Apoptosis in medial prefrontal cortex of PTSD rats

2011 ◽  
Vol 26 (S2) ◽  
pp. 1084-1084
Author(s):  
H.J. Zhang ◽  
M. Li ◽  
F. Han ◽  
X.Y. Shi
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Caspase 3 ◽  
Control Group ◽  
Mrna Levels ◽  
Post Traumatic Stress ◽  
Green Fluorescence ◽  
Caspase 9 ◽  
Post Traumatic ◽  
And Control

IntroductionA critical region of PTSD is the medial prefrontal cortex, which may be impaired in this disorder. Neuroimaging studies have reported reduced cortical volumes and neuronal integrity, as well as decreased function in medial prefrontal structures in this disorder.ObjectivesThe aim of this study is to find whether mPFC neurons have cell apoptosis, which may lead to the dysfunction of mPFC of PTSD.MethodsThe group to test apotosis was divided into SPS after1d, 4d, 7d, 14d and control group. Expression of caspase-9 and caspase-3 were detected by immunohistochemistry, immunofluorescence, western blotting and RT-PCR.ResultsCaspase-3 was located in cytoplasm. Evaluation of Caspase-3 immunohistochemistry showed a significant increased in the SPS-1d, SPS-4d and SPS-7d compared with the normal control group, then gradually decreased in SPS-14d. Caspase-9-positive cells were expressed in the control group and the SPS groups, The positive expression was green fluorescence, which in cell body, membrane, and processes. The mRNA levels of Caspase-9 in the SPS rats were significant increased on days 1d and 4d then gradually decreased. The Caspase-3 mRNA levels peaked at SPS-7d, then decreased on SPS-14d.ConclusionsThe mPFC neuronal apoptosis through mintochodrial pathway would play an important role in the dysfunction of mPFC in post traumatic stress disorder patients.

scholarly journals Identification of DNA Methylation Changes That Predict Onset of Post-traumatic Stress Disorder and Depression Following Physical Trauma

2021 ◽  
Vol 15 ◽  
Author(s):  
Carina A. Martin ◽  
Rany Vorn ◽  
Martin Schrieber ◽  
Chen Lai ◽  
Sijung Yun ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Stressful Events ◽  
Control Group ◽  
Post Traumatic Stress ◽  
Physical Trauma ◽  
Post Traumatic ◽  
And Control

Post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) are commonly experienced after exposure to highly stressful events, including physical trauma, yet, biological predictors remain elusive. Methylation of DNA may provide key insights, as it likely is reflective of factors that may increase the risk in trauma patients, as DNA methylation is altered by previous stressors. Here, we compared DNA methylation patterns using bisulfite sequencing in patients with a physical trauma that required more than a 24-h hospitalization (n = 33). We then compared DNA methylation in patients who developed and compared the following groups (1) PTSD and MDD; n = 12), (2) MDD (patients with MDD only; n = 12), and (3) control (patients who did not have PTSD or MDD; n = 9), determined by the PTSD Checklist (PCL-5) and Quick Inventory of Depressive Symptomatology (QIDS) at 6-months follow-up. We identified 17 genes with hypermethylated cytosine sites and 2 genes with hypomethylated sites in comparison between PTSD and control group. In comparison between MDD and control group, we identified 12 genes with hypermethylated cytosine sites and 6 genes with hypomethylated sites. Demethylation of these genes altered the CREB signaling pathway in neurons and may represent a promising therapeutic development target for PTSD and MDD. Our findings suggest that epigenetic changes in these gene regions potentially relate to the onset and symptomology of PTSD and MDD and could be used as potential biomarkers in predicting the onset of PTSD or MDD following traumatic events.

scholarly journals Gasdermine E-Dependent Mitochondrial Pyroptotic Pathway in Dermatomyositis: A Possible Mechanism of Perifascicular Atrophy

2020 ◽  
Vol 79 (5) ◽  
pp. 551-561
Author(s):  
Meirong Liu ◽  
Ling Li ◽  
Tingjun Dai ◽  
Ying Hou ◽  
Wei Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Immunohistochemical Analysis ◽  
Positive Staining ◽  
Mrna Levels ◽  
Mitochondrial Apoptosis ◽  
Histologic Feature ◽  
Caspase 9 ◽  
Perifascicular Atrophy ◽  
And Control

