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A novel sprayable thermosensitive hydrogel coupled with zinc modified metformin promotes the healing of skin wound

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Bioactive Materials 2023年第2期20卷 610-626页

作者： Zhengwei Liu Wanze Tang Jiayi Liu Yingying Han qinnan yan Yuechao Dong Xiaomei Liu Dazhi yang Guixing Ma Huiling Cao Department of Biochemistry School of MedicineSouthern University of Science and TechnologyGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease ResearchShenzhen Key Laboratory of Cell MicroenvironmentShenzhen518055China Southern University of Science and Technology Shenzhen518055China Department of Biomedical Engineering Southern University of Science and TechnologyShenzhen518055China The First Affiliated Hospital Southern University of Science and TechnologyShenzhen518055China

A novel sprayable adhesive is established(ZnMet-PF127)by the combination of a thermosensitive hydrogel(Pluronic F127,PF127)and a coordination complex of zinc and metformin(ZnMet).Here we demonstrate that ZnMet-PF127 potently promotes the healing of traumatic skin defect and burn skin injury by promoting cell proliferation,angiogenesis,collagen ***,we find that ZnMet could inhibit reactive oxygen species(ROS)production through activation of autophagy,thereby protecting cell from oxidative stress induced damage and promoting healing of skin *** complex exerts better effects on promoting skin wound healing than ZnCl2 or metformin *** complex also displays excellent antibacterial activity against Staphylococcus aureus or Escherichia coli,which could reduce the incidence of skin wound ***,we demonstrate that sprayable PF127 could be used as a new drug delivery system for treatment of skin *** advantages of this sprayable system are obvious:(1)It is convenient to use;(2)The hydrogel can cover irregular skin defect sites evenly in a liquid *** combination with this system,we establish a novel sprayable adhesive(ZnMet-PF127)and demonstrate that it is a potential clinical treatment for traumatic skin defect and burn skin injury.

关键词： Thermosensitive hydrogel Skin wound ZnMet-PF127 Reactive oxygen species(ROS) Autophagy

Targeting Kindlin-2 in adipocytes increases bone mass through inhibiting FAS/PPARγ/FABP4 signaling in mice

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Acta Pharmaceutica Sinica B 2023年第11期13卷 4535-4552页

作者： Wanze Tang Zhen Ding Huanqing Gao qinnan yan Jingping Liu Yingying Han Xiaoting Hou Zhengwei Liu Litong Chen Dazhi yang Guixing Ma Huiling Cao Department of Biochemistry School of MedicineGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease ResearchKey University Laboratory of Metabolism and Health of GuangdongSouthern University of Science and TechnologyShenzhen 518055China The First Affiliated Hospital Southern University of Science and TechnologyShenzhen 518055China Clinical Laboratory of the Third Affiliated Hospital of Southern Medical University Guangzhou 510630China

Osteoporosis(OP)is a systemic skeletal disease that primarily affects the elderly population,which greatly increases the risk of *** we report that Kindlin-2 expression in adipose tissue increases during aging and high-fat diet fed and is accompanied by decreased bone ***-2 specific deletion(K2KO)controlled by Adipoq-Cre mice or adipose tissue-targeting AAV(AAV-Rec2-CasRx-sgK2)significantly increases bone ***,Kindlin-2 promotes peroxisome proliferator-activated receptor gamma(PPARγ)activation and downstream fatty acid binding protein 4(FABP4)expression through stabilizing fatty acid synthase(FAS),and increased FABP4 inhibits insulin expression and decreases bone ***-2 inhibition results in accelerated FAS degradation,decreased PPARγactivation and FABP4 expression,and therefore increased insulin expression and bone ***,we find that FABP4 is increased while insulin is decreased in serum of OP *** FABP4 expression through PPARγactivation by rosiglitazone reverses the high bone mass phenotype of K2KO *** of FAS by C75 phenocopies the high bone mass phenotype of K2KO ***,our study establishes a novel Kindlin-2/FAS/PPARγ/FABP4/insulin axis in adipose tissue modulating bone mass and strongly indicates that FAS and Kindlin-2 are new potential targets and C75 or AAV-Rec2-CasRx-sgK2 treatment are potential strategies for OP treatment.

