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Irisin-loaded electrospun core-shell nanofibers as calvarial periosteum accelerate vascularized bone regeneration by activating the mitochondrial SIRT3 pathway

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Regenerative Biomaterials 2024年第1期3卷 44-57页

作者： Xi Hua Mingzhuang Hou Lei Deng Nanning Lv Yong Xu Xuesong Zhu Huilin Yang Qin Shi Hao Liu Fan He Department of Orthopaedics The First Affiliated Hospital of Soochow UniversitySoochow UniversitySuzhou 215006China Orthopaedic Institute Suzhou Medical CollegeSoochow UniversitySuzhou 215000China Department of Orthopedics Suzhou Wuzhong People’s HospitalSuzhouJiangsu Province 215128China Department of Orthopedic Surgery Lianyungang Clinical College of Xuzhou Medical UniversityLianyungang 222003China

The scarcity of native periosteum poses a significant clinical barrier in the repair of critical-sized bone defects.The challenge of enhancing regenerative potential in bone healing is further compounded by oxidative stress at the fracture site.However,the introduction of artificial periosteum has demonstrated its ability to promote bone regeneration through the provision of appropriate mechanical support and controlled release of proosteogenic factors.In this study,a poly(L-lactic acid)(PLLA)/hyaluronic acid(HA)-based nanofibrous membrane was fabricated using the coaxial electrospinning technique.The incorporation of irisin into the core-shell structure of PLLA/HA nanofibers(PLLA/HA@Irisin)achieved its sustained release.In vitro experiments demonstrated that the PLLA/HA@Irisin membranes exhibited favorable biocompatibility.The osteogenic differentiation of bone marrow mesenchymal stem cells(BMMSCs)was improved by PLLA/HA@Irisin,as evidenced by a significant increase in alkaline phosphatase activity and matrix mineralization.Mechanistically,PLLA/HA@Irisin significantly enhanced the mitochondrial function of BMMSCs via the activation of the sirtuin 3 antioxidant pathway.To assess the therapeutic effectiveness,PLLA/HA@Irisin membranes were implanted in situ into critical-sized calvarial defects in rats.The results at 4 and 8 weeks post-surgery indicated that the implantation of PLLA/HA@Irisin exhibited superior efficacy in promoting vascularized bone formation,as demonstrated by the enhancement of bone matrix synthesis and the development of new blood vessels.The results of our study indicate that the electrospun PLLA/HA@Irisin nanofibers possess characteristics of a biomimetic periosteum,showing potential for effectively treating critical-sized bone defects by improving the mitochondrial function and maintaining redox homeostasis of BMMSCs.

关键词： periosteum irisin mitochondrial function critical-sized bone defect redox homeostasis

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Hif-1α/Hsf1/Hsp70 signaling pathway regulates redox homeostasis and apoptosis in large yellow croaker(Larimichthys crocea)under environmental hypoxia

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Zoological Research 2021年第6期42卷 746-760页

作者： Sheng-Yu Luo Jing-Qian Wang Cheng Liu Xin-Ming Gao Yi-Bo Zhang Jie Ding Cong-Cong Hou Jun-Quan Zhu Bao Lou Wei-Liang Shen Xiong-Fei Wu Chun-Dan Zhang Dao-Jun Tang Key Laboratory of Applied Marine Biotechnology by the Ministry of Education School of Marine SciencesNingbo UniversityNingboZhejiang 315211China Zhejiang Academy of Agricultural Sciences HangzhouZhejiang 310021China State Key Laboratory of Large Yellow Croaker Breeding Ningbo Academy of Oceanology and FisheryNingboZhejiang 315012China

