Blister wounds are featured with over-generated wound exudate and extensive skin peeling,call for breathable temporary skin with effective exudate management,and function as an extracellular matrix to accelerate regen...Blister wounds are featured with over-generated wound exudate and extensive skin peeling,call for breathable temporary skin with effective exudate management,and function as an extracellular matrix to accelerate regeneration of wound skin.Traditional extracellular matrix(ECM)mimicked nanofibrous 3D scaffold and corresponding hydrogel composites suffer from poor mechanical strength,and the wound exudate management behavior is seldom studied.Herein,we proposed the strategy to enhance the mechanical properties of a 3D nanofiber scaffold via constructing a long nanofiber(NF)and sodium alginate(SA)aerogel interpenetrated architecture(NF/SA).The as-prepared scaffold was then evaluated as temporary skin for a full-thickness defect wound.After absorption of blister fluid,the aerogel transferred into a hydrogel and imparted a wet wound care environment with a water-vapor transmission rate of(6001.90±522.04)g/(m^(2)·24 h),and Young s modulus of(2.97±0.38)MPa.The exudate was continuously refreshed by a directed and dynamic pump,followed by volatilization driven by Brownian motion.Meanwhile,the NF/SA scaffold exhibited decent compatibility with blister fluid.The basic fibroblast growth factor(bFGF)-loaded NF/SA improved the wound healing rate by 36.46%on Day 3 and 15.34%on Day 7 in the full-thickness defect wound model.展开更多
The growth of Caenorhabditis elegans involves multiple molting processes,during which old cuticles are shed and new cuticles are rapidly formed.This process requires the regulated bulk secretion of cuticle components....The growth of Caenorhabditis elegans involves multiple molting processes,during which old cuticles are shed and new cuticles are rapidly formed.This process requires the regulated bulk secretion of cuticle components.The transmembrane protein-39(TMEM-39)mutant exhibits distinct dumpy and ruptured phenotypes characterized by notably thin cuticles.TMEM-39 primarily co-localizes with the coat protein II complex(COPII)in large vesicles rather than small COPII vesicles.These TMEM-39-associated large vesicles(TMEM-39-LVs)form robustly during the molting period and co-localize with various extracellular matrix components,including BLI-1 collagen,BLI-3 dual oxidase,and carboxypeptidases.Through immunoprecipitation using TMEM39A-FLAG and proteomics analysis in human sarcoma cells,we identify TMEM39A-associated proteins,including TMEM131.Knockdown of TMEM131 results in reduced TMEM39A-LV formation and collagen secretion in both C.elegans and human sarcoma cells,indicating a cooperative role between TMEM39A and TMEM131 in the secretion of extracellular components through the formation of large COPII vesicles.Given the conservation of TMEM39A and its associated proteins between C.elegans and humans,TMEM39A-LVs may represent a fundamental machinery for rapid and extensive secretion across metazoans.展开更多
Oral submucous fibrosis(OSF),characterized by excessive deposition of extracellular matrix(ECM)that causes oral mucosal tissue sclerosis,and even cancer transformation,is a chronic,progressive fibrosis disease.However...Oral submucous fibrosis(OSF),characterized by excessive deposition of extracellular matrix(ECM)that causes oral mucosal tissue sclerosis,and even cancer transformation,is a chronic,progressive fibrosis disease.However,despite some advancements in recent years,no targeted antifibrotic strategies for OSF have been approved;likely because the complicated mechanisms that initiate and drive fibrosis remain to be determined.In this review,we briefly introduce the epidemiology and etiology of OSF.Then,we highlight how cell-intrinsic changes in significant structural cells can drive fibrotic response by regulating biological behaviors,secretion function,and activation of ECM-producing myofibroblasts.In addition,we also discuss the role of innate and adaptive immune cells and how they contribute to the pathogenesis of OSF.Finally,we summarize strategies to interrupt key mechanisms that cause OSF,including modulation of the ECM,inhibition of inflammation,improvement of vascular disturbance.This review will provide potential routes for developing novel anti-OSF therapeutics.展开更多
基金Natural Science Foundation of Shanghai(General Program,22ZR1409500)China Postdoctoral Science Foundation(23M742317,GZB240446)+3 种基金Shanghai Science and Technology Innovation Action Plan(22S31905500)Medical Engineering Fund of Fudan University(yg2021-032)Fundamental Research Project of CNTAC(J202104)Program of Introducing Talents of Discipline to Universities(BP0719035)。
文摘Blister wounds are featured with over-generated wound exudate and extensive skin peeling,call for breathable temporary skin with effective exudate management,and function as an extracellular matrix to accelerate regeneration of wound skin.Traditional extracellular matrix(ECM)mimicked nanofibrous 3D scaffold and corresponding hydrogel composites suffer from poor mechanical strength,and the wound exudate management behavior is seldom studied.Herein,we proposed the strategy to enhance the mechanical properties of a 3D nanofiber scaffold via constructing a long nanofiber(NF)and sodium alginate(SA)aerogel interpenetrated architecture(NF/SA).The as-prepared scaffold was then evaluated as temporary skin for a full-thickness defect wound.After absorption of blister fluid,the aerogel transferred into a hydrogel and imparted a wet wound care environment with a water-vapor transmission rate of(6001.90±522.04)g/(m^(2)·24 h),and Young s modulus of(2.97±0.38)MPa.The exudate was continuously refreshed by a directed and dynamic pump,followed by volatilization driven by Brownian motion.Meanwhile,the NF/SA scaffold exhibited decent compatibility with blister fluid.The basic fibroblast growth factor(bFGF)-loaded NF/SA improved the wound healing rate by 36.46%on Day 3 and 15.34%on Day 7 in the full-thickness defect wound model.
