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SportSync health: revolutionizing patient care in sports medicine through integrated follow-up technologies. SportSync health:通过综合随访技术彻底改变运动医学中的病人护理。
IF 6.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-11-04 eCollection Date: 2024-01-01 DOI: 10.1093/burnst/tkae064
Zhiwen Luo, Chen Chen, Quan Gan, Renwen Wan, Zhenghua Hong, Min Zhu, Xiaohan Wu, Linlin Sha, Yisheng Chen, Yanwei He, Xingting Feng, Junbo Liang, Shiyi Chen, Xiaobo Zhou
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引用次数: 0
Dexmedetomidine regulates exosomal miR-29b-3p from macrophages and alleviates septic myocardial injury by promoting autophagy in cardiomyocytes via targeting glycogen synthase kinase 3β. 右美托咪定通过靶向糖原合酶激酶3β促进心肌细胞自噬,从而调节巨噬细胞外泌体miR-29b-3p并减轻脓毒症心肌损伤。
IF 6.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-11-04 eCollection Date: 2024-01-01 DOI: 10.1093/burnst/tkae042
Tianyi Yu, Hsinying Liu, Min Gao, Dan Liu, JiaQiang Wang, Jie Zhang, Jizhuang Wang, Peilang Yang, Xiong Zhang, Yan Liu

Background: Our previous research suggested that dexmedetomidine (Dex) promotes autophagy in cardiomyocytes, thus safeguarding them against apoptosis during sepsis. However, the underlying mechanisms of Dex-regulated autophagy have remained elusive. This study aimed to explore the role of exosomes and how they participate in Dex-induced cardioprotection in sepsis. The underlying microRNA (miRNA) mechanisms and possible therapeutic targets for septic myocardial injury were identified.

Methods: We first collected plasma exosomes from rats with sepsis induced by caecal ligation and puncture (CLP) with or without Dex treatment, and then incubated them with H9c2 cells to observe the effect on cardiomyocytes. Subsequently, the differential expression of miRNAs in plasma exosomes from each group of rats was identified through miRNA sequencing. miR-29b-3p expression in circulating exosomes of septic or non-septic patients, as well as in lipopolysaccharide-induced macrophages after Dex treatment, was analysed by quantitative real-time polymerase chain reaction (qRT-PCR). The autophagy level of cardiomyocytes after macrophage-derived exosome treatment was assessed by an exosome tracing assay, western blotting, and an autophagic flux assay. Specific miRNA mimics and inhibitors or small interfering RNAs were used to predict and evaluate the function of candidate miRNA and its target genes by qRT-PCR, annexin V/propyl iodide staining, autophagy flux analysis, and western blotting.

Results: We found that plasma-derived exosomes from Dex-treated rats promoted cardiomyocyte autophagy and exerted antiapoptotic effects. Additionally, they exhibited a high expression of miRNA, including miR-29b-3p. Conversely, a significant decrease in miR-29b-3p was observed in circulating exosomes from CLP rats, as well as in plasma exosomes from sepsis patients. Furthermore, Dex upregulated the lipopolysaccharide-induced decrease in miR-29b-3p expression in macrophage-derived exosomes. Exosomal miR-29b-3p from macrophages is thought to be transferred to cardiomyocytes, thus leading to the promotion of autophagy in cardiomyocytes. Database predictions, luciferase reporter assays, and small interfering RNA intervention confirmed that glycogen synthase kinase 3β (GSK-3β) is a target of miR-29b-3p. miR-29b-3p promotes cardiomyocyte autophagy by inhibiting GSK-3β expression and activation.

Conclusions: These findings demonstrate that Dex attenuates sepsis-associated myocardial injury by modulating exosome-mediated macrophage-cardiomyocyte crosstalk and that the miR-29b-3p/GSK-3β signaling pathway represents a hopeful target for the treatment of septic myocardial injury.