关键词： Kindlin-2 Adipocyte FAS Bone homeostasis AAV-Rec2-CasRx-sgK2 Osteoporosis C75 mRNA editing

Kindlin-2 loss in condylar chondrocytes causes spontaneous osteoarthritic lesions in the temporomandibular joint in mice

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International Journal of Oral Science 2022年第3期14卷 371-380页

作者： Yumei Lai Wei Zheng Minghao Qu Christopher C.Xiao Sheng Chen Qing Yao Weiyuan Gong Chu Tao qinnan yan Peijun Zhang Xiaohao Wu Guozhi Xiao Department of Orthopedic Surgery Rush University Medical CenterChicagoILUSA Department of Orthopaedic Center Xinjiang Production and Construction Corps HospitalUrumqiChina Department of Biochemistry School of MedicineSouthern University of Science and TechnologyGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease ResearchShenzhen Key Laboratory of Cell MicroenvironmentShenzhenChina Department of Orthopedics Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina

The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint(TMJ) osteoarthritis(OA);however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4(Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore,Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis.

关键词： Kindlin-2 loss in condylar chondrocytes causes spontaneous osteoarthritic lesions in the temporomandibular joint in mice TMJ

Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice

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Signal Transduction and Targeted Therapy 2021年第1期6卷 131-143页

作者： Xuekun Fu Bo Zhou qinnan yan Chu Tao Lei Qin Xiaohao Wu Sixiong Lin Sheng Chen Yumei Lai Xuenong Zou Zengwu Shao Meiqing Wang Di Chen Wenfei Jin Youqiang Song Huiling Cao Ge Zhang Guozhi Xiao School of Medicine Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Researchand Shenzhen Key Laboratory of Cell MicroenvironmentSouthern University of Science and Technology1088 Xue Yuan Road518055 ShenzhenGuangdongChina Law Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases School of Chinese MedicineHong Kong Baptist University999077 Hong KongSARChina Department of Biology Southern University of Science and Technology518055 ShenzhenChina School of Biomedical Sciences University of Hong Kong21 Sassoon RoadHong KongChina Department of Spine Surgery Orthopedic Research InstituteThe First Affiliated Hospital of Sun Yat-sen UniversityGuangdong Provincial Key Laboratory of Orthopedics and Traumatology510080 GuangzhouChina Department of Orthopedics Union HospitalTongji Medical CollegeHuazhong University of Science and Technology430022 WuhanChina Department of Orthopedic Surgery Rush University Medical CenterChicagoIL 60612USA State Key Laboratory of Military Stomatology National Clinical Research Center for Oral DiseasesShanxi International Joint Research Center for Oral DiseasesDepartment of Oral Anatomy and Physiology and TMDSchool of Stomatologythe Fourth Military Medical University145 Changle West RoadXi’anChina Research Center for Human Tissues and Organs Degeneration Shenzhen Institutes of Advanced TechnologyChinese Academy of Sciences518055 ShenzhenChina

In vertebrates,the type 1 parathyroid hormone receptor(PTH1R)is a critical regulator of skeletal development and homeostasis;however,how it is modulated is incompletely *** we report that deleting Kindlin-2 in osteoblastic cells using the mouse 10-kb Dmp1-Cre largely neutralizes the intermittent PTH-stimulated increasing of bone volume fraction and bone mineral density by impairing both osteoblast and osteoclast formation in murine adult ***-cell profiling reveals that Kindlin-2 loss increases the proportion of osteoblasts,but not mesenchymal stem cells,chondrocytes and fibroblasts,in non-hematopoietic bone marrow cells,with concomitant depletion of osteoblasts on the bone surfaces,especially those stimulated by ***,haploinsufficiency of Kindlin-2 and Pth1r genes,but not that of either gene,in mice significantly decreases basal and,to a larger extent,PTH-stimulated bone mass,supporting the notion that both factors function in the same genetic ***,Kindlin-2 interacts with the C-terminal cytoplasmic domain of PTH1R via aa 474–475 and Gsα.Kindlin-2 loss suppresses PTH induction of cAMP production and CREB phosphorylation in cultured osteoblasts and in ***,PTH promotes Kindlin-2 expression in vitro and in vivo,thus creating a positive feedback regulatory ***,estrogen deficiency induced by ovariectomy drastically decreases expression of Kindlin-2 protein in osteocytes embedded in the bone matrix and Kindlin-2 loss essentially abolishes the PTH anabolic activity in bone in ovariectomized ***,we demonstrate that Kindlin-2 functions as an intrinsic component of the PTH1R signaling pathway in osteoblastic cells to regulate bone mass accrual and homeostasis.

