Altered expression of randomly selected genes in mouse hippocampus after traumatic brain injury

Long, Yan; Zou, Linglong; H, Liu; Lu, Holly; Yuan, Xiaoqing; Robertson, Claudia S.; Yang, Kuo-Hsin

doi:10.1002/jnr.10524

Cited by 62 publications

(27 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hemoglobin alpha and beta chain (Hbb and Hba-a1) were also upregulated at 4 h. This mirrors the work of Natale and colleagues 32 in fluid percussion injury (FPI) and may reflect local tissue hypoxia, because apnea accounted for 25-27% acute mortality in our model 11 and is noted after FPI. However, downregulation of mitochondrial genes has been reported by others at 3-4 h after CCI, 33,34 contrasting our findings. Thus, unlike the previous reports of downregulation of mitochondrial genes in CCI, we noted general upregulation of mitochondrial metabolic genes at 2 h. This could reflect our sampling time, differences in injury level, or a unique profile for blast.…”

contrasting

confidence: 99%

Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

Kochanek

Dixon

Shellington

et al. 2013

Journal of Neurotrauma

100

View full text Add to dashboard Cite

Explosive blast-induced traumatic brain injury (TBI) is the signature insult in modern combat casualty care and has been linked to post-traumatic stress disorder, memory loss, and chronic traumatic encephalopathy. In this article we report on blast-induced mild TBI (mTBI) characterized by fiber-tract degeneration and axonal injury revealed by cupric silver staining in adult male rats after head-only exposure to 35 psi in a helium-driven shock tube with head restraint. We now explore pathways of secondary injury and repair using biochemical/molecular strategies. Injury produced *25% mortality from apnea. Shams received identical anesthesia exposure. Rats were sacrificed at 2 or 24 h, and brain was sampled in the hippocampus and prefrontal cortex. Hippocampal samples were used to assess gene array (RatRef-12 Expression BeadChip; Illumina, Inc., San Diego, CA) and oxidative stress (OS; ascorbate, glutathione, low-molecular-weight thiols [LMWT], protein thiols, and 4-hydroxynonenal [HNE]). Cortical samples were used to assess neuroinflammation (cytokines, chemokines, and growth factors; Luminex Corporation, Austin, TX) and purines (adenosine triphosphate [ATP], adenosine diphosphate, adenosine, inosine, 2¢-AMP [adenosine monophosphate], and 5¢-AMP). Gene array revealed marked increases in astrocyte and neuroinflammatory markers at 24 h (glial fibrillary acidic protein, vimentin, and complement component 1) with expression patterns bioinformatically consistent with those noted in Alzheimer's disease and long-term potentiation. Ascorbate, LMWT, and protein thiols were reduced at 2 and 24 h; by 24 h, HNE was increased. At 2 h, multiple cytokines and chemokines (interleukin [IL]-1a, IL-6, IL-10, and macrophage inflammatory protein 1 alpha ) were increased; by 24 h, only MIP-1a remained elevated. ATP was not depleted, and adenosine correlated with 2¢-cyclic AMP (cAMP), and not 5¢-cAMP. Our data reveal (1) gene-array alterations similar to disorders of memory processing and a marked astrocyte response, (2) OS, (3) neuroinflammation with a sustained chemokine response, and (4) adenosine production despite lack of energy failure-possibly resulting from metabolism of 2¢-3¢-cAMP. A robust biochemical/molecular response occurs after blast-induced mTBI, with the body protected from blast and the head constrained to limit motion.

show abstract

contrasting

confidence: 99%

Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

Kochanek

Dixon

Shellington

et al. 2013

Journal of Neurotrauma

100

View full text Add to dashboard Cite

show abstract

“…The HC also accumulated T 4 in the presence of TTR. Interestingly, TTR is abundantly expressed in BS, HC, and cerebral cortex (4,22), as well as CP (8), which may act to enhance T 4 uptake and retention by cells. Since THs may facilitate neuronal regeneration after CNS injury (32), it is interesting that the ER, which had high TTR 125 I-labeled T 4 uptake in this study, is also an area of active neurogenesis in the adult, which increases after brain injury (24).…”

Section: Ependyma As Reservoir For Brain Uptake Of Tmentioning

confidence: 99%

Role of transthyretin in thyroxine transfer from cerebrospinal fluid to brain and choroid plexus