背景:我们之前的研究表明,右美托咪定(Dex)可促进心肌细胞的自噬,从而在败血症期间保护心肌细胞免受凋亡。然而,Dex调控自噬的潜在机制仍然难以捉摸。本研究旨在探索外泌体的作用及其如何参与脓毒症中由 Dex 诱导的心脏保护。方法:我们首先收集了血浆外泌体:方法:我们首先收集了通过盲肠结扎和穿刺(CLP)诱导的败血症大鼠血浆外泌体,并将其与 H9c2 细胞培养,观察其对心肌细胞的影响。通过实时定量聚合酶链反应(qRT-PCR)分析了miR-29b-3p在败血症或非败血症患者循环外泌体中的表达,以及在Dex处理后脂多糖诱导的巨噬细胞中的表达。巨噬细胞衍生的外泌体处理后,心肌细胞的自噬水平通过外泌体追踪检测法、Western 印迹法和自噬通量检测法进行了评估。通过qRT-PCR、annexin V/丙基碘染色、自噬通量分析和Western印迹,使用特定的miRNA模拟物和抑制剂或小干扰RNA来预测和评估候选miRNA及其靶基因的功能:结果:我们发现,经 Dex 处理的大鼠血浆中的外泌体可促进心肌细胞自噬并发挥抗凋亡作用。此外,外泌体还表现出高表达 miRNA,包括 miR-29b-3p。相反,在中毒性大鼠的循环外泌体和败血症患者的血浆外泌体中,miR-29b-3p 的表达量明显下降。此外,Dex还能上调脂多糖诱导的巨噬细胞外泌体中miR-29b-3p表达的下降。巨噬细胞的外泌体 miR-29b-3p 被认为会转移到心肌细胞,从而促进心肌细胞的自噬。miR-29b-3p通过抑制GSK-3β的表达和激活促进心肌细胞自噬:这些研究结果表明,Dex 可通过调节外泌体介导的巨噬细胞-心肌细胞串联来减轻脓毒症相关心肌损伤,而且 miR-29b-3p/GSK-3β 信号通路是治疗脓毒症心肌损伤的希望靶点。
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引用次数: 0
Polylactic acid-based dressing with oxygen generation and enzyme-like activity for accelerating both light-driven biofilm elimination and wound healing 基于聚乳酸的敷料,具有氧气生成和类酶活性,可加速光驱动的生物膜消除和伤口愈合
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-10-25 DOI: 10.1093/burnst/tkae041
Tianci Wen, Shilang Xiong, Huihui Zhao, Junzhe Wang, Chunming Wang, Zhisheng Long, Long Xiong, Guowen Qian
Background Photodynamic therapy (PDT) is a widely used therapeutic approach for eradicating bacterial biofilms in infected wound, but its effectiveness is limited by the hypoxic environment within the biofilm. This study aimed to investigate whether the efficiency of photodynamic removing biofilm is improving by providing oxygen (O2), as well as the expression of cytokines involved in infected wound healing. Methods Manganese dioxide (MnO2) nanoparticles with catalase-like activity were grown in situ on graphitic phase carbon nitride (g-C3N4, CN) nanosheets to construct an all-in-one CN-MnO2 nanozyme, which was then incorporated into poly-L-lactic acid (PLLA) to prepare CN-MnO2/PLLA wound dressing by electrospinning. Subsequently, the in vitro antibacterial biofilm ratio and antibacterial ratio of CN-MnO2/PLLA wound dressing were examined by spread plate and crystal violet staining under irradiation with 808 nm near-infrared light and 660 nm visible light. Meanwhile, the rat skin injury model was established, and hematoxylin and eosin (H&E), Masson’s, tumor necrosis factor-α (TNF-α), Arginase 1 (Arg-1), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (BFGF) were evaluated in vivo to assess the effect of CN-MnO2/PLLA wound dressing on wound healing. Results Biofilm density caused by Staphylococcus aureus and Pseudomonas aeruginosa had elimination rates of 83 and 62%, respectively, when treated with CN-MnO2/PLLA dressing. Additionally, the dressing exhibited high antibacterial efficacy against both bacteria, achieving 99 and 98.7% elimination of Staphylococcus aureus and Pseudomonas aeruginosa, respectively. Furthermore, in vivo experiments showed that the CN-MnO2/PLLA wound dressing achieved complete healing of infected wounds on Day 14, with a wound healing rate of &gt;99% by increasing collagen deposition, expression of anti-inflammatory cytokine Arg-1, vascularization cytokine VEGF, and epithelial cell BFGF, and inhibiting the expression of inflammatory cytokine TNF-α. Conclusions The CN-MnO2/PLLA wound dressing exhibited excellent antibacterial properties in vitro and in vivo. In addition, CN-MnO2/PLLA wound dressing accelerated rapid wound healing through an anti-inflammatory, pro-vascular regeneration and skin tissue remodeling mechanism.
背景光动力疗法(PDT)是根除感染伤口中细菌生物膜的一种广泛使用的治疗方法,但其有效性受到生物膜内缺氧环境的限制。本研究旨在探讨光动力清除生物膜的效率是否会因提供氧气(O2)而提高,以及参与感染伤口愈合的细胞因子的表达情况。方法 在石墨相氮化碳(g-C3N4,CN)纳米片上原位生长具有类似催化剂活性的二氧化锰(MnO2)纳米颗粒,构建一体化的CN-MnO2纳米酶,然后将其与聚左旋乳酸(PLLA)结合,通过电纺丝制备CN-MnO2/PLLA伤口敷料。随后,在808 nm近红外线和660 nm可见光照射下,通过铺板和水晶紫染色法检测了CN-MnO2/PLLA伤口敷料的体外抗菌生物膜比例和抗菌率。同时,建立了大鼠皮肤损伤模型,并对苏木精和伊红(H&E)、Masson's、肿瘤坏死因子-α(TNF-α)、精氨酸酶 1(Arg-1)、血管内皮生长因子(VEGF)和碱性成纤维细胞生长因子(BFGF)进行了体内评价,以评估 CN-MnO2/PLLA 伤口敷料对伤口愈合的影响。结果 使用 CN-MnO2/PLLA 敷料处理金黄色葡萄球菌和铜绿假单胞菌引起的生物膜密度,消除率分别为 83% 和 62%。此外,该敷料对这两种细菌都有很高的抗菌效果,对金黄色葡萄球菌和铜绿假单胞菌的清除率分别达到 99% 和 98.7%。此外,体内实验表明,CN-MnO2/PLLA 伤口敷料通过增加胶原蛋白沉积、抗炎细胞因子 Arg-1、血管生成细胞因子 VEGF 和上皮细胞 BFGF 的表达以及抑制炎症细胞因子 TNF-α 的表达,使感染伤口在第 14 天完全愈合,伤口愈合率达 &gt;99% 。结论 CN-MnO2/PLLA伤口敷料在体外和体内均表现出优异的抗菌性能。此外,CN-MnO2/PLLA 伤口敷料还能通过抗炎、促进血管再生和皮肤组织重塑机制加速伤口快速愈合。
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引用次数: 0
Single-cell sequencing technology in skin wound healing 皮肤伤口愈合中的单细胞测序技术
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-10-23 DOI: 10.1093/burnst/tkae043
Xu Cheng Cheng, Wang Zi Tong, Wang Rui, Zhao Feng, Hou Shuai, Wang Zhe
