">Medical-Surgical Nursing</td></tr><tr class="item-address"><td class="label">Contact Address:</td><td class="value">845 S Damen (MC/802) Rm 229, Chicago, IL, 60612, USA</td></tr><tr class="item-phone"><td class="label">Contact Telephone:</td><td class="value">312-355-0282</td></tr><tr class="item-email"><td class="label">Email:</td><td class="value">hdarwish@uic.edu</td></tr><tr class="item-co-authors"><td class="label">Co-Authors:</td><td class="value">H. Darwish, T. Briones, Medical Surgical Nursing, Univ.of Illinois at Chicago, Chicago, IL;</td></tr><tr><td colspan="2" class="item-abstract">Studies show that epigenetic modifications such as DNA methylation and histone acetylation play a role in normal and pathological brain functioning. Although DNA methyltransferases (DNMT, enzymes that facilitate DNA methylation) are highly expressed in neurons, there is a dearth of information on epigenetic changes following traumatic brain injury (TBI). In the present study, we examined changes in DNA methylation and histone modifications following recovery from mild TBI. Adult male Wistar rats [n = 7 mild tbi and n = 6 shams] weighing approximately 300-350 grams were included in the study. Mild TBI was induced in anesthetized animals through controlled cortical impact injury (1.5 mm compression) while sham rats received the same anesthesia and surgical incision without cortical injury. Following surgery, rats were allowed to recover for 35 days with free access to food and water. Rats were sacrificed after the predetermined recovery period, brains were removed and the hippocampus, brain region involved in learning and memory and emotional processing, was prepared for immunohistochemistry. Our results showed that DNMT3b (marker for de novo methylation) is significantly increased in the hippocampus of mild TBI rats when compared to the sham animals. In contrast, DNMT1 (marker for development and maintenance methylation) is significantly reduced in mild TBI rats in comparison to the sham animals. In addition, we found that Sir2 (sirtuin, a histone deacetylase) expression was significantly decreased in the mild TBI animals compared to the sham rats. These results suggest that epigenetic changes following mild TBI can persist for weeks after injury. Since both DNA methylation and histone acetylation are involved in regulating gene expression, the clinical relevance of our data lies in understanding the changes in gene expression associated with neuroprotection and neurodegeneration. Supported by NR007666 and NINR T32 NR007075-14</td></tr></table>en_GB
dc.date.available2011-10-26T21:33:11Z-
dc.date.issued2011-10-17en_GB
dc.date.accessioned2011-10-26T21:33:11Z-
dc.description.sponsorshipMidwest Nursing Research Societyen_GB
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