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Transplantation of human placental chorionic plate-derived mesenchymal stem cells for repair of neurological damage in neonatal hypoxic-ischemic encephalopathy

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Neural Regeneration Research 2024年第9期19卷 2027-2035页

作者： Lulu Xue Ruolan Du Ning Bi Qiuxia Xiao Yifei Sun Ruize Niu Yaxin Tan Li Chen Jia Liu Tinghua Wang Liulin Xiong Transformation Research Laboratory The Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhou ProvinceChina State Key Laboratory of biotherapy Sichuan UniversityChengduSichuan ProvinceChina Institute of Neurological Disease Translational Neuroscience CenterWest China HospitalSichuan UniversityChengduSichuan ProvinceChina department of Animal Zoology Institute of NeuroscienceKunming Medical UniversityKunmingYunnan ProvinceChina department of Anesthesiology The Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhou ProvinceChina department of Pediatrics the People’s Liberation Army Rocket Force Characteristic Medical CenterBeijingChina

Neonatal hypoxic-ischemic encephalopathy is often associated with permanent cerebral palsy,neurosensory impairments,and cognitive deficits,and there is no effective treatment for complications related to hypoxic-ischemic encephalopathy.The therapeutic potential of human placental chorionic plate-derived mesenchymal stem cells for various diseases has been explored.However,the potential use of human placental chorionic plate-derived mesenchymal stem cells for the treatment of neonatal hypoxic-ischemic encephalopathy has not yet been investigated.In this study,we injected human placental chorionic plate-derived mesenchymal stem cells into the lateral ventricle of a neonatal hypoxic-ischemic encephalopathy rat model and observed significant improvements in both cognitive and motor function.Protein chip analysis showed that interleukin-3 expression was significantly elevated in neonatal hypoxic-ischemic encephalopathy model rats.Following transplantation of human placental chorionic plate-derived mesenchymal stem cells,interleukin-3 expression was downregulated.To further investigate the role of interleukin-3 in neonatal hypoxic-ischemic encephalopathy,we established an in vitro SH-SY5Y cell model of hypoxic-ischemic injury through oxygen-glucose deprivation and silenced interleukin-3 expression using small interfering RNA.We found that the activity and proliferation of SH-SY5Y cells subjected to oxygen-glucose deprivation were further suppressed by interleukin-3 knockdown.Furthermore,interleukin-3 knockout exacerbated neuronal damage and cognitive and motor function impairment in rat models of hypoxic-ischemic encephalopathy.The findings suggest that transplantation of hpcMSCs ameliorated behavioral impairments in a rat model of hypoxic-ischemic encephalopathy,and this effect was mediated by interleukin-3-dependent neurological function.

关键词： behavioral evaluations gene knockout human neuroblastoma cells(SH-SY5Y) human placental chorionic derived mesenchymal stem cells interleukin-3 neonatal hypoxic-ischemic encephalopathy nerve injury oxygen-glucose deprivation protein chip small interfering RNA

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Britanin–a beacon of hope against gastrointestinal tumors?

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World Journal of Clinical Oncology 2024年第4期15卷 523-530页

作者： Agnieszka Kajdanek Damian Kołat Lin-Yong Zhao Mateusz Kciuk Zbigniew Pasieka Żaneta Kałuzińska-Kołat department of Biomedicine and Experimental Surgery Medical University of LodzLodz 90-136LodzkiePoland department of Functional Genomics Medical University of LodzLodz 90-752LodzkiePoland department of General Surgery&Laboratory of Gastric Cancer State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer CenterWest China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina Gastric Cancer Center West China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina department of Molecular Biotechnology and Genetics University of LodzLodz 90-237LodzkiePoland