Skin wound healing is a complicated biological process that mainly occurs in response to injury, burns, or diabetic ulcers. It can also be triggered by other conditions such as dermatitis and melanoma-induced skin cancer. Delayed healing or non-healing after skin injury presents an important clinical issue; therefore, further explorations into the occurrence and development of wound healing at the cellular and molecular levels are necessary. Single-cell sequencing (SCS) is used to sequence and analyze the genetic messages of a single cell. Furthermore, SCS can accurately detect cell expression and gene sequences. The use of SCS technology has resulted in the emergence of new concepts pertaining to wound healing, making it an important tool for studying the relevant mechanisms and developing treatment strategies. This article discusses the application value of SCS technology, the effects of the latest research on skin wound healing, and the value of SCS technology in clinical applications. Using SCS to determine potential biomarkers for wound repair will serve to accelerate wound healing, reduce scar formation, optimize drug delivery, and facilitate personalized treatments.
皮肤伤口愈合是一个复杂的生物过程,主要发生在受伤、烧伤或糖尿病溃疡时。皮炎和黑色素瘤诱发的皮肤癌等其他疾病也会引发皮肤伤口愈合。皮肤损伤后延迟愈合或不愈合是一个重要的临床问题;因此,有必要从细胞和分子水平进一步探索伤口愈合的发生和发展。单细胞测序(SCS)用于对单个细胞的遗传信息进行测序和分析。此外,SCS 还能准确检测细胞表达和基因序列。单细胞测序技术的使用产生了有关伤口愈合的新概念,使其成为研究相关机制和制定治疗策略的重要工具。本文将讨论 SCS 技术的应用价值、最新研究对皮肤伤口愈合的影响以及 SCS 技术在临床应用中的价值。利用 SCS 确定伤口修复的潜在生物标志物将有助于加速伤口愈合、减少疤痕形成、优化给药和促进个性化治疗。
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引用次数: 0
Consensus on the prevention and repair of titanium mesh exposed wound after cranioplasty (2024 edition). 颅骨成形术后钛网暴露伤口的预防和修复共识(2024 年版)。
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-10-23 DOI: 10.1093/burnst/tkae055
Pihong Zhang,Xiaobing Fu,Yuesheng Huang,
Titanium mesh exposure after cranioplasty is the most serious complication of this procedure. Although some clinical experience has been gradually accumulated over the years in the diagnosis and treatment of titanium mesh exposure, the treatment is often not standardized and it is difficult to achieve satisfactory repair results due to insufficient understanding of its pathogenesis and concurrent infections. To normalize the diagnosis and treatment of titanium mesh exposed wounds after cranioplasty and improve the therapeutic effect and the quality of life of patients, the Wound Repair Professional Committee of Chinese Medical Doctor Association organized an expert discussion based on the literature and current diagnosis and treatment status of titanium mesh exposed wounds after cranioplasty at home and abroad, and reached a consensus on the pathogenesis, preventive measures, and diagnosis and treatment strategies of titanium mesh exposed wounds after cranioplasty to provide reference for relevant clinicians.
颅骨成形术后钛网暴露是该手术最严重的并发症。虽然多年来在钛网暴露的诊断和治疗方面逐渐积累了一些临床经验,但由于对其发病机制和并发感染的认识不足,治疗往往不够规范,难以达到满意的修复效果。为使开颅术后钛网暴露伤口的诊治规范化,提高疗效和患者的生活质量,中国医师协会伤口修复专业委员会根据国内外文献及开颅术后钛网暴露伤口的诊治现状,组织专家进行讨论,就开颅术后钛网暴露伤口的发病机制、预防措施、诊治策略等达成共识,为相关临床医生提供参考。
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引用次数: 0
Engineered extracellular vesicles for tissue repair and regeneration. 用于组织修复和再生的工程细胞外囊泡。
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-10-22 DOI: 10.1093/burnst/tkae062
Yan Zhang,Dan Wu,Chen Zhou,Muran Bai,Yucheng Wan,Qing Zheng,Zhijin Fan,Xianwen Wang,Chun Yang
Extracellular vesicles (EVs) are heterogeneous membrane-like vesicles secreted by living cells that are involved in many physiological and pathological processes and act as intermediaries of intercellular communication and molecular transfer. Recent studies have shown that EVs from specific sources regulate tissue repair and regeneration by delivering proteins, lipids, and nucleic acids to target cells as signaling molecules. Nanotechnology breakthroughs have facilitated the development and exploration of engineered EVs for tissue repair. Enhancements through gene editing, surface modification, and content modification have further improved their therapeutic efficacy. This review summarizes the potential of EVs in tissue repair and regeneration, their mechanisms of action, and their research progress in regenerative medicine. This review highlights their design logic through typical examples and explores the development prospects of EVs in tissue repair. The aim of this review is to provide new insights into the design of EVs for tissue repair and regeneration applications, thereby expanding their use in regenerative medicine.
