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Rapid GFAP and Iba1 expression changes in the female rat brain following spinal cord injury

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Neural Regeneration Research 2022年第2期17卷 378-385页

作者： Mawj Mandwie Jordan A.Piper Catherine A.Gorrie Kevin A.Keay Giuseppe Musumeci Ghaith Al-Badri Alessandro Castorina Laboratory of Cellular and Molecular Neuroscience(LCMN) School of Life ScienceFaculty of ScienceUniversity of Technology SydneySydneyNSWAustralia Neural Injury Research Unit School of Life ScienceFaculty of ScienceUniversity of Technology SydneySydneyNSWAustralia School of Medical Sciences(Neuroscience) The University of SydneySydneyNSWAustralia Department of Biomedical and Biotechnological Sciences AnatomyHistology and Movement Sciences SectionSchool of MedicineUniversity of CataniaCataniaItaly

Evidence suggests that rapid changes to supporting glia may predispose individuals with spinal cord injury(SCI) to such comorbidities. Here, we interrogated the expression of astrocyte-and microglial-specific markers glial fibrillary acidic protein(GFAP) and ionized calcium binding adaptor molecule 1(Iba1) in the rat brain in the first 24 hours following SCI. Female Sprague-Dawley rats underwent thoracic laminectomy;half of the rats received a mild contusion injury at the level of the T10 vertebral body(SCI group), the other half did not(Sham group). Twenty-four hours post-surgery the amygdala, periaqueductal grey, prefrontal cortex, hypothalamus, lateral thalamus, hippocampus(dorsal and ventral) in rats were collected. GFAP and Iba1 m RNA and protein levels were measured by real-time quantitative polymerase chain reaction and Western blot. In SCI rats, GFAP m RNA and protein expression increased in the amygdala and hypothalamus. In contrast, gene and protein expression decreased in the thalamus and dorsal hippocampus. Interestingly, Iba1 transcripts and proteins were significantly diminished only in the dorsal and ventral hippocampus, where gene expression diminished. These findings demonstrate that as early as 24 hours post-SCI there are region-specific disruptions of GFAP and Iba1 transcript and protein levels in higher brain regions. All procedures were approved by the University of Technology Sydney Institutional Animal Care and Ethics Committee(UTS ACEC13-0069).

关键词： affective disorders astrocytes glial fibrillary acidic protein ionized calcium binding adaptor molecule 1 memory microglia Neurotrauma spinal cord injury

Critical role of mitochondrial aldehyde dehydrogenase 2 in acrolein sequestering in rat spinal cord injury

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Neural Regeneration Research 2022年第7期17卷 1505-1511页

作者： Seth A.Herr Liangqin Shi Thomas Gianaris Yucheng Jiao Siyuan Sun Nick Race Scott Shapiro Riyi Shi Center for Paralysis Research&Department of Basic Medical Sciences College of Veterinary MedicinePurdue UniversityWest LafayetteINUSA Department of Orthopedics Ruijin HospitalSchool of MedicineShanghai Jiaotong UniversityInstitute of Trauma and OrthopedicsShanghaiChina Department of Neurological Surgery Indiana University School of MedicineIndianapolisINUSA

Lipid peroxidation-derived aldehydes,such as acrolein,the most reactive aldehyde,have emerged as key culprits in sustaining post-spinal cord injury(SCI)secondary pathologies leading to functional loss.Strong evidence suggests that mitochondrial aldehyde dehydrogenase-2(ALDH2),a key oxidoreductase and powerful endogenous anti-aldehyde machinery,is likely important for protecting neurons from aldehydesmediated degeneration.Using a rat model of spinal cord contusion injury and recently discovered ALDH2 activator(Alda-1),we planned to validate the aldehyde-clearing and neuroprotective role of ALDH2.Over an acute 2 day period post injury,we found that ALDH2 expression was significantly lowered post-SCI,but not so in rats given Alda-1.This lower enzymatic expression may be linked to heightened acrolein-ALDH2 adduction,which was revealed in co-immunoprecipitation experiments.We have also found that administration of Alda-1 to SCI rats significantly lowered acrolein in the spinal cord,and reduced cyst pathology.In addition,Alda-1 treatment also resulted in significant improvement of motor function and attenuated post-SCI mechanical hypersensitivity up to 28 days post-SCI.Finally,ALDH2 was found to play a critical role in in vitro protection of PC12 cells from acrolein exposure.It is expected that the outcome of this study will broaden and enhance anti-aldehyde strategies in combating post-SCI neurodegeneration and potentially bring treatment to millions of SCI victims.All animal work was approved by Purdue Animal Care and Use Committee(approval No.1111000095)on January 1,2021.