Britanin is a bioactive sesquiterpene lactone known for its potent anti-inflammatory and anti-oxidant properties.It also exhibits significant anti-tumor activity,suppressing tumor growth in vitro and in vivo.The current body of research on Britanin includes thirty papers predominantly related to neoplasms,the majority of which are gastrointestinal tumors that have not been summarized before.To drive academic debate,the present paper reviews the available research on Britanin in gastrointestinal tumors.It also outlines novel research directions using data not directly concerned with the digestive system,but which could be adopted in future gastrointestinal research.Britanin was found to counteract liver,colorectal,pancreatic,and gastric tumors,by regulating proliferation,apoptosis,autophagy,immune response,migration,and angiogenesis.As confirmed in pancreatic,gastric,and liver cancer,its most commonly noted molecular effects include nuclear factor kappa B and B-cell lymphoma 2 downregulation,as well as Bcl-2-associated X protein upregulation.Moreover,it has been found to induce the Akt kinase and Forkhead box O1 axis,activate the AMP-activated protein kinase pathway,elevate interleukin-2 and peroxisome proliferator-activated receptor-γlevels,reduce interleukin-10,as well as downregulate matrix metalloproteinase-9,Twist family bHLH transcription factor 1,and cyclooxygenase-2.It also inhibits Myc–HIF1αinteraction and programmed death ligand 1 transcription by interrupting the Ras/RAF/MEK/ERK pathway and mTOR/P70S6K/4EBP1 signaling.Future research should aim to unravel the link between Britanin and acetylcholinesterase,mast cells,osteolysis,and ischemia,as compelling data have been provided by studies outside the gastrointestinal context.Since the cytotoxicity of Britanin on noncancerous cells is significantly lower than that on tumor cells,while still being effective against the latter,further in-depth studies with the use of animal models are merited.The compound exhibits pleiotropic biological activity and offers

关键词： Britanin Sesquiterpene lactones Chemotherapeutics Gastrointestinal tumors In vitro In vivo

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Colony-stimulating factor-1 receptor inhibition combined with paclitaxel exerts effective antitumor effects in the treatment of ovarian cancer

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Genes & Diseases 2024年第3期11卷 400-416页

作者： Meijia Yu Yiming Wu Qingfang Li Weiqi Hong Yang Yang Xiaoyi Hu Yanfei Yang Tianqi Lu Xia Zhao Xiawei Wei Laboratory of Aging Research and Cancer Drug Target State Key Laboratory of Biotherapy and Cancer CenterNational Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityChengduSichuan 610041China department of Gynecology and Obstetrics Development and Related Disease of Women and Children Key Laboratory of Sichuan ProvinceKey Laboratory of Birth Defects and Related Diseases of Women and ChildrenMinistry of EducationWest China Second HospitalSichuan UniversityChengduSichuan 610041China department of Obstetrics and Gynecology The First Affiliated HospitalArmy Medical UniversityChongqing 400038China

Ovarian cancer is the tumor with the highest mortality among gynecological malig-nancies.Studies have confirmed that paclitaxel chemoresistance is associated with increased infiltration of tumor-associated macrophages(TAMs)in the microenvironment.Colony-stimu-lating factor 1(CSF-1)receptor(CSF-1R)plays a key role in regulating the number and differ-entiation of macrophages in certain solid tumors.There are few reports on the effects of targeted inhibition of CSF-1R in combination with chemotherapy on ovarian cancer and the tu-mor microenvironment.Here,we explored the antitumor efficacy and possible mechanisms of the CSF-1R inhibitor pexidartinib(PLX3397)when combined with the first-line chemothera-peutic agent paclitaxel in the treatment of ovarian cancer.We found that CSF-1R is highly ex-pressed in ovarian cancer cells and correlates with poor prognosis.Treatment by PLX3397 in combination with paclitaxel significantly inhibited the growth of ovarian cancer both in vitro and in vivo.Blockade of CSF-1R altered the macrophage phenotype and reprogrammed the immunosuppressive cell population in the tumor microenvironment.

关键词： CSF-1R Ovariancancer Paclitaxel PLX3397 Targeted therapy Tumor-associated macrophages

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Telomerase inhibition and telomere loss in BEL-7404 human hepatoma cells treated with doxorubicin

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World Journal of Gastroenterology 2002年第5期8卷 827-831页

作者： Ru-Gang Zhang Li-Xia Guo Xing-Wang Wang Hong Xie department of biotherapy,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,the Chinese Academy of Sciences,Shanghai 200031,China department of biotherapy Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences the Chinese Academy of Sciences Shanghai 200031 China.

AIM：To study the effects of doxorub icin on telomerase activity and telomere length in hepatocellular carcinoma.METHODS:Telomerase activity was assayed with a non-radioisotopic quantitative telomerase repeat amplification protocal-based method.The effect of doxorubicin(DOX) on the growth of BEL-7404 human hepatoma cells was the growth of BEL-7404human hepatoma cells was determined by microculture tetrazoloum assay.Mean telomere length(terminal restriction fragment)was detected by Southern blot method.The expression of telomerase subunits genes was investigated by RT-PCR,Cell apoptosis and cell cycle distribution were evaluated by flow cytometry.RESULTS:Telomerase activity was inhibited in a dose and time-depandent manner in BEL-7404human hepatoma cells treated with DOXfor24,48or72h in concentrations from 0.156to 2.5μMwhich was crrelated with the inhibition of cell growth.No changes were found in the mRNA expression of three telomerase subunits(hTERT,hTR and TP1)after drug exposure for 72h with indicated concentrations.The cells treated with DOX showed shortened mean telomer length and accumulated at he G2/M phase.However,there was almost no effects on cell apoptosis by DOX.CONCLUSION:The telomerase inhibition an d the telomere shortening by ODXmay contribute to its efficiency in the treatment in hepatocellular carcinoma.

