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Article ; Online: Neuroinflammation Profiling of Brain Cytokines Following Repeated Blast Exposure.

Heyburn, Lanier / Batuure, Andrew / Wilder, Donna / Long, Joseph / Sajja, Venkatasivasai Sujith

International journal of molecular sciences

2023 Volume 24, Issue 16

Abstract: Due to use of explosive devices and heavy weapons systems in modern conflicts, the effect of BW on the brain and body is of increasing concern. These exposures have been commonly linked with neurodegenerative diseases and psychiatric disorders in veteran ...

Abstract	Due to use of explosive devices and heavy weapons systems in modern conflicts, the effect of BW on the brain and body is of increasing concern. These exposures have been commonly linked with neurodegenerative diseases and psychiatric disorders in veteran populations. A likely neurobiological link between exposure to blasts and the development of neurobehavioral disorders, such as depression and PTSD, could be neuroinflammation triggered by the blast wave. In this study, we exposed rats to single or repeated BW (up to four exposures-one per day) at varied intensities (13, 16, and 19 psi) to mimic the types of blast exposures that service members may experience in training and combat. We then measured a panel of neuroinflammatory markers in the brain tissue with a multiplex cytokine/chemokine assay to understand the pathophysiological process(es) associated with single and repeated blast exposures. We found that single and repeated blast exposures promoted neuroinflammatory changes in the brain that are similar to those characterized in several neurological disorders; these effects were most robust after 13 and 16 psi single and repeated blast exposures, and they exceeded those recorded after 19 psi repeated blast exposures. Tumor necrosis factor-alpha and IL-10 were changed by 13 and 16 psi single and repeated blast exposures. In conclusion, based upon the growing prominence of negative psychological health outcomes in veterans and soldiers with a history of blast exposures, identifying the molecular etiology of these disorders, such as blast-induced neuroinflammation, is necessary for rationally establishing countermeasures and treatment regimens.
MeSH term(s)	Animals ; Rats ; Cytokines ; Neuroinflammatory Diseases ; Brain ; Tumor Necrosis Factor-alpha ; Biological Assay
Chemical Substances	Cytokines ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2023-08-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241612564
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: TDP-43 overexpression impairs presynaptic integrity.

Heyburn, Lanier / Moussa, Charbel E-H

Neural regeneration research

2017 Volume 11, Issue 12, Page(s) 1910–1911

Language	English
Publishing date	2017-01-31
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.195272
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Article ; Online: TDP-43 in the spectrum of MND-FTLD pathologies.

Heyburn, Lanier / Moussa, Charbel E-H

Molecular and cellular neurosciences

2017 Volume 83, Page(s) 46–54

Abstract: The relationship between RNA-binding proteins, particularly TAR DNA binding protein 43 (TDP-43), and neurodegeneration is an important area of research. TDP-43 is involved in so many cellular processes that perturbation of protein homeostasis can lead to ...

Abstract	The relationship between RNA-binding proteins, particularly TAR DNA binding protein 43 (TDP-43), and neurodegeneration is an important area of research. TDP-43 is involved in so many cellular processes that perturbation of protein homeostasis can lead to countless downstream effects. Understanding what leads to this disease-related protein imbalance and the resulting cellular and molecular effects will help to develop targets for disease intervention, whether it be prevention of protein accumulation, or addressing a secondary effect of protein accumulation. Here we review the current literature of TDP-43 and TDP-43 pathologies, the effects of TDP-43 overexpression and disruption of synaptic proteins through its binding of messenger RNA, leading to synaptic dysfunction. This review highlights some of the still-limited knowledge of the protein TDP-43 and how it can contribute to disease.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/pathology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Frontotemporal Lobar Degeneration/genetics ; Frontotemporal Lobar Degeneration/metabolism ; Humans ; Motor Neuron Disease/genetics ; Motor Neuron Disease/metabolism ; Protein Aggregation, Pathological/genetics ; Protein Aggregation, Pathological/metabolism ; Synaptic Transmission
Chemical Substances	DNA-Binding Proteins ; TARDBP protein, human
Language	English
Publishing date	2017-07-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/j.mcn.2017.07.001
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Article: The Role of TDP-43 in Military-Relevant TBI and Chronic Neurodegeneration.