关键词： acrolein acrolein-lysine adduct alda-1 enzymatic catalyst lipid peroxidation mitochondrial aldehyde dehydrogenase-2 Neurotrauma oxidative stress reactive aldehydes spinal cord contusion

Basal cisternostomy for traumatic brain injury: A case report of unexpected good recovery

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Chinese Journal of Traumatology 2022年第5期25卷 302-305页

作者： Manuel De Jesus Encarnacion Ramirez Rossi Evelyn Barrientos Castilo Anton Vorobiev Nikita Kiselev Amaya Alvarez Aquino Ibrahim E.Efe Department of Neurosurgery Russian People's Friendship University MoscowRussia Department of Neurosurgery Municipal HospitalPodolskRusia Department of Neurosurgery International Center for Neurological Restoration HavanaCuba Charite-Universitatsmedizin Berlin Corporate Member of Freie Universitat BerlinHumbold-Universitat zu BerlinAnd Berlin Institute of HealthBerlinGermany

In subarachnoid hemorrhage following traumatic brain injury (TBI), the high intracisternal pressure drives the cerebrospinal fluid into the brain parenchyma, causing cerebral edema. Basal cisternostomy involves opening the basal cisterns to atmospheric pressure and draining cerebrospinal fluid in an attempt to reverse the edema. We describe a case of basal cisternostomy combined with decompressive craniectomy. A 35-year-old man with severe TBI following a road vehicle accident presented with acute subdural hematoma, Glasgow coma scale score of 6, fixed pupils and no corneal response. Opening of the basal cisterns and placement of a temporary cisternal drain led to immediate relaxation of the brain. The patient had a Glasgow coma scale score of 15 on postoperative day 6 and was discharged on day 10. We think basal cisternostomy is a feasible and effective procedure that should be considered in the management of TBI.

关键词： Basal cisternostomy Cerebral edema Decompressive craniectomy Neurotrauma Traumatic brain injury

WJSC 6^(th) Anniversary Special Issues(2):Mesenchymal stem cells Neurotrauma and mesenchymal stem cells treatment:From experimental studies to clinical trials

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World Journal of Stem Cells 2014年第2期6卷 179-194页

作者： Ana Maria Blanco Martinez Camila de Oliveira Goulart Bruna dos Santos Ramalho Júlia Teixeira Oliveira Fernanda Martins Almeida Laboratory of Neurodegeneration and Repair Institute of Biomedical SciencesHealth Science Center Pathology Department Faculty of MedicineFederal University of Rio de Janeiro Federal University of Rio de Janeiro Campus Macaé

Mesenchymal stem cell(MSC)therapy has attracted the attention of scientists and clinicians around the world.Basic and pre-clinical experimental studies have highlighted the positive effects of MSC treatment after spinal cord and peripheral nerve injury.These effects are believed to be due to their ability to differentiate into other cell lineages,modulate inflammatory and immunomodulatory responses,reduce cell apoptosis,secrete several neurotrophic factors and respond to tissue injury,among others.There are many pre-clinical studies on MSC treatment for spinal cord injury(SCI)and peripheral nerve injuries.However,the same is not true for clinical trials,particularly those concerned with nerve trauma,indicating the necessity of more well-constructed studies showing the benefits that cell therapy can provide for individuals suffering the consequences of nerve lesions.As for clinical trials for SCI treatment the results obtained so far are not as beneficial as those described in experimental studies.For these reasons basic and pre-clinical studies dealing with MSC therapy should emphasize the standardization of protocols that could be translated to the clinical set with consistent and positive outcomes.This review is based on pre-clinical studies and clinical trials available in the literature from 2010 until now.At the time of writing this article there were 43 and 36 pre-clinical and 19 and 1 clinical trials on injured spinal cord and peripheral nerves,respectively.

关键词： Neurotrauma Stem cell therapy Mesenchymal stem cells Pre-clinical studies Clinical trials

Regulation of neuroimmune processes by damage-and resolution-associated molecular patterns

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Neural Regeneration Research 2021年第3期16卷 423-429页

作者： Andis Klegeris Department of Biology University of British Columbia Okanagan CampusKelownaBCCanada