关键词：阿霉素肝细胞癌端粒酶化学疗法端粒丢失

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Antihepatoma effect of alpha-fetoprotein antisense phosphorothioate oligodeoxyribonucleotides in vitro and in mice

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World Journal of Gastroenterology 2001年第3期7卷 345-351页

作者： Xing Wang Wang~1 Jin Hui Yuan~1 Ru Gang Zhang~1 Li Xia Guo~1 Yong Xie~2 Hong Xie~1 ~1department of biotherapy,Shanghai Institute of Cell Biology,Chinese Academy of Sciences,Shanghai 200031,China ~2department of Biology,Hong Kong University of Science and Technology,ChinaDr.Xing Wang Wang earned Ph.D.from Shanghai Institute of Materia Medical,Chinese Academy of Sciences in 1997.Now a professor at Shanghai Institute of Cell Biology,Chinese Academy of Sciences. department of biotherapy Shanghai Institute of Cell Biology Chinese Academy of Sciences 320 Yue-Yang Road Shanghai 200031 China.

AIM To evaluate antihepatoma effect ofantisense phosphorothioate oligodeo-xyribonucleotides (S-ODNs) targeted to alpha-fetoprotein (AFP) genes in vitro and in nudemice.METHODS AFP gene expression was examinedby immunocytochemical method or enzyme-linked immunosorbent assay. Effect of S-ODNson SMMC-7721 human hepatoma cell growth invitro was determined using microculturetetrazolium assay. In vivo antitumor activitiesof S-ODNs were monitored by measuring tumorweight differences in treated and control micebearing SMMC-7721 xenografts. Induction of cellapoptosis was evaluated by fluorescence-activated cell sorter (FACS) analysis.RESULTS Antisense S-ODN treatment led toreduced AFP gene expression. Specificantisense S-ODNs, but not control S-ODNs,inhibited the growth of heaptoma cells in vitro.In vivo. only antisense S-ODNs exhibitedobvious antitumor activities. FACS analysisrevealed that the growth inhibition by antisenseS. ODNs was associated with their cell apoptosisinduction.CONCLUSION Antisense S-ODNs targeted toAFP genes inhibit the growth of human hepatomacells and solid hepatoma, which is related totheir cell apoptosis induction.

关键词： alpha-fetoproteins/genetics oligodeoxyribonucleotides, antisense/pharmacology liver neoplasms/pathology tumor cells, cultured/drug effects gene expression/drug effects

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Cancer-educated neutrophils promote lung cancer progression via PARP-1-ALOX5-mediated MMP-9 expression

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Cancer Biology & Medicine 2024年第2期21卷 175-192页

作者： Lulu Han Yuxin Chen Nan Huang Xiaowan Zhou Yanfang Lv Huizhong Li Dafei Chai Junnian Zheng Gang Wang Cancer Institute Xuzhou Medical University209 Tongshan RoadXuzhou 221004China Center of Clinical Oncology The Affiliated Hospital of Xuzhou Medical University99 West Huaihai RoadXuzhou 221002China Jiangsu Center for the Collaboration and Innovation of Cancer biotherapy Xuzhou Medical University209 Tongshan RoadXuzhou 221004China department of Oncology Suzhou Xiangcheng People’s HospitalSuzhou 215131China