关键词： homeostasis Kindlin skeletal

LIM domain proteins Pinch1/2 regulate chondrogenesis and bone mass in mice

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Bone Research 2020年第4期8卷 416-428页

作者： Yiming Lei Xuekun Fu Pengyu Li Sixiong Lin qinnan yan Yumei Lai Xin Liu Yishu Wang Xiaochun Bai Chuanju Liu Di Chen Xuenong Zou Xu Cao Huiling Cao Guozhi Xiao Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research Shenzhen Key Laboratory of Cell Microenvironmentand School of MedicineSouthern University of Science and TechnologyShenzhen 518055China Department of Spine Surgery Orthopedic Research InstituteThe First Affiliated Hospital of Sun Yat-sen UniversityGuangdong Provincial Key Laboratory of Orthopedics and TraumatologyGuangzhou 510080China Department of Orthopedic Surgery Rush University Medical CenterChicagoIL 60612USA Department of Cell Biology School of Basic Medical SciencesSouthern Medical UniversityGuangzhou 510515China Department of Orthopedic Surgery New York University School of MedicineNew YorkNY 10003USA Department of Cell Biology New York University School of MedicineNew YorkNY 10016USA Research Center for Human Tissues and Organs Degeneration Shenzhen Institutes of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China Department of Orthopedic Surgery The Johns Hopkins UniversityBaltimoreMD 21205USA

The LIM domain-containing proteins Pinch1/2 regulate integrin activation and cell–extracellular matrix interaction and ***,we report that deleting Pinch1 in limb mesenchymal stem cells(MSCs)and Pinch2 globally(double knockout;dKO)in mice causes severe chondrodysplasia,while single mutant mice do not display marked *** deletion decreases chondrocyte proliferation,accelerates cell differentiation and disrupts column *** loss drastically reduces Smad2/3 protein expression in proliferative zone(PZ)chondrocytes and increases Runx2 and Col10a1 expression in both PZ and hypertrophic zone(HZ)*** loss increases sclerostin and Rankl expression in HZ chondrocytes,reduces bone formation,and increases bone resorption,leading to low bone *** vitro studies revealed that Pinch1 and Smad2/3 colocalize in the nuclei of *** its C-terminal region,Pinch1 interacts with Smad2/3 *** loss increases Smad2/3 ubiquitination and degradation in primary bone marrow stromal cells(BMSCs).Pinch loss reduces TGF-β-induced Smad2/3 phosphorylation and nuclear localization in primary ***,compared to those from single mutant mice,BMSCs from dKO mice express dramatically lower protein levels ofβ-catenin and Yap1/Taz and display reduced osteogenic but increased adipogenic differentiation ***,ablating Pinch1 in chondrocytes and Pinch2 globally causes severe osteopenia with subtle limb ***,our findings demonstrate critical roles for Pinch1/2 and a functional redundancy of both factors in the control of chondrogenesis and bone mass through distinct mechanisms.

