Traumatic Brain Injury and Mitochondrial Dysfunction

Hiebert, John M.; Shen, Qiuhua; Thimmesch, Amanda R.; Pierce, Janet D.

doi:10.1097/maj.0000000000000506

Cited by 181 publications

(208 citation statements)

References 65 publications

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“…Intracellular mitochondrial dysfunction and molecules released from damaged mitochondria (DAMPs) are well documented for their contributions to disease states. [36][37][38][39][40] Our data further suggest that mtMPs possess a unique procoagulant activity that differs from intracellular mitochondrial dysfunctions and DAMPs.…”

Section: Discussionmentioning

confidence: 83%

Cardiolipin-mediated procoagulant activity of mitochondria contributes to traumatic brain injury–associated coagulopathy in mice

Zhao

Wang

Tian

et al. 2016

Blood

114

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Section: Discussionmentioning

confidence: 83%

Cardiolipin-mediated procoagulant activity of mitochondria contributes to traumatic brain injury–associated coagulopathy in mice

Zhao

Wang

Tian

et al. 2016

Blood

114

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“…Neuronal cells are critically dependent on mitochondrial integrity based on high rates of metabolic activity and need to response promptly to activity-dependent neurotransmission and hot spots of energy consumption, such as presynaptic and postsynaptic sites (Hiebert et al 2015;Robertson et al 2007). Mitochondria are one of the major sources of ROS, and are highly susceptible to oxidative damage because ROS damage mitochondrial enzymes directly, cause mtDNA mutation, and alter mitochondrial membrane permeability (Niizuma et al 2009;Schon and Manfredi 2003;Chen et al 2013a, b).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of IRF6 Attenuates Hydrogen Dioxide-Induced Oxidative Stress via Inhibiting Mitochondrial Dysfunction in HT22 Cells

Guo

Chen

et al. 2015

Cell Mol Neurobiol

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Oxidative stress-induced cell damage is involved in many neurological diseases. Interferon regulatory factor 6 (IRF6), a member of the IRF family of transcription factors, is required for the differentiation of skin, breast epithelium, and oral epithelium. However, the regulation and function of IRF6 in central nervous system remain unknown. This study aimed to investigate the role of IRF6 in hydrogen peroxide (H2O2)-induced oxidative neuronal injury in HT22 mouse hippocampal cells. Treatment with H2O2 significantly increased the expression of IRF6 at both mRNA and protein levels, and knockdown of IRF6 using specific small interfering RNA reduced H2O2-induced cytotoxicity, as evidenced by increased cell viability and decreased apoptosis. Knockdown of IRF6 attenuated intracellular reactive oxygen species (ROS) generation and lipid peroxidation, and also preserved endogenous antioxidant enzyme activities. The inhibitory effect of IRF6 knockdown on mitochondrial dysfunction was demonstrated by reduced mitochondrial oxidative level, preserved mitochondrial membrane potential (MMP) and ATP generation, as well as attenuated mitochondrial swelling. In addition, down-regulation of IRF6 inhibited the activation of mitochondrial apoptotic factors, whereas IRF6 knockdown together with caspase inhibitors had no extra effect on cell viability and LDH release. These results suggest that knockdown of IRF6 has protective effects against H2O2-induced oxidative stress by reducing ROS accumulation and apoptosis, and these protective effects are dependent on preservation of mitochondrial function.

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“…Significantly increased free radical production is one of the main causes of secondary injury in TBI, leading to further damage to neuronal tissue and vasculature (Corps, Roth, & McGavern, 2015;Hiebert, Shen, Thimmesch, & Pierce, 2015). Evidence strongly suggests that oxidative stress induced by the imbalance between free radicals and antioxidants propagates secondary injury mechanisms in TBI (Deng, 2010).…”

Section: Evidence Reviewmentioning

confidence: 99%

Systematic Review of Traumatic Brain Injury and the Impact of Antioxidant Therapy on Clinical Outcomes

Shen

Hiebert

Hartwell

et al. 2016

Worldviews Ev Based Nurs

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Background: Traumatic brain injury (TBI) is an acquired brain injury that occurs when there is sudden trauma that leads to brain damage. This acute complex event can happen when the head is violently or suddenly struck or an object pierces the skull or brain. The current principal treatment of TBI includes various pharmaceutical agents, hyperbaric oxygen, and hypothermia. There is evidence that secondary injury from a TBI is specifically related to oxidative stress. However, the clinical management of TBI often does not include antioxidants to reduce oxidative stress and prevent secondary injury.

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Traumatic Brain Injury and Mitochondrial Dysfunction

Cited by 181 publications

References 65 publications

Cardiolipin-mediated procoagulant activity of mitochondria contributes to traumatic brain injury–associated coagulopathy in mice

Cardiolipin-mediated procoagulant activity of mitochondria contributes to traumatic brain injury–associated coagulopathy in mice

Knockdown of IRF6 Attenuates Hydrogen Dioxide-Induced Oxidative Stress via Inhibiting Mitochondrial Dysfunction in HT22 Cells

Systematic Review of Traumatic Brain Injury and the Impact of Antioxidant Therapy on Clinical Outcomes

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