细胞外囊泡(EVs)是活细胞分泌的异质性膜状囊泡,参与许多生理和病理过程,是细胞间通信和分子传递的中介。最近的研究表明,来自特定来源的 EVs 可将蛋白质、脂类和核酸作为信号分子输送到靶细胞,从而调节组织的修复和再生。纳米技术的突破促进了用于组织修复的工程电动体的开发和探索。通过基因编辑、表面改性和内容改性等方法对其进行增强,进一步提高了其治疗效果。本综述总结了 EVs 在组织修复和再生中的潜力、作用机制以及在再生医学中的研究进展。本综述通过典型实例强调了 EVs 的设计逻辑,并探讨了 EVs 在组织修复中的发展前景。本综述旨在为组织修复和再生应用中的 EVs 设计提供新的见解,从而扩大 EVs 在再生医学中的应用。
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引用次数: 0
Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model 在一种新型小鼠模型中,缝线锚定皮肤张力诱发持续性肥厚性瘢痕
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-10-21 DOI: 10.1093/burnst/tkae051
Yashu Li, Anqi Liu, Jingyan Wang, Changsheng Yang, Kaiyang Lv, Weifeng He, Jun Wu, Wenbin Chen
Background Hypertrophic scars cause impaired skin appearance and function, seriously affecting physical and mental health. Due to medical ethics and clinical accessibility, the collection of human scar specimens is frequently restricted, and the establishment of scar experimental animal models for scientific research is urgently needed. The four most commonly used animal models of hypertrophic scars have the following drawbacks: the rabbit ear model takes a long time to construct; the immunodeficient mouse hypertrophic scar model necessitates careful feeding and experimental operations; female Duroc pigs are expensive to purchase and maintain, and their large size makes it difficult to produce a significant number of models; and mouse scar models that rely on tension require special skin stretch devices, which are often damaged and shed, resulting in unstable model establishment. Our group overcame the shortcomings of previous scar animal models and created a new mouse model of hypertrophic scarring induced by suture anchoring at the wound edge. Methods We utilized suture anchoring of incisional wounds to impose directional tension throughout the healing process, restrain wound contraction, and generate granulation tissue, thus inducing scar formation. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage and the wound edges on the lower back relaxed as a control. Macroscopic manifestation, microscopic histological analysis, mRNA sequencing, bioinformatics, and in vitro cell assays were also conducted to verify the reliability of this method. Results Compared with those in relaxed controls, the fibrotic changes in stretched wounds were more profound. Histologically, the stretched scars were hypercellular, hypervascular, and hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. In addition, the stretched scars exhibited transcriptional overlap with mechanically stretched scars, and human hypertrophic and keloid scars. Phosphatidylinositol 3-kinase-serine/threonine-protein kinase B signaling was implicated as a profibrotic mediator of apoptosis resistance under suture-induced tension. Conclusions This straightforward murine model successfully induces cardinal molecular and histological features of pathological hypertrophic scarring through localized suture tension to inhibit wound contraction. The model enables us to interrogate the mechanisms of tension-induced fibrosis and evaluate anti-scarring therapies.
背景增生性疤痕导致皮肤外观和功能受损,严重影响身心健康。由于医学伦理和临床可及性等原因,人类疤痕标本的采集往往受到限制,建立疤痕实验动物模型用于科学研究迫在眉睫。目前最常用的四种增生性疤痕动物模型存在以下缺点:兔耳模型制作时间长;免疫缺陷小鼠增生性疤痕模型需要精心饲养和实验操作;雌性杜洛克猪购买和饲养成本高,且体型较大,难以制作大量模型;依靠拉力的小鼠疤痕模型需要特殊的皮肤拉伸装置,而这种装置经常损坏和脱落,导致模型建立不稳定。我们的研究小组克服了以往疤痕动物模型的缺点,创建了一种通过缝合固定伤口边缘诱导增生性疤痕的新型小鼠模型。方法 我们利用缝合锚定切口伤口,在整个愈合过程中施加定向张力,抑制伤口收缩,生成肉芽组织,从而诱导疤痕形成。小鼠背侧切口成对,上背部伤口边缘与肋骨缝合,下背部伤口边缘放松作为对照。为验证该方法的可靠性,还进行了宏观表现、显微组织学分析、mRNA 测序、生物信息学和体外细胞实验。结果 与松弛对照组相比,拉伸伤口的纤维化变化更为深刻。从组织学角度看,拉伸的疤痕细胞增生、血管增生、增殖旺盛,细胞外基质沉积紊乱,显示出肥厚性纤维化的分子特征。此外,拉伸疤痕与机械拉伸疤痕、人类肥厚性瘢痕和瘢痕疙瘩在转录上有重叠。磷脂酰肌醇 3- 激酶-丝氨酸/苏氨酸蛋白激酶 B 信号转导被认为是缝合线诱导的张力下抵抗细胞凋亡的促组织坏死介质。结论 这种直接的小鼠模型通过局部缝合张力抑制伤口收缩,成功诱导了病理肥厚性瘢痕的主要分子和组织学特征。该模型使我们能够探究张力诱导纤维化的机制并评估抗瘢痕疗法。
{"title":"Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model","authors":"Yashu Li, Anqi Liu, Jingyan Wang, Changsheng Yang, Kaiyang Lv, Weifeng He, Jun Wu, Wenbin Chen","doi":"10.1093/burnst/tkae051","DOIUrl":"https://doi.org/10.1093/burnst/tkae051","url":null,"abstract":"Background Hypertrophic scars cause impaired skin appearance and function, seriously affecting physical and mental health. Due to medical ethics and clinical accessibility, the collection of human scar specimens is frequently restricted, and the establishment of scar experimental animal models for scientific research is urgently needed. The four most commonly used animal models of hypertrophic scars have the following drawbacks: the rabbit ear model takes a long time to construct; the immunodeficient mouse hypertrophic scar model necessitates