Sterile inflammatory processes are essential for the maintenance of central nervous system homeostasis,but they also contribute to various neurological disorders,including Neurotrauma,stroke,and demyelinating or neurodegenerative diseases.Immune mechanisms in the central nervous system and periphery are regulated by a diverse group of endogenous proteins,which can be broadly divided into the pro-inflammatory damageassociated molecular patterns(DAMPs)and anti-inflammatory resolution-associated molecular patterns(RAMPs),even though there is notable overlap between the DAMPand RAMP-like activities for some of these molecules.Both groups of molecular patterns were initially described in peripheral immune processes and pathologies;however,it is now evident that at least some,if not all,of these immunomodulators also regulate neuroimmune processes and contribute to neuroinflammation in diverse central nervous system disorders.The review of recent literature demonstrates that studies on DAMPs and RAMPs of the central nervous system still lag behind the much broader research effort focused on their peripheral counterparts.Nevertheless,this review also reveals that over the last five years,significant advances have been made in our understanding of the neuroimmune functions of several well-established DAMPs,including high-mobility group box 1 protein and interleukin 33.Novel neuroimmune functions have been demonstrated for other DAMPs that previously were considered almost exclusively as peripheral immune regulators;they include mitochondrial transcription factor A and cytochrome C.RAMPs of the central nervous system are an emerging area of neuroimmunology with very high translational potential since some of these molecules have already been used in preclinical and clinical studies as candidate therapeutic agents for inflammatory conditions,such as multiple sclerosis and rheumatoid arthritis.The therapeutic potential of DAMP antagonists and neutralizing antibodies in central nervous system neuroinflammatory diseases is al

关键词： Alzheimer's disease astrocytes DAMPs HMGB1 microglia neurodegeneration neuroimmune responses neuroinflammation Neurotrauma oligodendrocytes pattern-recognition receptors RAMPs

Fast-tracking regenerative medicine for traumatic brain injury

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Neural Regeneration Research 2020年第7期15卷 1179-1190页

作者： Brooke Bonsack Matt Heyck Chase Kingsbury Blaise Cozene Nadia Sadanandan Jea-Young Lee Cesar V. Borlongan Center of Excellence for Aging and Brain Repair University of South Florida College of Medicine

Traumatic brain injury remains a global health crisis that spans all demographics,yet there exist limited treatment options that may effectively curtail its lingering symptoms.Traumatic brain injury pathology entails a progression from primary injury to inflammation-mediated secondary cell death.Sequestering this inflammation as a means of ameliorating the greater symptomology of traumatic brain injury has emerged as an attractive treatment prospect.In this review,we recapitulate and evaluate the important developments relating to regulating traumatic brain injury-induced neuroinflammation,edema,and blood-brain barrier disintegration through pharmacotherapy and stem cell transplants.Although these studies of stand-alone treatments have yielded some positive results,more therapeutic outcomes have been documented from the promising area of combined drug and stem cell therapy.Harnessing the facilitatory properties of certain pharmaceuticals with the anti-inflammatory and regenerative effects of stem cell transplants creates a synergistic effect greater than the sum of its parts.The burgeoning evidence in favor of combined drug and stem cell therapies warrants more elaborate preclinical studies on this topic in order to pave the way for later clinical trials.

关键词： clinical trials combined therapy inflammatory cascade neuroinflammation neuroprotection Neurotrauma pharmacotherapy preclinical studies secondary cell death stem cells

Restoring nervous system structure and function using tissue engineered living scaffolds

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Neural Regeneration Research 2015年第5期10卷 679-685页

作者： Laura A.Struzyna James P.Harris Kritika S.Katiyar H.Isaac Chen D.Kacy Cullen Center for Brain Injury and Repair Department of NeurosurgeryPerelman School of MedicineUniversity of Pennsylvania Center for Neurotrauma Neurodegenerationand RestorationPhiladelphia Veterans Affairs Medical Center School of Biomedical Engineering Drexel University

Neural tissue engineering is premised on the integration of engineered living tissue with the host nervous system to directly restore lost function or to augment regenerative capacity following ner- vous system injury or neurodegenerative disease. Disconnection of axon pathways - the long-distance fibers connecting specialized regions of the central nervous system or relaying peripheral signals - is a common feature of many neurological disorders and injury. However, functional axonal regenera- tion rarely occurs due to extreme distances to targets, absence of directed guidance, and the presence of inhibitory factors in the central nervous system, resulting in devastating effects on cognitive and sensorimotor function. To address this need, we are pursuing multiple strategies using tissue engi- neered ＂living scaffolds＂, which are preformed three-dimensional constructs consisting of living neural cells in a defined, often anisotropic architecture. Living scaffolds are designed to restore function by serving as a living labeled pathway for targeted axonal regeneration - mimicking key developmental mechanisms- or by restoring lost neural circuitry via direct replacement of neurons and axonal tracts. We are currently utilizing preformed living scaffolds consisting of neuronal dusters spanned by long axonal tracts as regenerative bridges to facilitate long-distance axonal regeneration and for targeted neurosurgical reconstruction of local circuits in the brain. Although there are formidable challenges in predinical and clinical advancement, these living tissue engineered constructs represent a promising strategy to facilitate nervous system repair and functional recovery.

