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Treatment of spinal cord injury with biomaterials and stem cell therapy in non-human primates and humans

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Neural Regeneration Research 2025年第2期20卷 343-353页

作者： Ana Milena Silva Olaya Fernanda Martins Almeida Ana Maria Blanco Martinez Suelen Adriani Marques PhD Program in Pathological anatomy Federal University of Rio de JaneiroRio de JaneiroBrazil Biomedical science institute Federal University of Rio de JaneiroRio de JaneiroBrazil Graduate Program in Pathological anatomy Federal University of Rio de JaneiroRio de JaneiroBrazil Graduate Program in Pathological anatomy(PPGAP/UFRJ) Department of Neurobiology/Institute of BiologyCampus do GragoatáNiteróiRio de JaneiroBrazil

Spinal cord injury results in the loss of sensory,motor,and autonomic functions,which almost always produces permanent physical ***,in the search for more effective treatments than those already applied for years,which are not entirely efficient,researches have been able to demonstrate the potential of biological strategies using biomaterials to tissue manufacturing through bioengineering and stem cell therapy as a neuroregenerative approach,seeking to promote neuronal recovery after spinal cord *** of these strategies has been developed and meticulously evaluated in several animal models with the aim of analyzing the potential of interventions for neuronal repair and,consequently,boosting functional *** the majority of experimental research has been conducted in rodents,there is increasing recognition of the importance,and need,of evaluating the safety and efficacy of these interventions in non-human primates before moving to clinical trials involving therapies potentially promising in *** article is a literature review from databases(PubMed,science Direct,Elsevier,Scielo,Redalyc,Cochrane,and NCBI)from 10 years ago to date,using keywords(spinal cord injury,cell therapy,non-human primates,humans,and bioengineering in spinal cord injury).From 110 retrieved articles,after two selection rounds based on inclusion and exclusion criteria,21 articles were ***,this review arises from the need to recognize the experimental therapeutic advances applied in non-human primates and even humans,aimed at deepening these strategies and identifying the advantages and influence of the results on extrapolation for clinical applicability in humans.

关键词： bioengineering biomaterials cell therapy humans non-human primates spinal cord injury stem cell therapy

Cigarette Smoke Induces Apoptosis by Activation of Caspase-3 in Isolated Fetal Rat Lung Type II Alveolar Ep-ithelial cells in Vitro

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Open Journal of Respiratory Diseases 2013年第1期3卷 4-12页

作者： Asra Ahmed James A. Thliveris Anthony Shaw Michael Sowa James Gilchrist J. Elliott Scott Departments of Oral Biology University of Manitoba and Manitoba Institute for Child Health Winnipeg Canada human anatomy and cell science university of manitoba and manitoba institute for child health Winnipeg Canada The Biology of Breathing Group University of Manitoba and Manitoba Institute for Child Health Winnipeg Canada The National Research Council Biodiagnostics institute university of manitoba and manitoba institute for child health Winnipeg Canada

Smoking during pregnancy is a major source of fetal exposure to numerous harmful agents present in tobacco smoke. Lung development involves complex biochemical processes resulting in dramatic changes which continue even after birth. In addition to type I cells which form the blood-air barrier, type II alveolar epithelial (AE) cells have important and diverse functions related to immunological protection and stabilization of the alveolus through synthesis and secretion of the pulmonary surfactant. Apoptosis or programmed cells death is an important physiological process during lung embryogenesis and for the proper maintenance of homeostasis. Caspases are proteases that play important roles in regulating apoptosis. Caspase-3 is the key executioner caspase in the cascade of events leading to cell death by apoptosis. We explored the hypothesis that cigarette smoke extract (CSE) induces apoptosis in fetal rat lung type II AE cells by activation of caspase-3. To analyze these factors, isolated fetal rat lung type II AE cells were used. The cells were exposed to different concentrations of CSE (5%, 10% or 15%) (v/v) for 60 min. The results of the present study showed that CSE induced apoptosis in fetal rat lung type II AE cells with a significant increase (p 0.05) in caspase-3 activity and decrease in cell proliferation at CSE concentrations of 10% and 15% (v/v). These observations indicate that cigarette smoke extract induces apoptosis by activation of caspase-3 in fetal rat lung type II AE cells in a dose-dependent manner and may potentially alter the regulated development of the lung and the appearance of the surfactant-producing type II alveolar cells which are critical for the establishment of adequate gas exchange at birth.