基金supported by the National Institutes of Health-Office of Research Infrastructure Programs(P40 OD010440)supported in part by grants from the National Cancer Center of Korea(NCC-2110160,NCC-2110263,and NCC-2310750)supported by the Basic Science Research Program of the National Research Foundation of Korea,funded by the Ministry of Science,ICT,and Future Planning(NRF-2015R1C1A1A01053611).
文摘The growth of Caenorhabditis elegans involves multiple molting processes,during which old cuticles are shed and new cuticles are rapidly formed.This process requires the regulated bulk secretion of cuticle components.The transmembrane protein-39(TMEM-39)mutant exhibits distinct dumpy and ruptured phenotypes characterized by notably thin cuticles.TMEM-39 primarily co-localizes with the coat protein II complex(COPII)in large vesicles rather than small COPII vesicles.These TMEM-39-associated large vesicles(TMEM-39-LVs)form robustly during the molting period and co-localize with various extracellular matrix components,including BLI-1 collagen,BLI-3 dual oxidase,and carboxypeptidases.Through immunoprecipitation using TMEM39A-FLAG and proteomics analysis in human sarcoma cells,we identify TMEM39A-associated proteins,including TMEM131.Knockdown of TMEM131 results in reduced TMEM39A-LV formation and collagen secretion in both C.elegans and human sarcoma cells,indicating a cooperative role between TMEM39A and TMEM131 in the secretion of extracellular components through the formation of large COPII vesicles.Given the conservation of TMEM39A and its associated proteins between C.elegans and humans,TMEM39A-LVs may represent a fundamental machinery for rapid and extensive secretion across metazoans.
基金study was supported by the National Key Research and Development Program of China(2022YFC2402900)National Natural Science Foundation of China(82470989,52103327)+3 种基金The Joint Funds of the Hunan Provincial Natural Science Foundation(2023JJ60509)The Science and Technology Talent Support Project of the Hunan Provincial Science Popularization Special Project(2023TJ-Z08)Hunan Provincial Innovation Foundation for Postgraduate(2023ZZTS0218)The Postgraduate Inde-pendent Exploration Innovation Fund of the Central South University(2023ZZTS0987)。
文摘Oral submucous fibrosis(OSF),characterized by excessive deposition of extracellular matrix(ECM)that causes oral mucosal tissue sclerosis,and even cancer transformation,is a chronic,progressive fibrosis disease.However,despite some advancements in recent years,no targeted antifibrotic strategies for OSF have been approved;likely because the complicated mechanisms that initiate and drive fibrosis remain to be determined.In this review,we briefly introduce the epidemiology and etiology of OSF.Then,we highlight how cell-intrinsic changes in significant structural cells can drive fibrotic response by regulating biological behaviors,secretion function,and activation of ECM-producing myofibroblasts.In addition,we also discuss the role of innate and adaptive immune cells and how they contribute to the pathogenesis of OSF.Finally,we summarize strategies to interrupt key mechanisms that cause OSF,including modulation of the ECM,inhibition of inflammation,improvement of vascular disturbance.This review will provide potential routes for developing novel anti-OSF therapeutics.