关键词： living scaffolds neural tissue engineering cell transplant biomaterials regeneration Neurotrauma neurodegeneration axon pathfinding cell migration

Neutrophil extracellular traps mediate neuro-immunothrombosis

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Neural Regeneration Research 2024年第8期19卷 1734-1740页

作者： Jianbo Lou Jianning Zhang Quanjun Deng Xin Chen Department of Neurosurgery Tianjin Medical University General HospitalTianjinChina Tianjin Neurological Institute Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous SystemMinistry of EducationTianjin Key Laboratory of InjuriesVariations and Regeneration of Nervous SystemTianjinChina

Neutrophil extracellular traps are primarily composed of DNA and histones and are released by neutrophils to promote inflammation and thrombosis when stimulated by various inflammato ry reactions.Neutrophil extracellular trap formation occurs through lytic and non-lytic pathways that can be further classified by formation mechanisms.Histones,von Willebrand factor,fibrin,and many other factors participate in the interplay between inflammation and thrombosis.Neuroimmunothrombosis summarizes the intricate interplay between inflammation and thrombosis during neural development and the pathogenesis of neurological diseases,providing cutting-edge insights into post-Neurotrauma thrombotic events.The blood-brain barrier defends the brain and spinal cord against external assaults,and neutrophil extracellular trap involvement in blood-brain barrier disruption and immunothrombosis contributes substantially to secondary injuries in neurological diseases.Further research is needed to understand how neutrophil extracellular traps promote blood-brain barrier disruption and immunothrombosis,but recent studies have demonstrated that neutrophil extracellular traps play a crucial role in immunothrombosis,and identified modulators of neuro-immunothrombosis.However,these neurological diseases occur in blood vessels,and the mechanisms are unclear by which neutrophil extracellular traps penetrate the blood-brain barrier to participate in immunothrombosis in traumatic brain injury.This review discusses the role of neutrophil extracellular traps in neuro-immunothrombosis and explores potential therapeutic interventions to modulate neutrophil extracellular traps that may reduce immunothrombosis and improve traumatic brain injury outcomes.

关键词： inflammation neuro-immunothrombosis neurologic diseases Neurotrauma neutrophil extracellular traps platelet thrombosis traumatic brain injury

c-Jun N-terminal kinase 3 deficiency protects axotomized retinal ganglion cells via affecting mitochondria involved apoptosis pathway

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International Journal of Ophthalmology(English edition) 2019年第1期12卷 30-37页

作者： Rong-Rong Wang Cheng-Fang Li De-Zu Wang Cheng-Wu Zhang Gui-Xiang Liu Qingdao University Department of Ophthalmology Jimo Traditional Chinese Medicine Hospital Department of Ophthalmology Affiliated Qingdao Hiser Hospital of Qingdao University Institute of Advanced Materials Nanjing Tech University Department of Ophthalmology Affiliated Hospital of the Medical College of Qingdao University

AIM: To illustrate the isoform-specific role and mechanism of c-Jun N-terminal kinases(JNKs) in mouse optic nerve axotomy induced Neurotrauma. METHODS: We firstly investigated the expression of JNK1, JNK2, and JNK3 in the retinal ganglion cells(RGCs) by double-immunofluorescent staining. Then we created optic nerve axotomy model in wild type as well as JNK1, JNK2, JNK3, isoform specific gene deficiency mice. With that, we checked the protein expression profile of JNKs and its active form, and quantified the survival RGCs number by immunofluorescence staining. We further explored the molecules underlying isoform specific protective effect by real-time polymerase chain reaction(PCR) and Western blotting assay. RESULTS: We found that all the three isoforms of JNKs were expressed in the RGCs. Deficiency of JNK3, but not JNK1 or JNK2, significantly alleviated optic nerve axotomyinduced RGCs apoptosis. We further established that expression of Noxa, a pro-apoptotic member of BH3 family, was significantly suppressed only in JNK3 gene deficiency mice. But tumor necrosis factor receptor 1(TNFR1) and Fas, two key modulators of death receptor mediated apoptosis pathway, did not display obvious change in the expression. CONCLUSION: It is suggested that mitochondria mediated apoptosis, but not death receptor mediated apoptosis got involved in the JNK3 gene deficiency induced RGCs protection. Our study provides a novel insight into the isoform-specific role of JNKs in Neurotrauma and indicates some cues for its therapeutics.

关键词： retinal ganglion cells c-Jun N-terminal kinases optic nerve mitochondria Noxa Neurotrauma