关键词： Cigarette Smoke Toxicity Fetal Rat Lung Type II Alveolar cells Apoptosis Protease Caspase-3 Lung Development Developmental Toxicity Maternal Smoking

Spatial transcriptomics combined with single-nucleus RNA sequencing reveals glial cell heterogeneity in the human spinal cord

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Neural Regeneration Research 2025年第11期20卷 3302-3316页

作者： Yali Chen Yiyong Wei Jin Liu Tao Zhu Cheng Zhou Donghang Zhang Department of Anesthesiology West China HospitalSichuan UniversityChengduSichuan ProvinceChina Laboratory of Anesthesia and Critical Care Medicine National-Local Joint Engineering Research Center of Translational Medicine of AnesthesiologyWest China HospitalSichuan UniversityChengduSichuan ProvinceChina Department of Anesthesiology Longgang District Maternity&Child Healthcare Hospital of Shenzhen City(Longgang Maternity and Child Institute of Shantou University Medical College)ShenzhenGuangdong ProvinceChina Department of Anesthesiology Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhou ProvinceChina

Glial cells play crucial roles in regulating physiological and pathological functions,including sensation,the response to infection and acute injury,and chronic neurodegenerative *** cells include astrocytes,microglia,and oligodendrocytes in the central nervous system,and satellite glial cells and Schwann cells in the peripheral nervous *** the greater understanding of glial cell types and functional heterogeneity achieved through single-cell and single-nucleus RNA sequencing in animal models,few studies have investigated the transcriptomic profiles of glial cells in the human spinal ***,we used high-throughput single-nucleus RNA sequencing and spatial transcriptomics to map the cellular and molecular heterogeneity of astrocytes,microglia,and oligodendrocytes in the human spinal *** explore the conservation and divergence across species,we compared these findings with those from *** the human spinal cord,astrocytes,microglia,and oligodendrocytes were each divided into six distinct transcriptomic *** the mouse spinal cord,astrocytes,microglia,and oligodendrocytes were divided into five,four,and five distinct transcriptomic subclusters,*** comparative results revealed substantial heterogeneity in all glial cell types between humans and ***,we detected sex differences in gene expression in human spinal cord glial ***,in all astrocyte subtypes,the levels of NEAT1 and CHI3L1 were higher in males than in females,whereas the levels of CST3 were lower in males than in *** all microglial subtypes,all differentially expressed genes were located on the sex *** addition to sex-specific gene differences,the levels of MT-ND4,MT2A,MT-ATP6,MT-CO3,MT-ND2,MT-ND3,and MT-CO_(2) in all spinal cord oligodendrocyte subtypes were higher in females than in ***,the present dataset extensively characterizes glial cell heterogeneity and offers a valuable resource for explo

关键词： astrocyte glial cell human microglia oligodendrocyte sex differentiation single-nucleus RNA sequencing spatial transcriptomics species variation spinal cord

PCAF-mediated acetylation of METTL3 impairs mRNA translation efficiency in response to oxidative stress

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science China(Life sciences) 2024年第10期67卷 2157-2168页

作者： Cheng Liu Miao Yu Mengyuan Wang Siyuan Yang Yenan Fu Lei Zhang Chaoyang Zhu Hongquan Zhang Program for Cancer and cell Biology Department of Human AnatomyHistology and EmbryologySchool of Basic Medical SciencesPeking University International Cancer Instituteand State Key Laboratory of Molecular OncologyPeking University Health Science CenterBeijing 100191China Department of General Surgery and Urological Surgery Huaihe HospitalHenan UniversityKaifeng 100084China Department of human anatomy Histologyand EmbryologyShenzhen University School of MedicineShenzhen 518055China

