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Connecting cellular mechanisms and extracellular vesicle cargo in traumatic brain injury

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Neural Regeneration Research 2024年第10期19卷 2119-2131页

作者： Nikita Ollen-Bittle Austyn D.Roseborough Wenxuan Wang Jeng-liang D.Wu Shawn N.Whitehead Department of Anatomy and cell biology Western UniversityLondonONCanada Schulich School of Medicine and Dentistry Western UniversityLondonONCanada Deparment of clinical Neurological Sciences Western UniversityLondonONCanada

Traumatic brain injury is followed by a cascade of dynamic and complex events occurring at the cellular level. These events include: diffuse axonal injury, neuronal cell death, blood-brain barrier break down, glial activation and neuroinflammation, edema, ischemia, vascular injury, energy failure, and peripheral immune cell infiltration. The timing of these events post injury has been linked to injury severity and functional outcome. Extracellular vesicles are membrane bound secretory vesicles that contain markers and cargo pertaining to their cell of origin and can cross the blood-brain barrier. These qualities make extracellular vesicles intriguing candidates for a liquid biopsy into the pathophysiologic changes occurring at the cellular level post traumatic brain injury. Herein, we review the most commonly reported cargo changes in extracellular vesicles from clinical traumatic brain injury samples. We then use knowledge from animal and in vitro models to help infer what these changes may indicate regrading cellular responses post traumatic brain injury. Future research should prioritize labeling extracellular vesicles with markers for distinct cell types across a range of timepoints post traumatic brain injury.

关键词： axonal injury biomarkers blood-brain barrier chronic traumatic encephalopathy extracellular vesicles glial activation neuroinflammation traumatic brain injury

Drug repurposing: A novel strategy to target cancer stem cells and therapeutic resistance

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Genes & Diseases 2024年第1期11卷 148-175页

作者： Divya Ajmeera Rajanna Ajumeera cell biology Department ICMR-National Institute of Nutrition(NIN)HyderabadTelangana 500007India

Chemotherapy is an effortless and frequently used approach in cancer therapy.However,in most cases,it can only prolong life expectancy and does not guarantee a complete cure.Furthermore,chemotherapy is associated with severe adverse effects,one of the major complications of effective cancer therapy.In addition,newly published research outputs show that cancer stem cells are involved in cancer disease progression,drug resistance,metastasis,and recurrence and that they are functional in the trans-differentiation capacity of cancer stem cells to cancer cells in response to treatments.Novel strategies are therefore required for better management of cancer therapy.The prime approach would be to synthesize and develop novel drugs that need extensive resources,time,and endurance to be brought into therapeutic use.The subsequent approach would be to screen the anti-cancer activity of avail-able non-cancerous drugs.This concept of repurposing non-cancer drugs as an alternative to current cancer therapy has become popular in recent years because using existing anticancer drugs has several adverse effects.Micronutrients have also been investigated for cancer ther-apy due to their significant anti-cancer effects with negligible or no side effects and availabil-ity in food sources.In this paper,we discuss an ideal hypothesis for screening available non-cancerous drugs with anticancer activity,with a focus on cancer stem cells and their clinical application for cancer treatment.Further,drug repurposing and the combination of micronu-trients that can target both cancers and cancer stem cells may result in a better therapeutic approach leading to maximum tumor growth control.

关键词： Cancerstem cells Chemotherapy Combination therapy micronutrients Non-cancer drugs Novel strategies

New insights into the role of the endoplasmic reticulum in microglia

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Neural Regeneration Research 2024年第7期19卷 1397-1398页

作者： Veronika E.Neubrand M.Rosario Sepúlveda Department of cell biology Faculty of SciencesUniversity of GranadaGranadaSpain

Microglial cells are the only resident immune cells in the central nervous system and constitute its frontline guardian.They are extremely reactive against infections,trauma,or toxins,but are also responsible for mediating inflammation,taking part in the pathogenic course of many neuropathologies(Sierra et al.,2019).cell-specific staining,ultrastructural analysis by transmission electron microscopy(TEM),or two-photonmicroscopy imaging have been relevant for the characterization of microglia as well as their cell-cell interactions。

关键词： inflammation reticulum

Physical exercise and traumatic brain injury: is it question of time?