Oxygen is an essential molecule for animal respiration,growth,and survival.Unlike in terrestrial environments,contamination and climate change have led to the frequent occurrence of hypoxia in aquatic environments,thus impacting aquatic animal survival.However,the adaptative mechanisms underlying fish responses to environmental hypoxia remain largely unknown.Here,we used large yellow croaker(Larimichthys crocea)and large yellow croaker fry(LYCF)cells to investigate the roles of the Hif-1α/Hsf1/Hsp70 signaling pathway in the regulation of cellular redox homeostasis,and apoptosis.We confirmed that hypoxia induced the expression of Hif-1α,Hsf1,and Hsp70 in vivo and in vitro.Genetic Hsp70 knockdown/overexpression indicated that Hsp70 was required for maintaining redox homeostasis and resisting oxidative stress in LYCF cells under hypoxic stress.Hsp70 inhibited caspase-dependent intrinsic apoptosis by maintaining normal mitochondrial membrane potential,enhancing Bcl-2 mRNA and protein expression,inhibiting Bax and caspase3 mRNA expression,and suppressing caspase-3 and caspase-9 activation.Hsp70 suppressed caspaseindependent intrinsic apoptosis by inhibiting nuclear translocation of apoptosis-inducing factor(AIF)and disturbed extrinsic apoptosis by inactivating caspase-8.Genetic knockdown/overexpression of Hif-1αand dual-luciferase reporter assay indicated that Hif-1αactivated the Hsf1 DNA promoter and enhanced Hsf1 mRNA transcription.Hsf1 enhanced Hsp70 mRNA transcription in a similar manner.In summary,the Hif-1α/Hsf1/Hsp70 signaling pathway plays an important role in regulating redox homeostasis and anti-apoptosis in L.crocea under hypoxic stress.

关键词： Hypoxia Larimichthys crocea Apoptosis redox homeostasis Hif-1α/Hsf1/Hsp70

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LSL1 controls cell death and grain production by stabilizing chloroplast in rice

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Science China(Life Sciences) 2022年第11期65卷 2148-2161页

作者： Deyong Ren Wei Xie Qiankun Xu Jiang Hu Li Zhu Guangheng Zhang Dali Zeng Qian Qian State Key Lab of Rice Biology China National Rice Research InstituteHangzhou 310006China College of Modern Agriculure Zhejiang A&F UniversityHangzhou 31006China National Nanfan Research Institute Chinese Academy of Agricultural SciencesSanya 572024China

Lesion mutants can be valuable tools to reveal the interactions between genetic factors and environmental signals and to improve grain production.Here we identified a rice(Oryza sativa)mutant,lesion spotleaf1(lsl1),which produces necrotic leaf lesions throughout its life cycle.LSL1 encodes a protein of unknown function and belongs to a grass-specific clade.The lesion phenotype of the lsl1 mutant was sharply induced by shading,and its detached leaves incubated in 6-benzylamino purine similarly formed lesions in the dark.In addition,the lsl1 mutant exhibited reactive oxygen species accumulation and cell death.The terminal deoxynucleotidyl transferase d UTP nick end-labeling(TUNEL)and comet assays revealed that the lsl1 mutant contained severe DNA damage,resulting in reduced grain yield and quality.RNA sequencing,gene expression,and protein activity analyses indicate that LSL1 is required for chloroplast function.Furthermore,LSL1 interacts with Psa D and PAP10 to form a regulatory module that functions in chlorophyll synthesis and chloroplast development to maintain redox balance.Our results reveal that LSL1 maintains chloroplast structure,redox homeostasis,and DNA stability,and plays important roles in the interaction between genetic factors and environmental signals and in regulating grain size and quality.

关键词： lesion formation chloroplast function redox homeostasis grain size and quality LSL1 rice

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Targeting glutamine utilization to block metabolic adaptation of tumor cells under the stress of carboxyamidotriazole-induced nutrients unavailability

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Acta Pharmaceutica Sinica B 2022年第2期12卷 759-773页

作者： Jing Shi Rui Ju Hongting Gao Yuqing Huang Lei Guo Dechang Zhang Department of Pharmacology Institute of Basic Medical SciencesChinese Academy of Medical Sciences and School of Basic MedicinePeking Union Medical CollegeBeijing 100005China Department of Pharmacy Peking University Third HospitalBeijing 100191China

Tumor cells have unique metabolic programming that is biologically distinct from that of corresponding normal cells.Resetting tumor metabolic programming is a promising strategy to ameliorate drug resistance and improve the tumor microenvironment.Here,we show that carboxyamidotriazole(CAI),an anticancer drug,can function as a metabolic modulator that decreases glucose and lipid metabolism and increases the dependency of colon cancer cells on glutamine metabolism.CAI suppressed glucose and lipid metabolism utilization,causing inhibition of mitochondrial respiratory chain complex I,thus producing reactive oxygen species(ROS).In parallel,activation of the aryl hydrocarbon receptor(Ah R)increased glutamine uptake via the transporter SLC1A5,which could activate the ROS-scavenging enzyme glutathione peroxidase.As a result,combined use of inhibitors of GLS/GDH1,CAI could effectively restrict colorectal cancer(CRC)energy metabolism.These data illuminate a new antitumor mechanism of CAI,suggesting a new strategy for CRC metabolic reprogramming treatment.

