Alterations in brain-derived neurotrophic factor and insulin-like growth factor-1 protein levels after penetrating ballistic-like brain injury in rats

Madathil, Sindhu K.; Deng-Bryant, Ying; Wilfred, Bernard S.; Leung, Lai Yee; Gilsdorf, Janice; Shear, Deborah A.

doi:10.1097/ta.0000000000001471

Cited by 6 publications

(4 citation statements)

References 39 publications

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“…MiR-335 targets insulin-like growth factor receptor (IGF-R) (Gong et al, 2014). The IGF-1/IGF-R pathway is crucial to cellular metabolism affected by TBI and the ligand, IGF-1, is increased in damaged cortical and hippocampal regions 3-7 day after PBBI (Madathil and Saatman, 2015;Madathil et al, 2017). It is possible that this observation is relevant to neurogenesis during attempted repair (Madathil et al, 2013).…”

Section: Pbbi Leads To Temporally Specific Mirna Dysregulation Associmentioning

confidence: 99%

Penetrating Ballistic-Like Brain Injury Leads to MicroRNA Dysregulation, BACE1 Upregulation, and Amyloid Precursor Protein Loss in Lesioned Rat Brain Tissues

et al. 2020

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Severe traumatic brain injury (TBI) is a risk factor for neurodegenerative diseases. Yet, the molecular events involving dysregulated miRNAs that may be associated with protein degradation in the brain remains elusive. Quantitation of more than 800 miRNAs was conducted using rat ipsilateral coronal brain tissues collected 1, 3, or 7 days after penetrating ballistic-like brain injury (PBBI). As a control for each time-point, Sham-operated animals received craniotomy alone. Microarray and systems biology analysis indicated that the amplitude and complexity of miRNAs affected were greatest 7 day after PBBI. Arrays and Q-PCR inferred that dysregulation of miR-135a, miR-328, miR-29c, and miR-21 were associated with altered levels of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), PSEN1, PSEN2, and amyloid precursor protein (APP) genes. These events were followed by increased levels of mature BACE1 protein and concomitant loss of full length APP within 3-7 days, then elevation of amyloid beta (Aβ)-40 7 days after PBBI. This study indicates that miRNA arrays, coupled with systems biology, may be used to guide study design prior validation of miRNA dysregulation. Associative analysis of miRNAs, mRNAs, and proteins within a proposed pathway are poised for further validation as biomarkers and therapeutic targets relevant to TBI-induced APP loss and subsequent Aβ peptide generation during neurodegeneration.

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Section: Pbbi Leads To Temporally Specific Mirna Dysregulation Associmentioning

confidence: 99%

Penetrating Ballistic-Like Brain Injury Leads to MicroRNA Dysregulation, BACE1 Upregulation, and Amyloid Precursor Protein Loss in Lesioned Rat Brain Tissues

et al. 2020

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“…Most studies of TBI in juvenile rats have found greater BDNF protein concentration and BDNF mRNA expression up to 7 days after injury relative to sham or control animals [40][41][42]. In adult models, rats with TBI had higher BDNF expression acutely (within 6 h of injury) compared to shams, suggesting an upregulation of BDNF in the acute period, but similar or even lower BDNF expression compared to the sham group chronically after injury [43][44][45][46][47]. BDNF expression in adult models of ABI is associated with recovery in many of these studies [46,48,49].…”

Section: Bdnf In Preclinical Models Of Pediatric Abimentioning

confidence: 99%

Brain-Derived Neurotrophic Factor in Pediatric Acquired Brain Injury and Recovery

Treble-Barna,

Petersen,

Stec

et al. 2024

Biomolecules

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We review emerging preclinical and clinical evidence regarding brain-derived neurotrophic factor (BDNF) protein, genotype, and DNA methylation (DNAm) as biomarkers of outcomes in three important etiologies of pediatric acquired brain injury (ABI), traumatic brain injury, global cerebral ischemia, and stroke. We also summarize evidence suggesting that BDNF is (1) involved in the biological embedding of the psychosocial environment, (2) responsive to rehabilitative therapies, and (3) potentially modifiable. BDNF’s unique potential as a biomarker of neuroplasticity and neural repair that is reflective of and responsive to both pre- and post-injury environmental influences separates it from traditional protein biomarkers of structural brain injury with exciting potential to advance pediatric ABI management by increasing the accuracy of prognostic tools and informing clinical decision making through the monitoring of therapeutic effects.