METTL3 methylates RNA and regulates the fate of mRNA through its methyltransferase ***3 enhances RNA translation independently of its catalytic ***,the underlying mechanism is still ***,we report that METTL3 is both interacted with and acetylated at lysine 177 by the acetyltransferase PCAF and deacetylated by *** the methyltransferase activity nor the stability of METTL3 is affected by its acetylation at ***,acetylation of METTL3 blocks its interaction with EIF3H,a subunit of the translation initiation factor,thereby reducing mRNA translation ***,acetylation of METTL3 responds to oxidative ***,oxidative stress enhances the interaction of PCAF with METTL3,increases METTL3 acetylation,and suppresses the interaction of METTL3 with EIF3H,thereby decreasing the translation efficiency of ribosomes and inhibiting cell ***,we suggest a mechanism by which oxidative stress regulates RNA translation efficiency by the modulation of METTL3 acetylation mediated by PCAF.

关键词： METTL3 acetylation PCAF m^(6)A oxidative stress translation SIRT3

Stachybotrys chartarum(atra) spore extract alters surfactant protein expression and surfactant function in isolated fetal rat lung epithelial cells, fibroblasts and human A549 cells

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Open Journal of Pediatrics 2013年第3期3卷 243-256页

作者： Gail F. Pollard Anthony Shaw Michael Sowa Thomas Rand James A. Thliveris James E. Scott Department of Biology St. Mary’s University Halifax Nova Scotia Department of human anatomy and cell science University of Manitoba Winnipeg Canada Department of Oral Biology University of Manitoba Winnipeg Canada National Research Council Biodiagnostics Institute Winnipeg Canada

Moulds, notably Stachybotrys chartarum (atra), are constant contributors to air pollution particularly to air quality in buildings. The spores themselves or their volatile organic products are present in variable amounts in almost all environments, particularly in buildings affected by flooding. These moulds and products can account for the sick building syndrome and have been tied to such occurrences as the outbreak of pulmonary hemosiderosis and hemorrhage in infants in Cleveland, Ohio. The present study was designed to investigate the effects of S. chartarum extracts on surfactant protein expression, surfactant quality and cell survival in the developing lung. S. chartarum extracts were incubated with cultures of several cell types;isolated fetal lung type II cells and fetal lung fibroblasts, and human lung A549 cells, a continuously growing cell line derived from surfactant producing type II alveolar cells. MTT formazan assays were employed to test cell viability. The synthesis and release of the predominant surfactant protein A (SP-A), which is involved in the regulation of surfactant turnover and metabolism, and surfactant protein B (SP-B) involved in shuttling phospholipids between surfactant subcompartments was also assessed. Antibodies to these proteins and western blotting results were used to assess the quantity of protein produced by the various cell types. A novel approach utilizing captive bubble surfactometry was employed to investigate the quality of surfactant in terms of surface tension and bubble volume measurements. Electron microscopy was used to examine changes in cellular structure of control and S. chartarum-treated cells. Results of the study showed that exposure to the S. chartarum extracts had deleterious effects on fetal lung epithelial cell viability and their ability to produce pulmonary surfactant. S. chartarum extracts also induced deleterious changes to the developing fetal lung cells in terms of expression of SP-A and SP-B as well a

关键词： Fetal Lung Surfactant Surface Tension Black Mould Captive Bubble Surfactometer Surfactant Proteins

Hepatitis B and C virus-induced hepatitis: Apoptosis, autophagy, and unfolded protein response

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World Journal of Gastroenterology 2015年第47期21卷 13225-13239页

作者： Behzad Yeganeh Adel Rezaei Moghadam Javad Alizadeh Emilia Wiechec Seyed Moayed Alavian Mohammad Hashemi Bita Geramizadeh Afshin Samali Kamran Bagheri Lankarani Martin Post Payam Peymani Kevin M Coombs Saeid Ghavami Department of Physiology and Experimental Medicine Hospital for Sick Children Research Institute University of Toronto Young Researchers and Elite Club Ardabil Branch Islamic Azad University Department of human anatomy and cell science College of Medicine Faculty of Health Sciences University of Manitoba The children's Hospital Research institute of manitoba University of Manitoba Department of Clinical and Experimental Medicine Division of Otorhinolaryngology Link?ping University Baqiyatallah Research Center for Gastroenterology and Liver Diseases (BRCGL) Department of Clinical Biochemistry School of Medicine Zahedan University of Medical Sciences Department of Pathology and Organ Transplant Research Center Shiraz University of Medical Sciences Department of Biochemistry National University of Ireland Galway health Policy Research Centre Shiraz University of Medical Sciences manitoba Center for Proteomics and Systems Biology University of Manitoba Department of Medical Microbiology and Infectious Diseases The Children's Hospital Research Institute of Manitoba University of Manitoba