Kassem¹,

Deane²,

Segal³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

The transport of 125I-labeled thyroxine (T4) from the cerebrospinal fluid (CSF) into brain and choroid plexus (CP) was measured in anesthetized rabbit [0.5 mg/kg medetomidine (Domitor) and 10 mg/kg pentobarbitonal sodium (Sagatal) iv] using the ventriculocisternal (V-C) perfusion technique. 125I-labeled T4 contained in artificial CSF was continually perfused into the lateral ventricles for up to 4 h and recovered from the cisterna magna. The %recovery of 125I-labeled T4 from the aCSF was 47.2 ± 5.6% ( n = 10), indicating removal of 125I-labeled T4 from the CSF. The recovery increased to 53.2 ± 6.3% ( n = 4) and 57.8 ± 14.8% ( n = 3), in the presence of 100 and 200 μM unlabeled-T4, respectively ( P < 0.05), indicating a saturable component to T4 removal from CSF. There was a large accumulation of 125I-labeled T4 in the CP, and this was reduced by 80% in the presence of 200 μM unlabeled T4, showing saturation. In the presence of the thyroid-binding protein transthyretin (TTR), more 125I-labeled T4 was recovered from CSF, indicating that the binding protein acted to retain T4 in CSF. However, 125I-labeled T4 uptake into the ependymal region (ER) of the frontal cortex also increased by 13 times compared with control conditions. Elevation was also seen in the hippocampus (HC) and brain stem. Uptake was significantly inhibited by the presence of endocytosis inhibitors nocodazole and monensin by > 50%. These data suggest that the distribution of T4 from CSF into brain and CP is carrier mediated, TTR dependent, and via RME. These results support a role for TTR in the distribution of T4 from CSF into brain sites around the ventricular system, indicating those areas involved in neurogenesis (ER and HC).

show abstract

“…Although mechanisms that regulate this distribution pattern are not clear, it has been proposed that proinflammatory cytokines, chemokines, and costimulatory molecules that are upregulated in traumatic injuries play a role in these processes (Arand et al, 2001;Lenzlinger et al, 2001;Morganti-Kossmann et al, 2001, 2002Swartz et al, 2001;Hensler et al, 2002;Ray et al, 2002;Fee et al, 2003Fee et al, , 2004Long et al, 2003). Recently, it was also suggested that in the absence of infections, antigen expression and antigen-presenting cells could also direct the preferential localization of antigen-specific T-cells to nonlymphoid tissue (Ingulli et al, 2002;Reinhardt et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Traumatic Injury and the Presence of Antigen Differentially Contribute to T-Cell Recruitment in the CNS

Ling¹,

Sándor²,

Suresh³

et al. 2006

J. Neurosci.

View full text Add to dashboard Cite

T-cell recruitment into the brain is critical in inflammatory and autoimmune diseases of the CNS. We use intracerebral antigen microinjection and tetramer technology to track antigen-specific CD8ϩ T-cells in the CNS and to clarify the contribution of antigen deposition or traumatic injury to the accumulation of T-cells in the brain. We demonstrate that, after intracerebral microinjection of ovalbumin, ovalbumin-specific CD8ϩ T-cells expand systemically and then migrate into the brain where they complete additional proliferation cycles. T-cells in the brain are activated and respond to in vitro secondary antigen challenge. CD8ϩ T-cells accumulate and persist in sites of antigen in the brain without replenishment from the periphery. Persistent survival of CD8ϩ T-cells at sites of cognate antigen is significantly reduced by blocking CD154 molecules. A small traumatic injury itself does not lead to recruitment of CD8 ϩ T-cells into the brain but attracts activated antigen-specific CD8 ϩ T-cells from cognate antigen injection sites. This process is presumably antigen independent and cannot be inhibited by blocking CD154 molecules. These data show that activated antigen-specific CD8 ϩ T-cells accumulate in the CNS at both cognate antigen-containing and traumatic injury sites after intracerebral antigen delivery. The accumulation of activated antigen-specific T-cells at traumatic injury sites, in addition to antigen-containing areas, could amplify local inflammatory processes in the CNS. Combination therapies in neuroinflammatory diseases to block both of these processes should be considered.

show abstract

Altered expression of randomly selected genes in mouse hippocampus after traumatic brain injury

Cited by 62 publications

References 51 publications

Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

Role of transthyretin in thyroxine transfer from cerebrospinal fluid to brain and choroid plexus

Traumatic Injury and the Presence of Antigen Differentially Contribute to T-Cell Recruitment in the CNS

Contact Info

Product

Resources

About