Heyburn, Lanier / Sajja, Venkata S S S / Long, Joseph B

Frontiers in neurology

2019 Volume 10, Page(s) 680

Abstract: Due largely to the use of improvised explosive devices (IEDs) and other explosives in recent military conflicts, blast-related TBI has emerged as a prominent injury sustained by warfighters. In the recent wars in Iraq and Afghanistan, traumatic brain ... ...

Abstract	Due largely to the use of improvised explosive devices (IEDs) and other explosives in recent military conflicts, blast-related TBI has emerged as a prominent injury sustained by warfighters. In the recent wars in Iraq and Afghanistan, traumatic brain injury (TBI) has been one of the most common types of injury sustained by soldiers and military personnel; of the ~380,000 TBIs reported in service members from 2000 to 2017, 82.3% were classified as mild (mTBI). While mTBI is associated with normal structural imaging, brief or no loss of consciousness, and rapid recovery of mental state, mTBI can nevertheless lead to persistent behavioral and cognitive effects. As in other cases of mTBI, exposure to low-level blast often does not cause immediate overt neurological effects, but may similarly lead to persistent behavioral and cognitive deficits. These effects are likely to be compounded when multiple exposures to blast and/or impact are sustained, since there is increasing evidence that multiple mTBIs can lead to chronic neurodegeneration. One common form of this deleterious outcome is frontotemporal lobar degeneration (FTLD), which is a progressive neurodegenerative process marked by atrophy of the frontal and temporal lobes, leading to frontotemporal dementia, a common form of dementia affecting behavior, cognition and language. About half of all cases of FTLD are marked by TAR-DNA binding protein (TDP-43)-positive protein inclusions. TDP-43, a DNA/RNA binding protein, controls the expression of thousands of genes and is associated with several neurodegenerative diseases including amyotrophic lateral sclerosis, Alzheimer's disease, Huntington's disease, and chronic traumatic encephalopathy. TDP-43 abnormalities have also been associated with traumatic brain injury in both pre-clinical and clinical studies. The role of TDP-43 in the manifestation of FTLD pathology in military TBI cases is currently unclear, and to date there has been only a limited number of pre-clinical studies addressing the effects of repeated blast-related mild TBI (rbTBI) in relation to FTLD and TDP-43. This review will summarize some of these findings and address the concerns and critical knowledge gaps associated with FTLD manifestation with military populations, as well as clinical findings on other forms of mTBI.
Language	English
Publishing date	2019-06-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2019.00680
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Article: Differential effects on TDP-43, piezo-2, tight-junction proteins in various brain regions following repetitive low-intensity blast overpressure.

Heyburn, Lanier / Dahal, Shataakshi / Abutarboush, Rania / Reed, Eileen / Urioste, Rodrigo / Batuure, Andrew / Wilder, Donna / Ahlers, Stephen T / Long, Joseph B / Sajja, Venkatasivasai Sujith

Frontiers in neurology

2023 Volume 14, Page(s) 1237647

Abstract: Introduction: Mild traumatic brain injury (mTBI) caused by repetitive low-intensity blast overpressure (relBOP) in military personnel exposed to breaching and heavy weapons is often unrecognized and is understudied. Exposure to relBOP poses the risk of ... ...

Abstract	Introduction: Mild traumatic brain injury (mTBI) caused by repetitive low-intensity blast overpressure (relBOP) in military personnel exposed to breaching and heavy weapons is often unrecognized and is understudied. Exposure to relBOP poses the risk of developing abnormal behavioral and psychological changes such as altered cognitive function, anxiety, and depression, all of which can severely compromise the quality of the life of the affected individual. Due to the structural and anatomical heterogeneity of the brain, understanding the potentially varied effects of relBOP in different regions of the brain could lend insights into the risks from exposures. Methods: In this study, using a rodent model of relBOP and western blotting for protein expression we showed the differential expression of various neuropathological proteins like TDP-43, tight junction proteins (claudin-5, occludin, and glial fibrillary acidic protein (GFAP)) and a mechanosensitive protein (piezo-2) in different regions of the brain at different intensities and frequency of blast. Results: Our key results include (i) significant increase in claudin-5 after 1x blast of 6.5 psi in all three regions and no definitive pattern with higher number of blasts, (ii) significant increase in piezo-2 at 1x followed by significant decrease after multiple blasts in the cortex, (iii) significant increase in piezo-2 with increasing number of blasts in frontal cortex and mixed pattern of expression in hippocampus and (iv) mixed pattern of TDP-3 and GFAP expression in all the regions of brain. Discussion: These results suggest that there are not definitive patterns of changes in these marker proteins with increase in intensity and/or frequency of blast exposure in any particular region; the changes in expression of these proteins are different among the regions. We also found that the orientation of blast exposure (e.g. front vs. side exposure) affects the altered expression of these proteins.
Language	English
Publishing date	2023-10-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2023.1237647
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Article: Blast Waves Cause Immune System Dysfunction and Transient Bone Marrow Failure in a Mouse Model.