AIM: To investigate the co-incidence of apoptosis, autophagy, and unfolded protein response(UPR) in hepatitis B(HBV) and C(HCV) infected ***: We performed immunofluorescence confocal microscopy on 10 liver biopsies from HBV and HCV patients and tissue microarrays of HBV positive liver samples. We used specific antibodies for LC3β, cleaved caspase-3, BIP(GRP78), and XBP1 to detect autophagy, apoptosis and UPR, respectively. AntiHCV NS3 and anti-HBs antibodies were also used to confirm infection. We performed triple blind counting of events to determine the co-incidence of autophagy(LC3β punctuate), apoptosis(cleaved caspase-3), and unfolded protein response(GRP78) with HBV and HCV infection in hepatocytes. All statistical analyses were performed using SPSS software for Windows(Version 16 SPSS Inc, Chicago, IL, United States). P-values cells and adjacent noninfected ***: Our results showed that infection of hepatocytes with either HBV and HCV induces significant increase(P cells, as compared to non-infected cells of the same biopsy sections. Our tissue microarray immunohistochemical expression analysis of LC3β in HBV^(Neg) and HBV^(Pos) revealed that majority of HBVinfected hepatocytes display strong positive stainingfor LC3β. Interestingly, although XBP splicing in HBVinfected cells was significantly higher(P cells(P > 0.05). Furthermore, our evaluation of patients with HBV and HCV infection based on stage and grade of the liver diseases revealed no correlation between these pathological findings and induction of apoptosis, autophagy,

关键词： cell fate cell death Hepatocyte Viralinfection Endoplasmic reticulum stress

FERM domain-containing protein FRMD6 activates the mTOR signaling pathway and promotes lung cancer progression

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Frontiers of Medicine 2023年第4期17卷 714-728页

作者： Tianzhuo Wang Huiying Guo Lei Zhang Miao Yu Qianchen Li Jing Zhang Yan Tang Hongquan Zhang Jun Zhan Program for Cancer and cell Biology Department of Human AnatomyHistology and EmbryologySchool of Basic Medical SciencesBeijing 100191China Peking university International Cancer institute Beijing 100191China MOE Key Laboratory of Carcinogenesis and Translational Research and State Key Laboratory of Natural and Biomimetic Drugs Peking University Health Science CenterBeijing 100191China

FRMD6,a member of the 4.1 ezrin-radixin-moesin domain-containing protein family,has been reported to inhibit tumor progression in multiple ***,we demonstrate the involvement of FRMD6 in lung cancer *** find that FRMD6 is overexpressed in lung cancer tissues relative to in normal lung *** addition,the enhanced expression of FRMD6 is associated with poor outcomes in patients with lung squamous cell carcinoma(n=75,P=0.0054)and lung adenocarcinoma(n=94,P=0.0330).cell migration and proliferation in vitro and tumor formation in vivo are promoted by FRMD6 but are suppressed by the depletion of ***,FRMD6 interacts and colocalizes with mTOR and S6K,which are the key molecules of the mTOR signaling ***6 markedly enhances the interaction between mTOR and S6K,subsequently increasing the levels of endogenous pS6K and downstream pS6 in lung cancer ***,knocking out FRMD6 inhibits the activation of the mTOR signaling pathway in Frmd6^(−/−)gene KO MEFs and ***,our results show that FRMD6 contributes to lung cancer progression by activating the mTOR signaling pathway.