careful feeding and experimental operations; female Duroc pigs are expensive to purchase and maintain, and their large size makes it difficult to produce a significant number of models; and mouse scar models that rely on tension require special skin stretch devices, which are often damaged and shed, resulting in unstable model establishment. Our group overcame the shortcomings of previous scar animal models and created a new mouse model of hypertrophic scarring induced by suture anchoring at the wound edge. Methods We utilized suture anchoring of incisional wounds to impose directional tension throughout the healing process, restrain wound contraction, and generate granulation tissue, thus inducing scar formation. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage and the wound edges on the lower back relaxed as a control. Macroscopic manifestation, microscopic histological analysis, mRNA sequencing, bioinformatics, and in vitro cell assays were also conducted to verify the reliability of this method. Results Compared with those in relaxed controls, the fibrotic changes in stretched wounds were more profound. Histologically, the stretched scars were hypercellular, hypervascular, and hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. In addition, the stretched scars exhibited transcriptional overlap with mechanically stretched scars, and human hypertrophic and keloid scars. Phosphatidylinositol 3-kinase-serine/threonine-protein kinase B signaling was implicated as a profibrotic mediator of apoptosis resistance under suture-induced tension. Conclusions This straightforward murine model successfully induces cardinal molecular and histological features of pathological hypertrophic scarring through localized suture tension to inhibit wound contraction. The model enables us to interrogate the mechanisms of tension-induced fibrosis and evaluate anti-scarring therapies.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mechanical stimulation promotes fibrochondrocyte proliferation by activating the TRPV4 signaling pathway during tendon–bone insertion healing: CCN2 plays an important regulatory role 在肌腱骨插入愈合过程中,机械刺激通过激活 TRPV4 信号通路促进纤维软骨细胞增殖:CCN2 发挥着重要的调节作用
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-10-20 DOI: 10.1093/burnst/tkae028
Xuting Bian, Xiao Liu, Mei Zhou, Hong Tang, Rui Wang, Lin Ma, Gang He, Shibo Xu, Yunjiao Wang, Jindong Tan, Kanglai Tang, Lin Guo
Background We previously confirmed that mechanical stimulation is an important factor in the repair of tendon–bone insertion (TBI) injuries and that mechanoreceptors such as transient receptor potential ion-channel subfamily V member 4 (TRPV4; also known as transient receptor potential vanilloid 4) are key to transforming mechanical stimulation into intracellular biochemical signals. This study aims to elucidate the mechanism of mechanical stimulation regulating TRPV4. Methods Immunohistochemical staining and western blotting were used to evaluate cartilage repair at the TBI after injury. The RNA expression and protein expression of mechanoreceptors and key pathway molecules regulating cartilage proliferation were analyzed. TBI samples were collected for transcriptome sequencing to detect gene expression. Calcium-ion imaging and flow cytometry were used to evaluate the function of TPRV4 and cellular communication network factor 2 (CCN2) after the administration of siRNA, recombinant adenovirus and agonists. Results We found that treadmill training improved the quality of TBI healing and enhanced fibrochondrocyte proliferation. The transcriptome sequencing results suggested that the elevated expression of the mechanistically stimulated regulator CCN2 and the exogenous administration of recombinant human CCN2 significantly promoted TRPV4 protein expression and fibrochondrocyte proliferation. In vitro, under mechanical stimulation conditions, small interfering RNA (siRNA)-CCN2 not only inhibited the proliferation of primary fibrochondrocytes but also suppressed TRPV4 protein expression and activity. Subsequently, primary fibrochondrocytes were treated with the TRPV4 agonist GSK1016790A and the recombinant adenovirus TRPV4 (Ad-TRPV4), and GSK1016790A partially reversed the inhibitory effect of siRNA-CCN2. The phosphoinositide 3-kinase/ protein kinase B (PI3K/AKT) signaling pathway participated in the above process. Conclusions Mechanical stimulation promoted fibrochondrocyte proliferation and TBI healing by activating TRPV4 channels and the PI3K/AKT signaling pathway, and CCN2 may be a key regulatory protein in maintaining TRPV4 activation.