关键词： CAI Glutaminolysis Glutamine metabolism AhR Colorectal cancer metabolism Mitochondrial oxidative stress redox homeostasis Metabolic reprogramming

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Nuclear TIGAR mediates an epigenetic and metabolic autoregulatory loop via NRF2 in cancer therapeutic resistance

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Acta Pharmaceutica Sinica B 2022年第4期12卷 1871-1884页

作者： Hong Wang Qianqian Wang Guodi Cai Zhijian Duan Zoann Nugent Jie Huang Jianwei Zheng Alexander D.Borowsky Jian Jian Li Peiqing Liu Hsing-Jien Kung Leigh Murphy Hong-Wu Chen Junjian Wang School of Pharmaceutical Sciences Sun Yat-sen UniversityGuangzhou 510006China Department of Biochemistry and Molecular Medicine University of CaliforniaDavisSacramentoCA 95817USA Research Institute in Oncology and Hematology University of Manitoba and CancerCare ManitobaWinnipeg R3E 0V9Canada Guangdong Lung Cancer Institute Guangdong Provincial Key Laboratory of Translational Medicine in Lung CancerGuangdong Provincial People’s Hospital and Guangdong Academy of Medical SciencesGuangzhou 510080China Department of Pathology and Laboratory Medicine University of CaliforniaDavisSacramentoCA 95817USA Department of Radiation Oncology University of CaliforniaDavisSacramentoCA 95817USA National-Local Joint Engineering Laboratory of Druggability and New Drugs Evaluation Guangdong Provincial Key Laboratory of New Drug Design and EvaluationSun Yat-sen UniversityGuangzhou 510006China UC Davis Comprehensive Cancer Center School of MedicineUniversity of CaliforniaDavisSacramentoCA 95817USA

Metabolic and epigenetic reprogramming play important roles in cancer therapeutic resistance.However,their interplays are poorly understood.We report here that elevated TIGAR(TP53-induced glycolysis and apoptosis regulator),an antioxidant and glucose metabolic regulator and a target of oncogenic histone methyltransferase NSD2(nuclear receptor binding SET domain protein 2),is mainly localized in the nucleus of therapeutic resistant tumor cells where it stimulates NSD2 expression and elevates global H3K36me2 mark.Mechanistically,TIGAR directly interacts with the antioxidant master regulator NRF2 and facilitates chromatin recruitment of NRF2,H3K4me3 methylase MLL1 and elongating Pol-II to stimulate the expression of both new(NSD2)and established(NQO1/2,PRDX1 and GSTM4)targets of NRF2,independent of its enzymatic activity.Nuclear TIGAR confers cancer cell resistance to chemotherapy and hormonal therapy in vitro and in tumors through effective maintenance of redox homeostasis.In addition,nuclear accumulation of TIGAR is positively associated with NSD2 expression in clinical tumors and strongly correlated with poor survival.These findings define a nuclear TIGAR-mediated epigenetic autoregulatory loop in redox rebalance for tumor therapeutic resistance.

关键词： TIGAR NSD2 NRF2 Metabolism Oxidative stress Epigenetic reprogramming Therapeutic resistance redox homeostasis

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Dusp 1 regulates thermal tolerance limits in zebrafish by maintaining mitochondrial integrity

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Zoological Research 2023年第1期44卷 126-141页

作者： Ying Wang Hua-Min Wang Yan Zhou Ling-Hong Hu Jing-Ming Wan Ji-Hui Yang Hong-Bo Niu Xiu-Ping Hong Peng Hu Liang-Biao Chen International Research Center for Marine Biosciences Ministry of Science and TechnologyShanghai Ocean UniversityShanghai 200120China Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources Ministry of EducationShanghai Ocean UniversityShanghai 200120China Shanghai Collaborative Innovation for Aquatic Animal Genetics and Breeding Shanghai Ocean UniversityShanghai 200120China