Bergmann-Leitner, Elke S / Bobrov, Alexander G / Bolton, Jessica S / Rouse, Michael D / Heyburn, Lanier / Pavlovic, Radmila / Garry, Brittany I / Alamneh, Yonas / Long, Joseph / Swierczewski, Brett / Tyner, Stuart / Getnet, Derese / Sajja, Venkatasivasai S / Antonic, Vlado

Frontiers in bioengineering and biotechnology

2022 Volume 10, Page(s) 821169

Abstract: Explosive devices, either conventional or improvised, are common sources of injuries during combat, civil unrest, and terror attacks, resulting in trauma from exposure to blast. A blast wave (BW), a near-instantaneous rise in pressure followed by a ... ...

Abstract	Explosive devices, either conventional or improvised, are common sources of injuries during combat, civil unrest, and terror attacks, resulting in trauma from exposure to blast. A blast wave (BW), a near-instantaneous rise in pressure followed by a negative pressure, propagates through the body in milliseconds and can affect physiology for days/months after exposure. Epidemiological data show that blast-related casualties result in significantly higher susceptibility to wound infections, suggesting long-lasting immune modulatory effects from blast exposure. The mechanisms involved in BW-induced immune changes are poorly understood. We evaluated the effects of BW on the immune system using an established murine model. Animals were exposed to BWs (using an Advanced Blast Simulator), followed by longitudinally sampling for 14 days. Blood, bone marrow, and spleen were analyzed for changes in the 1) complete blood count (CBC), and 2) composition of bone marrow cells (BMC) and splenocytes, and 3) concentrations of systemic cytokines/chemokines. Our data demonstrate that BW results in transient bone marrow failure and long-term changes in the frequency and profile of progenitor cell populations. Viability progressively decreased in hematopoietic stem cells and pluripotent progenitor cells. Significant decrease of CD4
Language	English
Publishing date	2022-03-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2719493-0
ISSN	2296-4185
ISSN	2296-4185
DOI	10.3389/fbioe.2022.821169
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Article: Repeated Low-Level Blast Acutely Alters Brain Cytokines, Neurovascular Proteins, Mechanotransduction, and Neurodegenerative Markers in a Rat Model.

Heyburn, Lanier / Abutarboush, Rania / Goodrich, Samantha / Urioste, Rodrigo / Batuure, Andrew / Wheel, Jaimena / Wilder, Donna M / Arun, Peethambaran / Ahlers, Stephen T / Long, Joseph B / Sajja, Venkatasivasai Sujith

Frontiers in cellular neuroscience

2021 Volume 15, Page(s) 636707

Abstract: Exposure to the repeated low-level blast overpressure (BOP) periodically experienced by military personnel in operational and training environments can lead to deficits in behavior and cognition. While these low-intensity blasts do not cause overt ... ...

Abstract	Exposure to the repeated low-level blast overpressure (BOP) periodically experienced by military personnel in operational and training environments can lead to deficits in behavior and cognition. While these low-intensity blasts do not cause overt changes acutely, repeated exposures may lead to cumulative effects in the brain that include acute inflammation, vascular disruption, and other molecular changes, which may eventually contribute to neurodegenerative processes. To identify these acute changes in the brain following repeated BOP, an advanced blast simulator was used to expose rats to 8.5 or 10 psi BOP once per day for 14 days. At 24 h after the final BOP, brain tissue was collected and analyzed for inflammatory markers, astrogliosis (GFAP), tight junction proteins (claudin-5 and occludin), and neurodegeneration-related proteins (Aβ40/42, pTau, TDP-43). After repeated exposure to 8.5 psi BOP, the change in cytokine profile was relatively modest compared to the changes observed following 10 psi BOP, which included a significant reduction in several inflammatory markers. Reduction in the tight junction protein occludin was observed in both groups when compared to controls, suggesting cerebrovascular disruption. While repeated exposure to 8.5 psi BOP led to a reduction in the Alzheimer's disease (AD)-related proteins amyloid-β (Aβ)40 and Aβ42, these changes were not observed in the 10 psi group, which had a significant reduction in phosphorylated tau. Finally, repeated 10 psi BOP exposures led to an increase in GFAP, indicating alterations in astrocytes, and an increase in the mechanosensitive ion channel receptor protein, Piezo2, which may increase brain sensitivity to injury from pressure changes from BOP exposure. Overall, cumulative effects of repeated low-level BOP may increase the vulnerability to injury of the brain by disrupting neurovascular architecture, which may lead to downstream deleterious effects on behavior and cognition.
Language	English
Publishing date	2021-02-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2021.636707
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Article ; Online: Development of Novel 3-D Printed Scaffolds With Core-Shell Nanoparticles for Nerve Regeneration.