Objective:Neutrophils are one of the most predominant infiltrating leukocytes in lung cancer tissues and are associated with lung cancer progression.How neutrophils promote lung cancer progression,however,has not been established.Methods:Kaplan–Meier plotter online analysis and tissue immunohistochemistry were used to determine the relationship between neutrophils and overall survival in lung cancer patients.The effect of neutrophils on lung cancer was determined using the Transwell migration assay,a proliferation assay,and a murine tumor model.Gene knockdown was used to determine poly ADPribose polymerase(PARP)-1 function in lung cancer-educated neutrophils.Western blot analysis and gelatin zymography were used to demonstrate the correlation between PARP-1 and matrix metallopeptidase 9(MMP-9).Immunoprecipitation coupled to mass spectrometry(IP/MS)was used to identify the proteins interacting with PARP-1.Co-immunoprecipitation(Co-IP)was used to confirm that PARP-1 interacts with arachidonate 5-lipooxygenase(ALOX5).Neutrophil PARP-1 blockage by AG14361 rescued neutrophil-promoted lung cancer progression.Results:An increased number of infiltrating neutrophils was negatively associated with overall survival in lung cancer patients(P<0.001).Neutrophil activation promoted lung cancer cell invasion,migration,and proliferation in vitro,and murine lung cancer growth in vivo.Mechanistically,PARP-1 was shown to be involved in lung cancer cell-induced neutrophil activation to increase MMP-9 expression through interacting and stabilizing ALOX5 by post-translational protein modification(PARylation).Blocking PARP-1 by gene knockdown or AG14361 significantly decreased ALOX5 expression and MMP-9 production,and eliminated neutrophil-mediated lung cancer cell invasion and in vivo tumor growth.Conclusion:We identified a novel mechanism by which PARP-1 mediates lung cancer cell-induced neutrophil activation and PARylates ALOX5 to regulate MMP-9 expression,which exacerbates lung cancer progression.

关键词： Lung cancer neutrophils PARP-1 ALOX5 MMP-9

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Long non-coding RNA MALAT1 in hematological malignancies and its clinical applications

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中华医学杂志(英文版) 2024年第10期137卷 2024 Apr 1页

作者： Zhang Chunlan Qin Yun Wu Yu Xu Heng Shu Yang department of Hematology West China Hospital Sichuan University Chengdu Sichuan China department of Radiology West China Hospital Sichuan University Chengdu Sichuan China department of Laboratory Medicine/Research Center of Clinical Laboratory Medicine West China Hospital Sichuan University Chengdu Sichuan China department of biotherapy State Key Laboratory of Biotherapy and Cancer Center West China Hospital Sichuan University Chengdu Sichuan China Institute of General Surgery West China Hospital Sichuan University Chengdu Sichuan China department of General Surgery Gastric Cancer Center and Laboratory of Gastric Cancer West China Hospital Sichuan University Chengdu Sichuan China

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a well-established oncogenic long non-coding RNA, the higher expression of which is strongly correlated with cancer events such as tumorigenesis, progression, metastasis, drug resistance, and treatment outcome in solid cancers. Recently, a series of studies has highlighted its potential role in hematological malignancies in terms of these events. Similar to solid cancers,MALAT1 can regulate various target genes via sponging and epigenetic mechanisms, but the miRNAs sponged byMALAT1 differ from those identified in solid cancers. In this review, we systematically describe the role and underlying mechanisms ofMALAT1 in multiple types of hematological malignancies, including regulation of cell proliferation, metastasis, stress response, and glycolysis. Clinically,MALAT1 expression is related to poor treatment outcome and drug resistance, therefore exhibiting potential prognostic value in multiple myeloma, lymphoma, and leukemia. Finally, we discuss the evaluation ofMALAT1 as a novel therapeutic target against cancer in preclinical studies.

关键词： Long non-coding RNA MALAT1 Hematological malignancies Tumorigenesis Metastasis Drug resistance Prognostic biomarker

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Reduced macular thickness and vascular density in abnormal glucose metabolism patients: A meta-analysis of optical coherence tomography (OCT) and OCT angiography studies

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中华医学杂志(英文版) 2024年第9期137卷 2024 Apr 2页

作者： Fu Xiangyu Ren Xiang Chen Wenyue Chen Danian department of Ophthalmology West China Hospital Sichuan University Chengdu Sichuan China Research Laboratory of Ophthalmology and Vision Sciences State Key Laboratory of Biotherapy West China Hospital Sichuan University Chengdu Sichuan China department of Ophthalmology The People’s Hospital of Guizhou Province Guiyang Guizhou China