Abstract Different mechanisms have been proposed to explain the pathological basis of perifascicular atrophy (PFA), a pathognomonic histologic feature of dermatomyositis (DM); however, the detailed mechanisms remain to be elucidated. There is mitochondrial dysfunction in PFA and expression of mitochondrial apoptosis molecules has been reported in DM. Overexpression of gasdermin E (GSDME) can turn mitochondrial apoptosis to mitochondrial pyroptosis, a newly characterized form of programmed cell death. We determined the expression of proteins involved in the caspase-3- and GSDME-dependent mitochondrial pyroptotic pathway, including BAX, BAK, cytochrome C, caspase-9, caspase-3, GSDME, and IL-1α, in biopsied muscles from DM and control patients. Immunohistochemical analysis showed that those markers were expressed in most fibers in PFA in DM. GSDME-positive and IL-1α-positive staining was mainly localized around punched-out vacuoles or sarcolemma. These markers were significantly upregulated at the protein and mRNA levels in DM versus controls. Our results suggest that caspase-3- and GSDME-dependent mitochondrial pyroptosis are involved in the pathogenetic mechanisms of PFA in DM and that targeting GSDME-dependent mitochondrial pyroptosis may be an effective therapeutic approach for this condition.

scholarly journals Diminished medial prefrontal cortex activation during the recollection of stressful events is an acquired characteristic of PTSD

2017 ◽  
Vol 48 (7) ◽  
pp. 1128-1138 ◽  
Author(s):  
M. K. Dahlgren ◽  
L. M. Laifer ◽  
M. B. VanElzakker ◽  
R. Offringa ◽  
K. C. Hughes ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Twin Studies ◽  
Stressful Events ◽  
Functional Magnetic Resonance ◽  
Post Traumatic Stress ◽  
Post Traumatic

AbstractBackgroundPrevious research has shown relatively diminished medial prefrontal cortex activation and heightened psychophysiological responses during the recollection of personal events in post-traumatic stress disorder (PTSD), but the origin of these abnormalities is unknown. Twin studies provide the opportunity to determine whether such abnormalities reflect familial vulnerabilities, result from trauma exposure, or are acquired characteristics of PTSD.MethodsIn this case–control twin study, 26 male identical twin pairs (12 PTSD; 14 non-PTSD) discordant for PTSD and combat exposure recalled and imagined trauma-unrelated stressful and neutral life events using a standard script-driven imagery paradigm during functional magnetic resonance imaging and concurrent skin conductance measurement.ResultsDiminished activation in the medial prefrontal cortex during Stressful v. Neutral script-driven imagery was observed in the individuals with PTSD, relative to other groups.ConclusionsDiminished medial prefrontal cortex activation during Stressful v. Neutral script-driven imagery may be an acquired characteristic of PTSD. If replicated, this finding could be used prospectively to inform diagnosis and the assessment of treatment response.

Single-prolonged stress induced mitochondrial - dependent apoptosis in hippocampus in the rat model of post-traumatic stress disorder

2011 ◽  
Vol 26 (S2) ◽  
pp. 1083-1083
Author(s):  
M.X. Li ◽  
F. Han ◽  
J.D. Liu ◽  
X.Y. Shi
Keyword(s):  
Cytochrome C ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Caspase 3 ◽  
Stress Disorder ◽  
Post Traumatic Stress ◽  
Caspase 9 ◽  
Post Traumatic ◽  
Induced Apoptosis ◽  
Prolonged Stress

ObjectiveThe aim of this study was to reveal the possible mechanisms involved in apoptosis induced by single prolonged stress (SPS) in hippocampus of post-traumatic stress disorder (PTSD) rats.MethodsSPS is one of the animal models proposed for PTSD. Wistar rats were killed at 1, 4, 7, 14 and 28days after exposure to SPS. Expression of caspase-9, caspase-3, cytochrome c, Bcl-2 and Bax was detected by immunohistochemistry, immunofluorescence, western blotting and electron microscopy. Apoptotic cells were assessed by TUNEL method.ResultsOur results showed apoptotic cells were significantly increased in hippocampus of SPS rats, accompanied by release of cytochrome c from the mitochondria into the cytosol, increase of caspase-9 and caspase-3 expression and decrease of the Bcl-2 / Bax ratio.ConclusionThe results indicate that SPS induced apoptosis in hippocampus of PTSD rats, and the mitochondrial pathway was involved in the process of SPS induced apoptosis. *National Natural Science Foundation of China

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