关键词： FRMD6 lung cancer mTOR pathway

Multifaceted function of YAP/TEAD on chromatin:prospects of‘A non-canonical role of YAP/TEAD is required for activation of estrogen-regulated enhancers in breast cancer’

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Journal of Molecular cell Biology 2019年第12期11卷 1101-1103页

作者： Lizhen Chen Zhijie Liu Barshop institute for Longevity and Aging Studies Department of Cell Systems and AnatomyThe University of Texas Health Science Center at San AntonioSan AntonioTX 78229USA Department of Molecular Medicine Mays Cancer CenterThe University of Texas Health Science Center at San AntonioSan AntonioTX 78229USA

cellular function and behavior are controlled by various signals during development and disease progression in *** is important to understand how signals ultimately alter the function and structure of DNA regulatory elements,especially enhancers,causing the changes of gene expression *** average,each mature human cell harbors at least^100000 enhancers,but only a small percent of them have the function to activate gene *** instance,only^12%–18%of ERα-bound enhancers are active *** enhancers become functionally active is critical for our overall understanding of enhancer biology and gene *** are recognized by signaling-dependent DNA binding transcription factors(TFs),resulting in the recruitment of different enhancer activation components that allow distal enhancers to interact with their target promoters through chromatin looping(Plank and Dean,2014).Increasing evidence indicates that the recruitment and switching of enhancer components underlie enhancer activation and the deregulation in enhancer component or architecture profoundly alters signal-regulated transcriptional machineries,leading to developmental defects or diseases.

关键词： activation function instance

human embryonic stem cell-derived mesenchymal stem cells improved premature ovarian failure

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World Journal of Stem cells 2020年第8期12卷 857-878页

作者： Khadijeh Bahrehbar Mojtaba Rezazadeh Valojerdi Fereshteh Esfandiari Rouhollah Fathi Seyedeh-NafisehHassani Hossein Baharvand Department of Stem cells and Developmental Biology Cell Science Research CenterRoyan Institute for Stem Cell Biology and TechnologyTehran ***Iran Department of Developmental Biology University of Science and CultureTehran ***Iran Department of Embryology Reproductive Biomedicine Research CenterRoyan Institute for Reproductive BiomedicineTehran ***Iran Department of anatomy Faculty of Medical ScienceTarbiat Modares UniversityTehran ***Iran

BACKGROUND Premature ovarian failure(POF)affects many adult women less than 40 years of age and leads to *** to previous reports,various tissue-specific stem cells can restore ovarian function and folliculogenesis in mice with chemotherapy-induced *** embryonic stem cells(ES)provide an alternative source for mesenchymal stem cells(MSCs)because of their similarities in phenotype and immunomodulatory and anti-inflammatory *** stem cell-derived mesenchymal stem cells(ES-MSCs)are attractive candidates for regenerative medicine because of their high proliferation and lack of barriers for harvesting tissue-specific ***,possible therapeutic effects and underlying mechanisms of transplanted ES-MSCs on cyclophosphamide and busulfan-induced mouse ovarian damage have not been *** To evaluate ES-MSCs vs bone marrow-derived mesenchymal stem cells(BMMSCs)in restoring ovarian function in a mouse model of chemotherapy-induced premature ovarian *** Female mice received intraperitoneal injections of different doses of cyclophosphamide and busulfan to induce *** human ES-MSCs or BMMSCs were transplanted into these *** days after the mice were injected with cyclophosphamide and busulfan and 4 wk after transplantation of the ESMSCs and/or BM-MSCs,we evaluated body weight,estrous cyclicity,folliclestimulating hormone and estradiol hormone concentrations and follicle count were used to evaluate the POF model and cell ***,terminal deoxynucleotidyl transferase mediated 2-deoxyuridine 5-triphosphate nick end labeling,real-time PCR,Western blot analysis and immunohistochemistry and mating was used to evaluate cell ***-linked immunosorbent assay was used to analyze vascular endothelial growth factor,insulin-like growth factor 2 and hepatocyte growth factor levels in ES-MSC condition medium in order to investigate the mechanisms that underlie their *** Th

关键词： Premature ovarian failure human embryonic stem cells Chemotherapy drugs Mesenchymal stem cell Bone marrow Apoptosis