Background: Alterations in macular thickness and vascular density before clinically visible diabetic retinopathy (DR) remain inconclusive. This study aimed to determine whether retinal manifestations in abnormal glucose metabolism (AGM) patients differ from those in the healthy individuals.Methods: PubMed, Embase, and Web of Science were searched between 2000 and 2021. The eligibility criteria were AGM patients without DR. Primary and secondary outcomes measured by optical coherence tomography (OCT) and OCT angiography (OCTA) were analyzed and expressed as standardized mean differences (SMDs) with 95% confidence intervals (CIs). A random-effects model was used in the data synthesis. The potential publication bias for the variables was evaluated using Egger’s test.Results: A total of 86 observational studies involving 13,773 participants and 15,416 eyes were included. OCT revealed that compared to healthy controls, the total macular thickness of AGM patients was thinner, including the thickness of fovea (–0.24, 95% CI [–0.39, –0.08];P = 0.002,I2 = 87.7%), all regions of parafovea (–0.32, 95% CI [–0.54, –0.11];P = 0.003;I2 = 71.7%) and the four quadrants of perifovea; the thickness of peripapillary retinal nerve fiber layer (pRNFL), macular retinal nerve fiber layer (mRNFL), and ganglion cell layer (GCL) also decreased. OCTA indicated that the superficial and deep vascular density decreased, the foveal avascular zone (FAZ) area enlarged, and the acircularity index (AI) reduced in AGM individuals.Conclusions: Retinal thinning and microvascular lesions have occurred before the advent of clinically detectable DR; OCT and OCTA may have the potential to detect these preclinical changes.Registration: PROSPERO; http://www.***.york.***.uk/prospero/; No. CRD42021269885.

关键词： Abnormal glucose metabolism Optical coherence tomography Optical coherence tomography angiography Diabetic retinopathy Prediabetes Meta-analysis

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A retrospective analysis of mature T-and NK-cell lymphomas

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Cancer Biology & Medicine 2024年第3期21卷 223-229页

作者： Junlei Jia Xiaohui Wang Zheng Song Shen Meng Yue Fei Jingwei Yu Xia Liu Xue Han Lanfang Li Lihua Qiu Zhengzi Qian Shiyong Zhou Wenchen Gong Bin Meng Xiubao Ren Xianhuo Wang Huilai Zhang National Key Laboratory of Druggability Evaluation and Systematic Translational Medicine and Department of LymphomaTianjin Medical University Cancer Institute&HospitalNational Clinical Research Center for CancerTianjin's Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjinThe Sino-US Center for Lymphoma and Leukemia ResearchTianjin 300060China department of Radiation Oncology Shandong Cancer Hospital and InstituteShandong First Medical University and Shandong Academy of Medical SciencesJinan 250117China department of Pathology department of Immunology/biotherapy Tianjin Medical University Cancer Institute&HospitalNational Clinical Research Center for CancerTianjin's Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjinTianjin 300060China

Mature T-and natural killer(NK)-cell lymphomas are heterogeneous groups of malignant lymphoid neoplasms arising from T and NK cells. The incidence of mature T-and NK-cell lymphomas is 2.1 per 100,000 people, according... 详细信息

关键词： lymphoma neoplasms killer

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Mesenchymal stem cell-derived exosomes: Versatile nanomaterials for skin wound treatment

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Nano Research 2024年第4期17卷 2836-2856页

作者： Yuzhen Xiao Hexi Li Junhui Zhang Songyun Yang Chunsen Zhang Yizhou Huang Xin Tang Huiqi Xie department of Orthopedic Surgery and Orthopedic Research Institute Laboratory of Stem Cell and Tissue EngineeringState Key Laboratory of BiotherapyWest China HospitalSichuan UniversityChengdu 610041China West China School of Basic Medical Sciences and Forensic Medicine Sichuan UniversityChengdu 610041China West China School of Public Health and West China Fourth Hospital Sichuan UniversityChengdu 610041China Sports Medicine Center West China HospitalSichuan UniversityChengdu 610041China

Accumulating studies reveal that mesenchymal stem cells(MSCs)promote skin wound healing mainly through the paracrine effects.Exosomes,one of the crucial paracrine mediators in wound healing,are cell-derived nanosized membranous vesicles containing diverse bioactive cargoes.With the potent ability of modulating skin cell behaviors,MSC-derived exosomes(MSC-Exos)are regarded as a promising nanomaterial for regenerative wound therapy.Under hostile conditions,MSC-Exos are efficient in protecting skin cells from severe damage and restoring their function.According to recent studies,MSC-Exos possess remarkable pro-healing effects in a variety of skin wounds,typically resulting in increased wound closure,inhibited scar tissue formation,and better restoration of skin function.To further enhance the therapeutic potential of MSC-Exos,the development of applicable pretreatment strategies and the optimization of exosome delivery are under intensive investigation.Herein,we summarize current research progress of MSC-Exos for skin wound treatment,with an emphasis on the biological effects of these nanovesicles,the repair mechanisms,and future challenges in clinical translation.

关键词： exosomes mesenchymal stem cells diabetic wounds burn wounds scar wound healing

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