背景 我们之前证实,机械刺激是肌腱-骨插入(TBI)损伤修复的一个重要因素,而瞬时受体电位离子通道 V 亚家族成员 4(TRPV4;又称瞬时受体电位香草素 4)等机械感受器是将机械刺激转化为细胞内生化信号的关键。本研究旨在阐明机械刺激调控 TRPV4 的机制。方法 采用免疫组化染色法和 Western 印迹法评估损伤后 TBI 处的软骨修复情况。分析机械感受器和调控软骨增殖的关键通路分子的 RNA 表达和蛋白表达。收集 TBI 样本进行转录组测序,以检测基因表达。使用钙离子成像和流式细胞术评估了服用 siRNA、重组腺病毒和激动剂后 TPRV4 和细胞通讯网络因子 2(CCN2)的功能。结果 我们发现跑步机训练提高了创伤性脑损伤的愈合质量,并增强了纤维软骨细胞的增殖。转录组测序结果表明,机理刺激调节因子 CCN2 表达升高,外源性给予重组人 CCN2 能显著促进 TRPV4 蛋白表达和纤维软骨细胞增殖。在体外,在机械刺激条件下,小干扰 RNA(siRNA)-CCN2 不仅能抑制原代纤维软骨细胞的增殖,还能抑制 TRPV4 蛋白的表达和活性。随后,用 TRPV4 激动剂 GSK1016790A 和重组腺病毒 TRPV4(Ad-TRPV4)处理原代纤维软骨细胞,GSK1016790A 可部分逆转 siRNA-CCN2 的抑制作用。磷酸肌酸 3- 激酶/蛋白激酶 B(PI3K/AKT)信号通路参与了上述过程。结论 机械刺激通过激活TRPV4通道和PI3K/AKT信号通路促进纤维软骨细胞增殖和创伤性脑损伤愈合,而CCN2可能是维持TRPV4激活的关键调控蛋白。
{"title":"Mechanical stimulation promotes fibrochondrocyte proliferation by activating the TRPV4 signaling pathway during tendon–bone insertion healing: CCN2 plays an important regulatory role","authors":"Xuting Bian, Xiao Liu, Mei Zhou, Hong Tang, Rui Wang, Lin Ma, Gang He, Shibo Xu, Yunjiao Wang, Jindong Tan, Kanglai Tang, Lin Guo","doi":"10.1093/burnst/tkae028","DOIUrl":"https://doi.org/10.1093/burnst/tkae028","url":null,"abstract":"Background We previously confirmed that mechanical stimulation is an important factor in the repair of tendon–bone insertion (TBI) injuries and that mechanoreceptors such as transient receptor potential ion-channel subfamily V member 4 (TRPV4; also known as transient receptor potential vanilloid 4) are key to transforming mechanical stimulation into intracellular biochemical signals. This study aims to elucidate the mechanism of mechanical stimulation regulating TRPV4. Methods Immunohistochemical staining and western blotting were used to evaluate cartilage repair at the TBI after injury. The RNA expression and protein expression of mechanoreceptors and key pathway molecules regulating cartilage proliferation were analyzed. TBI samples were collected for transcriptome sequencing to detect gene expression. Calcium-ion imaging and flow cytometry were used to evaluate the function of TPRV4 and cellular communication network factor 2 (CCN2) after the administration of siRNA, recombinant adenovirus and agonists. Results We found that treadmill training improved the quality of TBI healing and enhanced fibrochondrocyte proliferation. The transcriptome sequencing results suggested that the elevated expression of the mechanistically stimulated regulator CCN2 and the exogenous administration of recombinant human CCN2 significantly promoted TRPV4 protein expression and fibrochondrocyte proliferation. In vitro, under mechanical stimulation conditions, small interfering RNA (siRNA)-CCN2 not only inhibited the proliferation of primary fibrochondrocytes but also suppressed TRPV4 protein expression and activity. Subsequently, primary fibrochondrocytes were treated with the TRPV4 agonist GSK1016790A and the recombinant adenovirus TRPV4 (Ad-TRPV4), and GSK1016790A partially reversed the inhibitory effect of siRNA-CCN2. The phosphoinositide 3-kinase/ protein kinase B (PI3K/AKT) signaling pathway participated in the above process. Conclusions Mechanical stimulation promoted fibrochondrocyte proliferation and TBI healing by activating TRPV4 channels and the PI3K/AKT signaling pathway, and CCN2 may be a key regulatory protein in maintaining TRPV4 activation.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Twist-related protein 1 promotes transforming growth factor β receptor 1 in keloid fibroblasts via regulating the stability of myocyte enhancer factor 2A 扭转相关蛋白1通过调节肌细胞增强因子2A的稳定性促进瘢痕纤维母细胞中转化生长因子β受体1的形成
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-10-19 DOI: 10.1093/burnst/tkae024
Tianhao Li, Mingzi Zhang, Yunzhu Li, Yixin Sun, Jiuzuo Huang, Ang Zeng, Nanze Yu, Xiao Long
Background Keloid scarring is caused by a fibroproliferative disorder due to abnormal activation of genes, the underlying mechanism of which is still unclear. The basic helix–loop–helix transcription factor Twist-related protein 1 (TWIST1) controls cell proliferation and differentiation in tissue development and disease processes. In this study, we aimed to clarify the essential role of TWIST1 in the pathogenesis of keloids. Methods Immunohistochemistry, cell counting kit-8 assays, western blotting, PCR, matrigel invasion assays and immunofluorescence assays were applied to demonstrate the effects and mechanisms of TWIST1 in fibroblasts derived from normal skin and keloids. Mass spectrometry, ubiquitination assays, chromatin immunoprecipitation and dual luciferase reporter assay were applied to explore the interaction of TWIST1 with downstream molecules. Results In the present study, we confirmed that TWIST1 was upregulated in keloid tissue of patients and in keloid-derived fibroblasts (KFBs). In vitro, TWIST1 inhibition prevented KFB proliferation, invasion and activation. We also discovered a link between TWIST1 and the transforming growth factor β (TGF-β) signaling related molecules TGF-β receptor 1 (TΒR1), SMAD family member 2 (Smad2) and Smad3, and the fibrosis markers α-smooth muscle actin, collagen type I and collagen type III in KFBs. Mechanistically, we uncovered a brand-new mechanism by which TWIST1 interacts with myocyte enhancer factor 2A (MEF2A) and suppresses its ubiquitination and degradation. Using chromatin immunoprecipitation and dual-luciferase reporter assay, TΒR1 was identified as a novel downstream target of MEF2A, which directly binds to its promoter. Overexpression of TWIST1 promoted the recruitment of MEF2A to the TΒR1 promoter and restored TΒR1 functional expression. Conclusions Our research highlights a significant function of TWIST1 in the development of keloid and its related fibroblasts, partially facilitated by elevated MEF2A-dependent TΒR1 expression. Blocking the expression of TWIST1 in KFBs could potentially pave a novel therapeutic avenue for keloid treatment.