Temperature tolerance restricts the distribution of a species. However, the molecular and cellular mechanisms that set the thermal tolerance limits of an organism are poorly understood. Here, we report on the function of dual-specificity phosphatase 1(DUSP1) in thermal tolerance regulation. Notably, we found that dusp1-/- zebrafish grew normally but survived within a narrowed temperature range. The higher susceptibility of these mutant fish to both cold and heat challenges was attributed to accelerated cell death caused by aggravated mitochondrial dysfunction and over-production of reactive oxygen species in the gills. The DUSP1-MAPK-DRP1 axis was identified as a key pathway regulating these processes in both fish and human cells. These observations suggest that DUSP1 may play a role in maintaining mitochondrial integrity and redox homeostasis. We therefore propose that maintenance of cellular redox homeostasis may be a key mechanism for coping with cellular thermal stress and that the interplay between signaling pathways regulating redox homeostasis in the most thermosensitive tissue(i.e., gills) may play an important role in setting the thermal tolerance limit of zebrafish.

关键词： redox homeostasis Zebrafish Ectothermal Mitochondrial fission Thermal stress MAPK

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Non-enzymatic antioxidant blood plasma profile in the period of high training loads of elite speed skaters in the altitude

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Sports Medicine and Health Science 2023年第2期5卷 120-127页

作者： Elena Proskurnina Dmitry Martynov Andrey Yakushkin Irina Zelenkova Laboratory of Molecular Biology Research Centre for Medical GeneticsMoscow115522Russia Faculty of Fundamental Medicine Lomonosov Moscow State UniversityMoscow119991Russia The Federal Training Sport Center of the Representative Teams of Russia Moscow105064Russia GENUD(Growth ExerciseNutritionand Development)Research GroupDepartment of Physiatry and NursingUniversity of Zaragoza50009Spain

At the altitude,hypoxia and training load are key factors in the development of oxidative stress.Altitude-induced oxidative stress is developed due to the depletion of antioxidant potential.In the current study,we examined the non-enzymatic antioxidant profile of blood plasma in 7 males and 5 females specializing in speed skating at a 21-day training camp at 1850m above sea level.Training included:cycling,roller skating,ice skating,strength training,and special training.At the start point and the endpoint,total hemoglobin mass(tHb-mass),hemoglobin concentration,and circulating blood volume were determined.Antioxidant profiles,hypoxic doses,hypoxic impulses,and training impulses were assessed at 3,6,10,14,and 18 days.Antioxidant profiles consisting of“urate”and“thiol”parts were registered with chemiluminometry.In the training dynamics,antioxidant parameters changed individually,but in total there was a decrease in the“urate”capacity by a factor of 1.6(p=0.001)and an increase in the“thiol”capacity by a factor of 1.8(p=0.013).The changes in“urate”capacity positively correlated(r_(S)=0.40)and the changes in“thiol”capacity negatively correlated(r_(S)=−0.45)with changes in tHb-mass.Both exercise and hypoxic factors affect the antioxidant parameters bidirectionally.They correlated with a decrease in thiol capacity and with an increase in urate capacity.The assessment of the non-enzymatic antioxidant profile can be a simple and useful addition to screening the reactive oxygen species homeostasis and can help choose the personalized training schedule,individualize recovery and ergogenic support.

关键词： Elite athletes High training loads Oxidative stress Blood antioxidants redox homeostasis Altitude training Speed skating

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A Reactive Oxygen Species-Tyrosinase Cascade-Activated Prodrug for Selectively Suppressing Melanoma

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CCS Chemistry 2022年第5期4卷 1654-1670页

作者： Guorui Li Yi Yang Yaya Zhang Peiling Huang Jiangyu Yan Zhibin Song Quan Yuan Jing Huang Institute of Chemical Biology and Nanomedicine(ICBN) State Key Laboratory of Chemo/Biosensing and ChemometricsCollege of BiologyCollege of Chemistry and Chemical EngineeringHunan Provincial Key Laboratory of Biomacromolecular Chemical BiologyHunan UniversityChangsha 410082 Key Laboratory of Functional Small Organic Molecules Ministry of EducationCollege of Chemistry and Chemical EngineeringJiangxi Normal UniversityNanchang 330022