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Neural Regeneration Research 2024年第3期19卷 475-476页

作者： Valentina Mastrorilli Stefano Farioli Vecchioli Institute of Biochemistry and cell biology Institute of Biochemistry and Cell BiologyNational Research Council(IBBC/CNR)MonterotondoRomeItaly Plaisant S.R.L. RomeItaly

Is it better to be safe than sorry?This Hamletic dilemma has always stimulated medical-scientific debates in numerous fields of biomedicine.And among these,the preventive-therapeutic approach to the treatment of brain trauma is one of the most striking examples.Traumatic brain injury(TBI)is a leading cause of brain damage among young and elderly populations with a very high hospitalization and death rate.TBI is characterized by two pathologically distinct but strictly consequential phases:a first characterized by an immediate and highly variable mechanical dysfunction of the brain tissue,which involves widespread cell death and tissue degeneration,followed by a second phase which can last from days to even years depending on the severity of the TBI and the patient’s pre-existing health status.Secondary processes,including inflammatory phenomena,oxidative stress associated with metabolic,vascular,and neuro-modulatory deficits,are very often responsible for neuro-motor and psychological deficits leading to long-term disabilities(Kaur and Sharma,2018).

关键词： injury striking modulator

c-myb is involved in CML progression and is a therapeutic target in the zebrafish CML model

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Animal Models and Experimental Medicine 2024年第2期7卷 136-144页

作者： Yin Ye Xiaojun Yang Feifei Li Wei Liu Wenqing Zhang Zhibin Huang Division of cell Developmental and Integrative BiologySchool of MedicineSouth China University of TechnologyGuangzhouChina

Background:Despite the success of tyrosine kinase inhibitors in chronic myeloid leukemia(CML)therapy,CML still faces the challenges of drug resistance and progression to blast crisis.Twenty-five percent of patients have imatinib resistance and treatment difficulties due to heterogeneity after progression,but little is known about the mechanism.A key transcription factor in hematopoiesis,MYB,has been reported to increase abnormally in several types of aggressive blood disorders including CML.Methods:This study used a zebrafish model to explore the relationship between BCR/ABL1 and c-myb in CML progression.A CML zebrafish model was crossed with a c-myb hyperactivity transgenic line.Results:It was found that both exogenous BCR/ABL1 and c-myb could up-regulate the expression of neutrophil-related genes.More seriously,neutrophil accumulation was observed when BCR/ABL1 was combined with c-myb overexpression.Further studies showed that c-myb may be one of the downstream targets of BCR/ABL1 and the effect of BCR/ABL1 on neutrophils was c-myb dependent.Taking advantage of this inheritable in vivo model,it was shown that a combination of imatinib and flavopiridol,a cyclin-dependent kinase inhibitor targeting MYB,could more effectively alleviate the aggressive phenotype of the double transgene line.Conclusion:In summary,this study suggests that c-myb acts downstream of BCR/ABL1 and is involved in CML progression and is therefore a risk factor and a valuable target for the treatment of CML progression.The model used in the study could be helpful in high-throughput drug screening in CML transformation.

关键词： chronic myeloid leukemia c-myb flavopiridol zebrafish model

A toast to a zebrafish germ cell induction cocktail

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Science China(Life Sciences) 2024年第6期67卷 1314-1315页

作者： Mary C.Mullins Department of cell and Developmental biology University of Pennsylvania Perelman School of MedicinePhiladelphia 19104USA

The zebrafish field is ringing in the new year with a publication from Yonghua Sun's laboratory(Wang et al.,2023)of a cocktail of germline factors that can induce all cells of the zebrafish embryo into primordial germ cells(PGCs)at phenomenal rates.This major advance is not only of great interest to germ cell biologists,but it has important applications to the entire zebrafish field,as shown in Wang et al.(2023).