背景瘢痕疙瘩是由基因异常激活引起的纤维增生性疾病,其基本机制尚不清楚。基本螺旋环螺旋转录因子 Twist-related protein 1 (TWIST1) 在组织发育和疾病过程中控制着细胞的增殖和分化。本研究旨在阐明 TWIST1 在瘢痕疙瘩发病机制中的重要作用。方法 应用免疫组化、细胞计数试剂盒-8 检测、Western 印迹、PCR、matrigel 侵袭检测和免疫荧光检测来证明 TWIST1 在正常皮肤和瘢痕疙瘩成纤维细胞中的作用和机制。质谱分析、泛素化分析、染色质免疫沉淀和双荧光素酶报告分析被用来探讨 TWIST1 与下游分子的相互作用。结果 在本研究中,我们证实 TWIST1 在瘢痕疙瘩患者组织和瘢痕疙瘩衍生成纤维细胞(KFBs)中上调。在体外,抑制 TWIST1 可阻止 KFB 的增殖、侵袭和活化。我们还发现了 TWIST1 与转化生长因子 β(TGF-β)信号相关分子 TGF-β 受体 1(TΒR1)、SMAD 家族成员 2(Smad2)和 Smad3 以及 KFB 中的纤维化标志物 α-平滑肌肌动蛋白、I 型胶原和 III 型胶原之间的联系。从机理上讲,我们发现了TWIST1与肌细胞增强因子2A(MEF2A)相互作用并抑制其泛素化和降解的全新机制。通过染色质免疫沉淀和双荧光素酶报告分析,TΒR1被确定为MEF2A的一个新的下游靶点,它直接结合到MEF2A的启动子上。过表达 TWIST1 能促进 MEF2A 募集到 TΒR1 启动子并恢复 TΒR1 的功能表达。结论 我们的研究强调了 TWIST1 在瘢痕疙瘩及其相关成纤维细胞的发育过程中的重要功能,而 MEF2A 依赖性 TΒR1 表达的升高在一定程度上促进了这一功能。阻断 TWIST1 在 KFB 中的表达有可能为瘢痕疙瘩的治疗开辟一条新的治疗途径。
{"title":"Twist-related protein 1 promotes transforming growth factor β receptor 1 in keloid fibroblasts via regulating the stability of myocyte enhancer factor 2A","authors":"Tianhao Li, Mingzi Zhang, Yunzhu Li, Yixin Sun, Jiuzuo Huang, Ang Zeng, Nanze Yu, Xiao Long","doi":"10.1093/burnst/tkae024","DOIUrl":"https://doi.org/10.1093/burnst/tkae024","url":null,"abstract":"Background Keloid scarring is caused by a fibroproliferative disorder due to abnormal activation of genes, the underlying mechanism of which is still unclear. The basic helix–loop–helix transcription factor Twist-related protein 1 (TWIST1) controls cell proliferation and differentiation in tissue development and disease processes. In this study, we aimed to clarify the essential role of TWIST1 in the pathogenesis of keloids. Methods Immunohistochemistry, cell counting kit-8 assays, western blotting, PCR, matrigel invasion assays and immunofluorescence assays were applied to demonstrate the effects and mechanisms of TWIST1 in fibroblasts derived from normal skin and keloids. Mass spectrometry, ubiquitination assays, chromatin immunoprecipitation and dual luciferase reporter assay were applied to explore the interaction of TWIST1 with downstream molecules. Results In the present study, we confirmed that TWIST1 was upregulated in keloid tissue of patients and in keloid-derived fibroblasts (KFBs). In vitro, TWIST1 inhibition prevented KFB proliferation, invasion and activation. We also discovered a link between TWIST1 and the transforming growth factor β (TGF-β) signaling related molecules TGF-β receptor 1 (TΒR1), SMAD family member 2 (Smad2) and Smad3, and the fibrosis markers α-smooth muscle actin, collagen type I and collagen type III in KFBs. Mechanistically, we uncovered a brand-new mechanism by which TWIST1 interacts with myocyte enhancer factor 2A (MEF2A) and suppresses its ubiquitination and degradation. Using chromatin immunoprecipitation and dual-luciferase reporter assay, TΒR1 was identified as a novel downstream target of MEF2A, which directly binds to its promoter. Overexpression of TWIST1 promoted the recruitment of MEF2A to the TΒR1 promoter and restored TΒR1 functional expression. Conclusions Our research highlights a significant function of TWIST1 in the development of keloid and its related fibroblasts, partially facilitated by elevated MEF2A-dependent TΒR1 expression. Blocking the expression of TWIST1 in KFBs could potentially pave a novel therapeutic avenue for keloid treatment.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142451453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Silk fibroin–gelatine haemostatic sponge loaded with thrombin for wound haemostasis and tissue regeneration 含有凝血酶的丝纤维凝胶止血海绵,用于伤口止血和组织再生