Lee, Se-Jun / Zhu, Wei / Heyburn, Lanier / Nowicki, Margaret / Harris, Brent / Zhang, Lijie Grace

IEEE transactions on bio-medical engineering

2017 Volume 64, Issue 2, Page(s) 408–418

Abstract: A traumatic injury of peripheral nerves is serious clinical problem that may lead to major loss of nerve function, affecting quality of patient's life. Currently, nerve autograft is widely used to reconstruct the nerve gap. However, such surgical ... ...

Abstract	A traumatic injury of peripheral nerves is serious clinical problem that may lead to major loss of nerve function, affecting quality of patient's life. Currently, nerve autograft is widely used to reconstruct the nerve gap. However, such surgical procedure suffers from many disadvantages including donor site morbidity and limited availability. In order to address these issues, neural tissue engineering has focused on the development of synthetic nerve scaffolds to support bridging a larger gap and improving nerve generation. For this purpose, we fabricated a novel 3-D biomimetic scaffold, which has tunable porous structure and embedded core-shell nanoparticles with sustained neurogenic factor delivery system, using stereolithography based 3-D printing and coaxial electrospraying techniques. Our results showed that scaffolds with larger porosity significantly improve PC-12 neural cell adhesion compared to ones with smaller porosity. Furthermore, scaffolds embedded with bovine serum albumin containing nanoparticles showed an enhancement in cell proliferation relative to bared control scaffolds. More importantly, confocal microscopy images illustrated that the scaffold with nerve growth factor nanoparticles greatly increased the length of neurites and directed neurite extension of PC-12 cells along the fiber. In addition, the 3-D printed nanocomposite scaffolds also improved the average neurite length of primary cortical neurons. The results in this study demonstrate the potential of this 3-D printed scaffold in improving neural cell function and nerve growth.
MeSH term(s)	Animals ; Biocompatible Materials/chemistry ; Biocompatible Materials/pharmacology ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Cerebral Cortex/cytology ; Drug Carriers ; Nanoparticles/chemistry ; Nanoparticles/toxicity ; Nerve Regeneration/drug effects ; Neurons/drug effects ; PC12 Cells ; Rats ; Spectrometry, Mass, Electrospray Ionization ; Tissue Engineering/methods ; Tissue Scaffolds
Chemical Substances	Biocompatible Materials ; Drug Carriers
Language	English
Publishing date	2017-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	160429-6
ISSN	1558-2531 ; 0018-9294
ISSN (online)	1558-2531
ISSN	0018-9294
DOI	10.1109/TBME.2016.2558493
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Article: Repeated Low-Level Blast Overpressure Leads to Endovascular Disruption and Alterations in TDP-43 and Piezo2 in a Rat Model of Blast TBI.

Heyburn, Lanier / Abutarboush, Rania / Goodrich, Samantha / Urioste, Rodrigo / Batuure, Andrew / Statz, Jonathan / Wilder, Donna / Ahlers, Stephen T / Long, Joseph B / Sajja, Venkata Siva Sai Sujith

Frontiers in neurology

2019 Volume 10, Page(s) 766

Abstract: Recent evidence linking repeated low-level blast overpressure exposure in operational and training environments with neurocognitive decline, neuroinflammation, and neurodegenerative processes has prompted concern over the cumulative deleterious effects ... ...

