Traumatic brain injury induced matrix metalloproteinase2 cleaves CXCL12α (stromal cell derived factor 1α) and causes neurodegeneration

Abdul-Muneer, P. M.; Conte, Adriano Andrea; Haldar, Debanjan; Long, Mathew; Patel, Raf; Santhakumar, Vijayalakshmi; Overall, Christopher M.; Pfister, Bryan J.

doi:10.1016/j.bbi.2016.09.002

Cited by 33 publications

(24 citation statements)

References 53 publications

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“…Four animals per group are sufficient to get statistically significant results as per our previously reported studies and power analysis [9,12,13,23]. On 8 th day after the injury, behavioral tests were conducted, and on 9 th day, animals were anesthetized with ketamine/xylazine mixture and transcardially perfused with 1X PBS and 4% paraformaldehyde.…”

Section: Traumatic Brain Injury (Tbi) Is Defined As a Debilitating Efmentioning

confidence: 99%

“…Recently, we have found that reactive oxygen species (ROS) generated by the enzymatic action of NADPH oxidase-1 (NOX1) leads to activation of matrix metalloproteinase-2 (MMP-2) that cleaves stromal cell-derived factor 1α (SDF-1α) to neurotoxic SDF-1(5-67) fragment and ultimately leads to caspase-3 dependent apoptotic cell death [9]. In another recent study, we reported that the NOX1 activation causes upregulation of transforming growth factor-beta 1 (TGF-β1) that leads to caspase-3 mediated apoptosis via the phosphorylation of Smad2 and Smad3…”

Section: Traumatic Brain Injury (Tbi) Is Defined As a Debilitating Efmentioning

confidence: 99%

“…Based on power analysis and previous studies [9,12,13,23], we estimated a sample size of n=6 for detecting a significant effect of injury. No mortality were involved with the injury procedures and tissues samples from all animals were collected for analysis.…”

Section: Statistical Analysesmentioning

confidence: 99%

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Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

Bhowmick

D’Mello

Ponery

et al. 2017

Preprint

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Abstract:Traumatic brain injury (TBI) can result in persistent sensorimotor and cognitive deficits, which occur through a cascade of deleterious pathophysiological events over time. In this study, we investigated the hypothesis that neurodegeneration caused by TBI leads to impairments in sensorimotor function. TBI induces the activation of the caspase-3 enzyme, which triggers cell apoptosis in an in vivo model of fluid percussion injury (FPI).We analyzed caspase-3 mediated apoptosis by TUNEL staining and PARP and annexin V western blotting. We correlated the neurodegeneration with sensorimotor deficits by conducting the animal behavioral tests including grid walk, balance beam, inverted screen test, and climb test. Our study demonstrated that the excess cell death or neurodegeneration correlated with the neuronal dysfunction and sensorimotor impairments associated with TBI.

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Section: Traumatic Brain Injury (Tbi) Is Defined As a Debilitating Efmentioning

confidence: 99%

Section: Traumatic Brain Injury (Tbi) Is Defined As a Debilitating Efmentioning

confidence: 99%

See 1 more Smart Citation

Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

Bhowmick

D’Mello

Ponery

et al. 2017

Preprint

Self Cite

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“…The mechanisms involved in secondary neurodegeneration in the aftermath of mTBI are not yet fully elucidated. However, oxidative stress has emerged as a central component of the process [ 8 , 9 , 10 , 11 , 12 , 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies from our lab and others have demonstrated that oxidative stress, Ca 2+ influx, transforming growth factor-β (TGF-β) signaling and neuroinflammation are major mechanisms contributing to post-traumatic neurodegeneration [ 7 , 8 , 10 , 12 , 13 , 14 , 15 , 16 ]. Recently, we have found that reactive oxygen species (ROS) generated by the enzymatic action of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-1 (NOX1) leads to activation of matrix metalloproteinase-2 (MMP-2) that cleaves stromal cell-derived factor 1α (SDF-1α) to neurotoxic SDF-1 (5–67) fragment and ultimately leads to caspase-3 dependent apoptotic cell death [ 9 ]. In another recent study, we reported that the NOX1 activation causes upregulation of transforming growth factor-beta 1 (TGF-β1) that leads to caspase-3 mediated apoptosis via the phosphorylation of Smad2 and Smad3 proteins.…”

Section: Introductionmentioning

confidence: 99%

Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

et al. 2018

View full text Add to dashboard Cite

Traumatic brain injury (TBI) can result in persistent sensorimotor and cognitive deficits, which occur through a cascade of deleterious pathophysiological events over time. In this study, we investigated the hypothesis that neurodegeneration caused by TBI leads to impairments in sensorimotor function. TBI induces the activation of the caspase-3 enzyme, which triggers cell apoptosis in an in vivo model of fluid percussion injury (FPI). We analyzed caspase-3 mediated apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and poly (ADP-ribose) polymerase (PARP) and annexin V western blotting. We correlated the neurodegeneration with sensorimotor deficits by conducting the animal behavioral tests including grid walk, balance beam, the inverted screen test, and the climb test. Our study demonstrated that the excess cell death or neurodegeneration correlated with the neuronal dysfunction and sensorimotor impairments associated with TBI.

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Microenvironment‐Responsive Hydrogel Reduces Seizures After Traumatic Brain Injury in Juvenile Rats by Reducing Oxidative Stress and Hippocampal Inflammation

Han,

Zhao,

et al. 2024

Macromolecular Bioscience

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Traumatic brain injury (TBI) is the primary cause of child mortality and disability worldwide. It can result in severe complications that significantly impact children's quality of life, including post‐traumatic epilepsy (PTE). An increasing number of studies suggest that TBI‐induced oxidative stress and neuroinflammatory sequelae (especially inflammation in the hippocampus region) may lead to the development of PTE. Due to the blood‐brain barrier (BBB), typical systemic pharmacological therapy for TBI cannot deliver berberine (BBR) to the targeted location in the early stages of the injury, although BBR has strong anti‐inflammatory properties. To break through this limitation, we developed a microenvironment‐responsive Gelatin methacrylate hydrogel (GM/PB) to deliver BBR for regulating neuroinflammatory reactions and removing ROS in the brain trauma microenvironment through poly(propylene sulfide)60 (PPS60). In situ injection of the GM/PB hydrogel efficiently bypassed the BBB and was administered directly to the surface of brain tissue. In post‐traumatic brain injury models, GM/PB has the potential to mitigate oxidative stress and neuroinflammatory responses, facilitate functional recovery, and lessen seizing. These findings could lead to a new treatment for brain injuries that minimizes complications and improves the quality of life.This article is protected by copyright. All rights reserved

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Traumatic brain injury induced matrix metalloproteinase2 cleaves CXCL12α (stromal cell derived factor 1α) and causes neurodegeneration

Cited by 33 publications

References 53 publications

Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

Microenvironment‐Responsive Hydrogel Reduces Seizures After Traumatic Brain Injury in Juvenile Rats by Reducing Oxidative Stress and Hippocampal Inflammation

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