关键词： fish zebra field

Use of induced pluripotent stem cell-derived brain cells,organoids,assembloids,and blood-brain barrier models in understanding alcohol and anesthetic-induced brain injuries:an emerging perspective

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Neural Regeneration Research 2024年第5期19卷 953-954页

作者： Xiaowen Bai Department of cell biology Neurobiology&AnatomyMedical College of WisconsinMilwaukeeWIUSA

Neurological disorders,including developmental disorders,Alzheimer’s disease(AD),and psychiatric conditions,have significant social and economic impacts globally.Despite extensive research into the underlying mechanisms of these disorders,effective treatments remain elusive,partly due to the complexity of the brain,the limited availability of human brain tissue,and the blood-brain barrier(BBB)’s impermeability to certain drugs.This perspective article discusses the potential of human induced pluripotent stem cell(iPSC)-based models of brain cells,organoids,assembloids,and BBB to advance our understanding of the etiology,progression,and mechanisms of brain injuries induced by alcohol consumption and general anesthesia.These models could also be used to develop protective and therapeutic approaches.

关键词： injuries protective drugs

A perspective on age-related changes in cell environment and risk of neurodegenerative diseases

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Neural Regeneration Research 2024年第4期19卷 719-720页

作者： Alice Y.Liu Department of cell biology and Neuroscience Rutgers State University of New JerseyPiscatawayNJUSA

“Age-related neurodegenerative disease”underscores human age as the primary risk factor for disease development:Alzheimer’s,Parkinson’s,and Huntington’s disease(HD)as examples.Reasons for the age-dependent delay in disease manifestation,in particular for autosomal dominant forms of the disease,and the underlying cause(s)of specific neuron dysfunction and death to manifest as memory loss,anxiety,depression,and agitation in disease subjects remain unclear.We are interested in understanding age-related changes in cell environment that can modulate the structure,function,aggregation.

关键词： Huntington Alzheimer death

AtVQ25 promotes salicylic acid-related leaf senescence by fine-tuning the self-repression of AtWRKY53

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Journal of Integrative Plant biology 2024年第6期66卷 1126-1147页

作者： Qi Tan Mingming Zhao Jingwei Gao Ke Li Mengwei Zhang Yunjia Li Zeting Liu Yujia Song Xiaoyue Lu Zhengge Zhu Rongcheng Lin Pengcheng Yin Chunjiang Zhou Geng Wang Ministry of Education Key Laboratory of Molecular and cellular biology Hebei Research Center of the Basic Discipline of Cell BiologyHebei Collaboration Innovation Center for Cell Signaling and Environmental Adaptation Hebei Key Laboratory of Molecular and Cellular Biology College of Life Sciences Hebei Normal University College of Chemical Engineering Shijiazhuang University Institute of Botany Chinese Academy of Sciences

Most mechanistic details of chronologically ordered regulation of leaf senescence are unknown.Regulatory networks centered on AtWRKY53 are crucial for orchestrating and integrating various senescence-related signals. Notably, AtWRKY53binds to its own promoter and represses transcription of AtWRKY53, but the biological significance and mechanism underlying this selfrepression remain unclear. In this study, we identified the VQ motif-containing protein AtVQ25as a cooperator of AtWRKY53. The expression level of AtVQ25 peaked at mature stage and was specifically repressed after the onset of leaf senescence. AtVQ25-overexpressing plants and atvq25 mutants displayed precocious and delayed leaf senescence, respectively. Importantly, we identified AtWRKY53 as an interacting partner of AtVQ25. We determined that interaction between AtVQ25 and AtWRKY53 prevented AtWRKY53from binding to W-box elements on the AtWRKY53promoter and thus counteracted the selfrepression of AtWRKY53. In addition, our RNA-sequencing data revealed that the AtVQ25-AtWRKY53 module is related to the salicylic acid(SA) pathway. Precocious leaf senescence and SA-induced leaf senescence in AtVQ25-overexpressing lines were inhibited by an SA pathway mutant, atsid2, and Nah G transgenic plants; AtVQ25-overexpressing/atwrky53 plants were also insensitive to SA-induced leaf senescence. Collectively, we demonstrated that AtVQ25 directly attenuates the self-repression of AtWRKY53 during the onset of leaf senescence,which is substantially helpful for understanding the timing of leaf senescence onset modulated by AtWRKY53.

关键词： AtWRKY53 leaf senescence salicylic acid transcriptional regulation VQ motif-containing proteins