Abstract	Recent evidence linking repeated low-level blast overpressure exposure in operational and training environments with neurocognitive decline, neuroinflammation, and neurodegenerative processes has prompted concern over the cumulative deleterious effects of repeated blast exposure on the brains of service members. Repetitive exposure to low-level primary blast may cause symptoms (subclinical) similar to those seen in mild traumatic brain injury (TBI), with progressive vascular and cellular changes, which could contribute to neurodegeneration. At the cellular level, the mechanical force associated with blast exposure can cause cellular perturbations in the brain, leading to secondary injury. To examine the cumulative effects of repetitive blast on the brain, an advanced blast simulator (ABS) was used to closely mimic "free-field" blast. Rats were exposed to 1-4 daily blasts (one blast per day, separated by 24 h) at 13, 16, or 19 psi peak incident pressures with a positive duration of 4-5 ms, either in a transverse or longitudinal orientation. Blood-brain barrier (BBB) markers (vascular endothelial growth factor (VEGF), occludin, and claudin-5), transactive response DNA binding protein (TDP-43), and the mechanosensitive channel Piezo2 were measured following blast exposure. Changes in expression of VEGF, occludin, and claudin-5 after repeated blast exposure indicate alterations in the BBB, which has been shown to be disrupted following TBI. TDP-43 is very tightly regulated in the brain and altered expression of TDP-43 is found in clinically-diagnosed TBI patients. TDP-43 levels were differentially affected by the number and magnitude of blast exposures, decreasing after 2 exposures, but increasing following a greater number of exposures at various intensities. Lastly, Piezo2 has been shown to be dysregulated following blast exposure and was here observed to increase after multiple blasts of moderate magnitude, indicating that blast may cause a change in sensitivity to mechanical stimuli in the brain and may contribute to cellular injury. These findings reveal that cumulative effects of repeated exposures to blast can lead to pathophysiological changes in the brain, demonstrating a possible link between blast injury and neurodegenerative disease, which is an important first step in understanding how to prevent these diseases in soldiers exposed to blast.
Language	English
Publishing date	2019-07-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2019.00766
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Article ; Online: Oxidative stress-induced mutagenesis in single-strand DNA occurs primarily at cytosines and is DNA polymerase zeta-dependent only for adenines and guanines.

Degtyareva, Natalya P / Heyburn, Lanier / Sterling, Joan / Resnick, Michael A / Gordenin, Dmitry A / Doetsch, Paul W

Nucleic acids research

2013 Volume 41, Issue 19, Page(s) 8995–9005

Abstract: Localized hyper-mutability caused by accumulation of lesions in persistent single-stranded (ss) DNA has been recently found in several types of cancers. An increase in endogenous levels of reactive oxygen species (ROS) is considered to be one of the ... ...

Abstract	Localized hyper-mutability caused by accumulation of lesions in persistent single-stranded (ss) DNA has been recently found in several types of cancers. An increase in endogenous levels of reactive oxygen species (ROS) is considered to be one of the hallmarks of cancers. Employing a yeast model system, we addressed the role of oxidative stress as a potential source of hyper-mutability in ssDNA by modulation of the endogenous ROS levels and by exposing cells to oxidative DNA-damaging agents. We report here that under oxidative stress conditions the majority of base substitution mutations in ssDNA are caused by erroneous, DNA polymerase (Pol) zeta-independent bypass of cytosines, resulting in C to T transitions. For all other DNA bases Pol zeta is essential for ROS-induced mutagenesis. The density of ROS-induced mutations in ssDNA is lower, compared to that caused by UV and MMS, which suggests that ssDNA could be actively protected from oxidative damage. These findings have important implications for understanding mechanisms of oxidative mutagenesis, and could be applied to development of anticancer therapies and cancer prevention.
MeSH term(s)	Adenine/chemistry ; Cytosine/chemistry ; DNA/biosynthesis ; DNA, Single-Stranded/chemistry ; DNA, Single-Stranded/drug effects ; DNA-Directed DNA Polymerase/metabolism ; DNA-Directed DNA Polymerase/physiology ; Guanine/chemistry ; Hydrogen Peroxide/toxicity ; Mutagenesis ; Oxidative Stress ; Paraquat/toxicity ; Reactive Oxygen Species/metabolism ; Saccharomycetales/genetics
Chemical Substances	DNA, Single-Stranded ; Reactive Oxygen Species ; Guanine (5Z93L87A1R) ; Cytosine (8J337D1HZY) ; DNA (9007-49-2) ; Hydrogen Peroxide (BBX060AN9V) ; DNA polymerase zeta (EC 2.7.7.-) ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; Adenine (JAC85A2161) ; Paraquat (PLG39H7695)
Language	English
Publishing date	2013-08-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkt671
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