“Off-target effect”is one of the obstacles for targeted prodrugs in chemotherapy.To circumvent this issue,herein we propose a dual biomarker cascadeactivated prodrug strategy based on high levels of reactive oxygen species(ROS)and tyrosinase(TYR)in melanoma cells.A representative prodrug,Coumarin-Quinazolinone-phenylBoronic acid pinacol ester(CQB),was prepared.The prodrug contained Coumarin-Quinazolinone(CQ)as mitochondria targeting and monitoring moiety and phenylboronic acid pinacol ester as a cascade-activated prowarhead.After activation by the endogenous ROS and subsequent TYR in melanoma cells,CQB can be converted to the final active reagent Coumarin-Quinazolinone-o-Quinone(CQQ)that contains o-quinone group as the reactive species.CQQ may interact with cellular nucleophiles to exert its genotoxic effect and disrupt the cellular redox balance.This enables CQB to selectively suppress melanoma.CQB accumulates in the mitochondria and causes mitochondrial dysfunction via affecting mitochondrial DNA integrity.This cascade-activated prodrug may provide a precise strategy for melanoma theranostics.

关键词： prodrug cascade activated ROS TYR melanoma mitochondria redox homeostasis theranostics

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Regulation of multidrug resistance by microRNAs in anti-cancer therapy

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Acta Pharmaceutica Sinica B 2017年第1期7卷 38-51页

作者： Xin An Cesar Sarmiento Tao Tan Hua Zhu State Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer Medicine Department of Surgery Davis Heart and Lung Research InstituteThe Ohio State University Wexner Medical Center

Multidrug resistance(MDR) remains a major clinical obstacle to successful cancer treatment.Although diverse mechanisms of MDR have been well elucidated, such as dysregulation of drugs transporters, defects of apoptosis and autophagy machinery, alterations of drug metabolism and drug targets, disrupti on of redox homeostasis, the exact mechanisms of MDR in a specific cancer patient and the cross-talk among these different mechanisms and how they are regulated are poorly understood.Micro RNAs(mi RNAs) are a new class of small noncoding RNAs that could control the global activity of the cell by post-transcriptionally regulating a large variety of target genes and proteins expression.Accumulating evidence shows that mi RNAs play a key regulatory role in MDR through modulating various drug resistant mechanisms mentioned above, thereby holding much promise for developing novel and more effective individualized therapies for cancer treatment. This review summarizes the various MDR mechanisms and mainly focuses on the role of mi RNAs in regulating MDR in cancer treatment.

关键词： Multidrug resistance miRNA Cancer Therapy Autophagy redox homeostasis

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Current Opinions on the Functions of Tocopherol Based on the Genetic Manipulation of Tocopherol Biosynthesis in Plants

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Journal of Integrative Plant Biology 2008年第9期50卷 1057-1069页

作者： Yin Li Zinan Wang Xiaofen Sun Kexuan Tang State Key Laboratory of Genetic Engineering School of Life Sciences Fudan-SJTU-Nottingham Plant Biotechnology R&D Center Fudan University Shanghai 200433 China Plant Biotechnology Research Center School of Agriculture and Biology Fudan-SJTU-Nottingham Plant Biotechnology R&D Center Shanghai Jiao Tong University Shanghai 200030 China

As a member of an important group of lipid soluble antioxidants, tocopherols play a paramount role in the daily diet of humans and animals. Recently, genes required for tocochromanol biosynthesis pathway have been identified and cloned with the help of genomics-based approaches and molecular manipulation in the model organisms： Arabidopsis thaliana and Synechocystis sp. PCC 6803. At the basis of these foundations, genetic manipulation of tocochromanol biosynthesis pathway can give rise to strategies that enhance the level of tocochromanol content or convert the constitution of tocochromanol. In addition, genetic manipulations of the tocochromanol biosynthesis pathway provide help for the study of the function of tocopherol in plant systems. The present article summarizes recent advances and pays special attention to the functions of tocopherol in plants. The roles of tocopherol in the network of reactiv.e oxygen species, antioxidants and phytohormones to maintain redox homeostasis and the functions of tocopherol as a signal molecule in chloroplast-to- nucleus signaling to regulate carbohydrate metabolism are also discussed.

关键词： antioxidant carbohydrate metabolism genetic dissection programmed cell death redox homeostasis signal molecule tocopherol.

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