IF 5.3 1区 医学 Q1 DERMATOLOGY Pub Date : 2024-10-14 DOI: 10.1093/burnst/tkae026
Yajun Zhang, Ming Li, Jing Chang, Chang Li, Yuwen Hui, Yanhua Wang, Weiguo Xu
Background Wound haemostasis is an important part of clinical treatments, especially treatments for patients with avulsion injury, destructive injury and large-scale soft tissue injury. Therefore, developing fast and effective haemostatic materials is critical. This study aimed to design a novel and efficient silk fibroin–gelatine composite haemostatic sponge loaded with thrombin (SFG@TB) to assist in wound haemostasis. Methods The SFG@TB composite haemostatic sponge was formed with gelatine, silk fibroin and thrombin through a freeze-drying technique. First, the material characteristics of SFG@TB were measured, including the elastic modulus, swelling rate and porosity. Second, in vitro cell coculture experiments, in vivo embedding experiments and haemolytic analyses were performed to evaluate the biocompatibility of SFG@TB. Then, coagulation experiments and femoral artery and liver bleeding models were used to evaluate the haemostatic performance of SFG@TB. Finally, the ability of SFG@TB to promote tissue healing was evaluated through experiments with Sprague–Dawley rat models of injury. Results Compared with gelatine sponges, SFG@TB exhibited outstanding mechanical properties and water absorption properties. In addition, the excellent biosafety of the composite haemostatic sponge was confirmed by cell experiments, subcutaneous embedding experiments and haemolytic analysis. Based on the in vitro coagulation test results, SFG@TB exhibited greater adhesion of red blood cells and platelets and a shorter dynamic coagulation time. Compared to the use of silk fibroin–gelatine composite haemostatic sponges or gelatine sponges, the introduction of thrombin resulted in a shorter haemostasis time and a smaller bleeding volume, as revealed by in vivo coagulation tests. The experiments with Sprague–Dawley rat models of injury indicated that SFG@TB accelerated the wound healing process and reduced scar width, which was accompanied by thicker granulation tissue. Conclusions Overall, the SFG@TB composite haemostatic sponge, which exhibits outstanding mechanical properties, good haemostatic performance and high biosafety, promoted wound haemostasis and tissue repair. Therefore, the SFG@TB composite haemostatic sponge could be a promising material for wound haemostasis.
背景 伤口止血是临床治疗的重要组成部分,尤其是对撕脱伤、破坏性损伤和大面积软组织损伤患者的治疗。因此,开发快速有效的止血材料至关重要。本研究旨在设计一种新型、高效的丝纤维蛋白-明胶复合止血海绵(SFG@TB),该海绵含有凝血酶,可辅助伤口止血。方法 通过冷冻干燥技术将明胶、丝纤维素和凝血酶制成 SFG@TB 复合止血海绵。首先,测量了 SFG@TB 的材料特性,包括弹性模量、膨胀率和孔隙率。其次,进行了体外细胞共培养实验、体内包埋实验和溶血分析,以评估 SFG@TB 的生物相容性。然后,通过凝血实验和股动脉及肝脏出血模型来评估 SFG@TB 的止血性能。最后,通过 Sprague-Dawley 大鼠损伤模型实验评估了 SFG@TB 促进组织愈合的能力。结果 与明胶海绵相比,SFG@TB 具有出色的机械性能和吸水性能。此外,细胞实验、皮下包埋实验和溶血分析也证实了这种复合止血海绵具有良好的生物安全性。根据体外凝血试验结果,SFG@TB 对红细胞和血小板的粘附力更强,动态凝血时间更短。体内凝血试验显示,与使用丝纤维素-明胶复合止血海绵或明胶海绵相比,引入凝血酶后,止血时间更短,出血量更少。用 Sprague-Dawley 大鼠损伤模型进行的实验表明,SFG@TB 加快了伤口愈合过程,减少了疤痕宽度,同时肉芽组织也更厚实。结论 总体而言,SFG@TB 复合止血海绵具有优异的机械性能、良好的止血性能和较高的生物安全性,可促进伤口止血和组织修复。因此,SFG@TB 复合止血海绵有望成为一种伤口止血材料。
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