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“…The ability to predict mortality and injury severity may facilitate the development of clinical guidelines for managing pTBI. 15 Several biomarkers are reported to be altered after PBBI, including GFAP (glial fibrillary acidic protein; astrogliosis/astroglial injury), [16][17][18] brain-derived neurotrophic factor (BDNF; neurogenesis/neuroprotection), 19 ubiquitin C-terminal hydrolase-L1 (UCH-L1; neuronal cell body injury), 20 cathepsin B (CatB; apoptosis/ cell necrosis), 21 and microRNA (miRNA; astrogliosis/ inflammation/neurodegeneration). 22,23 Considering that pTBI and polytrauma often occur concurrently in the setting of emergency medicine, we hypothesized that the use of brain-specific and global injury biomarkers can reliably identify HX+HS and frontal PBBI with and without systemic insults (HX+HS) to diagnose and differentiate combined injury from isolated pTBI.…”

Section: Introductionmentioning

confidence: 99%

“…Several biomarkers are reported to be altered after PBBI, including GFAP (glial fibrillary acidic protein; astrogliosis/astroglial injury), 16–18 brain-derived neurotrophic factor (BDNF; neurogenesis/neuroprotection), 19 ubiquitin C-terminal hydrolase-L1 (UCH-L1; neuronal cell body injury), 20 cathepsin B (CatB; apoptosis/cell necrosis), 21 and microRNA (miRNA; astrogliosis/inflammation/neurodegeneration). 22 , 23 …”

Section: Introductionmentioning

confidence: 99%

Blood-Based Brain and Global Biomarker Changes after Combined Hypoxemia and Hemorrhagic Shock in a Rat Model of Penetrating Ballistic-Like Brain Injury

Pierre

Yang

et al. 2021

Neurotrauma Reports

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Penetrating traumatic brain injury (pTBI) often occurs with systemic insults such as hemorrhagic shock (HS) and hypoxemic (HX). This study examines rat models of penetrating ballistic-like brain injury (PBBI) and HX+HS to assess whether the blood levels of brain and systemic response biomarkers phosphorylated neurofilament-heavy protein (pNF-H), neurofilament-light protein (NF-L), aII-spectrin, heat shock protein (HSP70), and high mobility group box 1 protein (HMGB1) can distinguish pTBI from systemic insults and guide in pTBI diagnosis, prognosis, and monitoring. Thirty rats were randomly assigned to sham, PBBI, HS+HX, and PBBI+HS+HX groups. PBBI and sham groups underwent craniotomy with and without probe insertion and balloon expansion, respectively. HX and HS was then simulated by blood withdrawal and fraction of inspired oxygen (FIO 2 ) reduction. Biomarker serum concentrations were determined at one (D1) and two (D2) days post-injury with enzyme-linked immunosorbent assay (ELISA) methods. Axonal injury-linked biomarkers pNF-H and NF-L serum levels in PBBI groups were higher than those in sham and HX+HS groups at D1 and D2 post-injury. The same was true for PBBI+HX+HS compared with sham (D2 only for pNF-H) and HX+HS groups. However, pNF-H and NF-L levels in PBBI+HX+HS groups were not different than their PBBI counterparts. At D1, aII-spectrin levels in the HX+HS and PBBI+HS+HX groups were higher than the sham groups. aII-spectrin levels in the HX+HS group were higher than the PBBI group. This suggests HX+HS as the common insult driving aII-spectrin elevations. In conclusion, pNF-H and NF-L may serve as specific serum biomarkers of pTBI in the presence or absence of systemic insults. aII-spectrin may be a sensitive acute biomarker in detecting systemic insults occurring alone or with pTBI.

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Alterations in brain-derived neurotrophic factor and insulin-like growth factor-1 protein levels after penetrating ballistic-like brain injury in rats

Abstract: Our findings demonstrate that PBBI results in a brief upregulation of BDNF and IGF-1 during early posttraumatic period, providing critical information for interventions aiming to enhance neuronal survival and brain plasticity.

Cited by 6 publications

References 39 publications

Penetrating Ballistic-Like Brain Injury Leads to MicroRNA Dysregulation, BACE1 Upregulation, and Amyloid Precursor Protein Loss in Lesioned Rat Brain Tissues

Penetrating Ballistic-Like Brain Injury Leads to MicroRNA Dysregulation, BACE1 Upregulation, and Amyloid Precursor Protein Loss in Lesioned Rat Brain Tissues

Brain-Derived Neurotrophic Factor in Pediatric Acquired Brain Injury and Recovery

Blood-Based Brain and Global Biomarker Changes after Combined Hypoxemia and Hemorrhagic Shock in a Rat Model of Penetrating Ballistic-Like Brain Injury

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