关键词： Smad2/3 globally mass

Focal adhesion protein Kindlin-2 regulates bone homeostasis in mice

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Bone Research 2020年第1期8卷 26-38页

作者： Huiling Cao qinnan yan Dong Wang Yumei Lai Bo Zhou Qi Zhang Wenfei Jin Simin Lin Yiming Lei Liting Ma Yuxi Guo Yishu Wang Yilin Wang Xiaochun Bai Chuanju Liu Jian QFeng Chuanyue Wu Di Chen Xu Cao Guozhi Xiao Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research Shenzhen Key Laboratory of Cell Microenvironmentand Department of BiologySouthern University of Science and TechnologyShenzhen 518055China Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education Co-innovation Center of NeuroregenerationNantong UniversityNantong 226001China Department of Orthopedic Surgery Rush University Medical CenterChicagoIL 60612USA Department of Cell Biology School of Basic Medical SciencesSouthern Medical UniversityGuangzhou 510515China Department of Orthopedic Surgery New York University School of MedicineNew YorkNY 10003USA Department of Cell Biology New York University School of MedicineNew YorkNY 10016USA Department of Biomedical Sciences Texas A&M University College of DentistryDallasTX 75246USA Department of Orthopedic Surgery The Johns Hopkins UniversityBaltimoreMD 21205USA

Our recent studies demonstrate that the focal adhesion protein Kindlin-2 is critical for chondrogenesis and early skeletal development. Here, we show that deleting Kindlin-2 from osteoblasts using the 2.3-kb mouse Col1 a1-Cre transgene minimally impacts bone mass in mice, but deleting Kindlin-2 using the 10-kb mouse Dmp1-Cre transgene, which targets osteocytes and mature osteoblasts, results in striking osteopenia in mice. Kindlin-2 loss reduces the osteoblastic population but increases the osteoclastic and adipocytic populations in the bone microenvironment. Kindlin-2 loss upregulates sclerostin in osteocytes,downregulates β-catenin in osteoblasts, and inhibits osteoblast formation and differentiation in vitro and in vivo. Upregulation ofβ-catenin in the mutant cells reverses the osteopenia induced by Kindlin-2 deficiency. Kindlin-2 loss additionally increases the expression of RANKL in osteocytes and increases osteoclast formation and bone resorption. Kindlin-2 deletion in osteocytes promotes osteoclast formation in osteocyte/bone marrow monocyte cocultures, which is significantly blocked by an anti-RANKLneutralizing antibody. Finally, Kindlin-2 loss increases osteocyte apoptosis and impairs osteocyte spreading and dendrite ***, we demonstrate an important role of Kindlin-2 in the regulation of bone homeostasis and provide a potential target for the treatment of metabolic bone diseases.

关键词： homeostasis Kindlin cytes

High power and stable P-doped yolk-shell structured Si@C anode simultaneously enhancing conductivity and Li^(+)diffusion kinetics

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Nano Research 2021年第4期14卷 1004-1011页

作者： Ming Chen qinnan Zhou Jiantao Zai Asma Iqbal TsegayeTadesse Tsega Boxu Dong Xuejiao Liu Yuchi Zhang Changyu yan Liang Zhao Ali Nazakat SharelPeisan E CheeTongJohn Low Xuefeng Qian Shanghai Electrochemical Energy Devices Research Center School of Chemistry and Chemical Engineering and State Key Laboratory oj Metal Matrix CompositesShanghai Jiao Tong UniversityShanghai 200240China Warwick Electrochemical Engineering Group WMGEnergy Innovation CentreUniversity of WarwickCV47ALUK School of Health&Life Sciences Teesside UniversityMiddlesbroughTS13BXUK

Silicon is a low price and high capacity ancxje material for lithium-ion *** yolk-shell structure can effectively accommodate Si expansion to improve ***,the limited rate performance of Si anodes can't meet people's growing demand for high power ***,the phosphorus-doped yolk-shell Si@C materials(P-doped Si@C)were prepared through carbon coating on P-doped Si/SiO_(x)matrix to obtain high power and stable ***,the as-prepared P-doped Si@C electrodes delivered a rapid increase in Coulombic efficiency from 74.4%to 99.6%after only 6 cycles,high capacity retention of-95%over 800 cycles at 4 A·g^(-1),and great rate capability(510 mAh·g^(-1)at 35 A·g^(-1)).As a result,P-doped Si@C anodes paired with commercial activated carbon and LiFePO_(4)cathode to assemble lithium-ion capacitor(high power density of〜61,080 W·kg^(-1)at 20 A·g^(-1))and lithium-ion full cell(good rate performance with 68.3 mAh·g^(-1)at 5 C),*** work can provide an effective way tofurther improve power density and stability for energy storage devices.

关键词： P-doped yolk-shell structured Si@C anode excellent rate performance long life lithium-ion battery high power full cell

Effect of Metformin on Lactate Metabolism in Normal Hepatocytes under High Glucose Stress in Vitro

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Journal of Advances in Medicine Science 2021年第2期4卷 31-34页

作者： Jianhao Wu qinnan Zhang Yubiao yang Chunyue Wang Xindi Yue Zhilu Li Pingping yan School of International Education Hainan Medical UniversityHaikouHainan570100China The First Clinical College of Hainan Medical University HaikouHainan570100China Clinical Skills Center Hainan Medical UniversityHaikouHainan570100China

To study the effect of metformin on lactate metabolism in hepatocytes in vitro under high glucose ***:LO2 hepatocytes was cultured in vitro,hepatocytes were randomly divided into blank control group,25 mmol/L glucose solution,27 mmol/L glucose solution,29 mmol/L glucose solution,31 mmol/L glucose solution,33 mmol/L glucose solution,35 mmol/L glucose solution treatment group,after determining the optimal concentration as 31 mmol/L,use 30 mmol/L metformin solution,and then divided into blank control group,normal hepatocytes+the optimal concentration of glucose solution,normal hepatocytes+metformin solution,normal hepatocytes+.The optimal concentration of glucose solution normal hepatocytes+metformin solution,calculate the number of hepatocytes on cell count plate respectively in the 12 h,24 h,48 h,and use the lactic acid kit to determine the lactic acid value of the cell culture medium of normal liver cells+optimal concentration glucose solution and normal liver cells+optimal concentration glucose solution+metformin solution at 12 h,24 h,and 48 h,***:There was no significant change in the lactic acid concentration but significant increase in the number of surviving hepatocytes in the high-glycemic control group compared with that in the high-glycemic control group without ***:Metformin has no significant effect on lactic acid metabolism of hepatocytes under high glucose stress in vitro,and has a protective effect on hepatocytes under high glucose *** on this,it is preliminarily believed that metformin is not the direct factor leading to diabetic lactic acidosis.

关键词： Metformin Hepatocyte Metformin associated lactic acidosis(MALA)

中部地区急诊科护士付出回报失衡现状及其相关因素

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中国心理卫生杂志 2023年第5期37卷 429-434页

作者：安荣荣董月闫勤朱艺李钦楠颜时姣龚言红华中科技大学同济医学院公共卫生学院武汉430030 海南医学院公共卫生学院海口570216

目的:探讨中部地区急诊科护士付出回报失衡的现状及相关因素。方法:以中部六省3614名急诊科护士为研究对象,使用结构化问卷、改编版积极情感和消极情感量表、付出回报失衡量表进行调查,采用广义线性回归探讨其付出回报失衡的相关因素。... 详细信息

目的:探讨中部地区急诊科护士付出回报失衡的现状及相关因素。方法:以中部六省3614名急诊科护士为研究对象,使用结构化问卷、改编版积极情感和消极情感量表、付出回报失衡量表进行调查,采用广义线性回归探讨其付出回报失衡的相关因素。结果:男性、月收入少于2500元、月收入在2500~4000元之间、自觉护士短缺、消极情感得分较高者发生付出回报失衡的风险更高(β=0.17、0.12、0.05、0.19、0.24);工作年限小于1a、近一年未遭受和遭受1~3次语言暴力、近一年未遭受身体暴力、积极情感得分较高者发生付出回报失衡的风险较低(β=-0.08、-0.18、-0.13、-0.12、-0.14)。结论:中部地区急诊科护士的付出回报失衡与性别、自觉护士短缺、工作年限、月收入、工作场所暴力以及积极、消极情感有关。

关键词：急诊科护士付出-回报失衡工作场所暴力积极情感消极情感