Biomaterials research最新文献

External-Force-Offset Effects of ECM Coating Layers on hMSCs Subjected to External Physical Force. 外力作用下ECM涂层对hMSCs的外力偏移效应。

IF 9.6

Biomaterials research Pub Date : 2025-10-03 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0265

Cho Young Park, Kyoung Choi, Young-Jin Kim, Seok Chung, Jun Shik Choi, Sang Jun Park, Chun-Ho Kim

{"title":"External-Force-Offset Effects of ECM Coating Layers on hMSCs Subjected to External Physical Force.","authors":"Cho Young Park, Kyoung Choi, Young-Jin Kim, Seok Chung, Jun Shik Choi, Sang Jun Park, Chun-Ho Kim","doi":"10.34133/bmr.0265","DOIUrl":"https://doi.org/10.34133/bmr.0265","url":null,"abstract":"Mesenchymal stem cells (MSCs) used for cell-delivery-based therapy also undergo considerable external stresses upon entering the recipient site in the body. Here, we sought to develop a cell-protective barrier on the MSC surface that protects against stress-induced damage from physical external stresses. The barrier was fabricated from gelatin and hyaluronic acid (HyA) using a layer-by-layer (LbL) technique. In addition to assessing the stability and biological properties of extracellular matrix (ECM)-coated human bone marrow-derived MSCs (hMSCs) produced using the LbL, we also evaluated the cell-protective effects of this coating against 2 external stresses: low-attachment conditions and mechanical force induced by injection. Cell biological and morphological surface changes accompanying cell surface coating were analyzed using fluorescence-activated cell sorting and scanning electron microscopy. Viability and cell cycle characteristics were not substantially different between bare hMSCs and ECM-coated hMSCs with different numbers of layers after 7 days in culture. Stemness was also maintained, as reflected in >97.3% expression of positive markers and <0.5% expression of negative markers in 6-layered ECM-coated hMSCs, termed ECM-hMSCs. ECM-hMSCs showed 62.1% decrease in cell damage and 50.6% increase in DNA content after 3 days under low-attachment conditions. In addition, ECM-hMSCs injected at 100 and 200 kPa showed 27.2% and 41.8% higher viability, with damaged cells decreased by 54.9% and 45.6%, respectively, compared to bare hMSCs. These results show that LbL coating of hMSCs with gelatin and HyA does not impair the function of hMSCs and can physically protect cells from low-attachment conditions and the mechanical force associated with injection.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0265"},"PeriodicalIF":9.6,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12491781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Repairing Effect and Mechanism of the 4-Dimensionally Printed Limbal Stem Cell Strategy on Corneal Alkali Burns in Large Animals. 四维打印角膜缘干细胞策略对大型动物角膜碱烧伤的修复作用及机制。

IF 9.6

Biomaterials research Pub Date : 2025-10-02 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0262

Zhen Shang, Nailong Pan, Xiaomin Wang, Xiao Xu, Yanhan Dong, Dan Han, Liang Zhang, Junlin Lv, Yiwei Xu, Yan Tang, Xiaotong Li, Xiaoying Kong, Wenhua Xu

{"title":"Repairing Effect and Mechanism of the 4-Dimensionally Printed Limbal Stem Cell Strategy on Corneal Alkali Burns in Large Animals.","authors":"Zhen Shang, Nailong Pan, Xiaomin Wang, Xiao Xu, Yanhan Dong, Dan Han, Liang Zhang, Junlin Lv, Yiwei Xu, Yan Tang, Xiaotong Li, Xiaoying Kong, Wenhua Xu","doi":"10.34133/bmr.0262","DOIUrl":"https://doi.org/10.34133/bmr.0262","url":null,"abstract":"Alkali burn of corneas can induce corneal stromal fibrosis and limbal stem cell deficiency, which destroys corneal epithelial homeostasis, leading to scarring and impaired vision. Although stem cell therapy has shown potential therapeutic contributions to corneal injuries, it still faces the challenges of difficult retention and low survival rates due to the limitations of corneal curvature and an abnormal microenvironment. In this work, a 4D-printed chitosan-based hydrogel (4D-CTH) was prepared to load limbal stem cells (LSCs) for the regulation of epithelial microenvironment homeostasis and the repair of alkali-burned corneas. 4D-CTH, which has good biocompatibility and a regular spatial structure, was proven to be a candidate for use as a tissue engineering carrier that supplies highly active LSCs to a cornea injured by alkali. Both in vitro and in vivo studies confirmed that treatment with 4D-CTH + LSCs can provide more efficient corneal repair for alkali burn injuries compared to epidermal growth factor, which is the traditional treatment method for treating burned corneas. Based on single-cell sequencing analysis, 4D-CTH can markedly increase the proportion of LSCs in corneal tissue by promoting the residence and growth of LSCs. Additionally, 4D-CTH loaded with LSCs can inhibit and reverse corneal fibrosis by interfering with fibroblast differentiation, which is closely related to the down-regulation of cytochrome c oxidase subunit VIc expression by LSCs, thereby inhibiting oxidative phosphorylation in fibroblasts. In conclusion, this work not only confirmed the feasibility of 4D-CTH + LSCs for the treatment of corneas burned by alkali but also clarified the regulation mechanism of corneal epithelial homeostasis by 4D-CTH + LSCs, providing theoretical support and an application paradigm for corneal tissue engineering therapy.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0262"},"PeriodicalIF":9.6,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12489182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Self-Assembling Senolytic Prodrug with Enhanced Bioavailability and Selective Activation for Targeting Senescent Retinal Pigment Epithelium. 一种具有增强生物利用度和选择性激活的自组装抗衰老前药。

IF 9.6

Biomaterials research Pub Date : 2025-10-01 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0261

Haewon Ok, Hyun-Seo Park, Jungin Park, Sunyoung Hwang, Jiwon Jang, Jiye Kim, Gaeun Park, Dojoon Park, Tae-Eun Park, Chaekyu Kim, Ja-Hyoung Ryu

{"title":"A Self-Assembling Senolytic Prodrug with Enhanced Bioavailability and Selective Activation for Targeting Senescent Retinal Pigment Epithelium.","authors":"Haewon Ok, Hyun-Seo Park, Jungin Park, Sunyoung Hwang, Jiwon Jang, Jiye Kim, Gaeun Park, Dojoon Park, Tae-Eun Park, Chaekyu Kim, Ja-Hyoung Ryu","doi":"10.34133/bmr.0261","DOIUrl":"10.34133/bmr.0261","url":null,"abstract":"Senolytic therapy, which targets and selectively eliminates senescent cells, has emerged as a promising strategy for treating various age-related diseases. However, its clinical application is often limited by poor bioavailability, off-target toxicity, and the need for invasive administration routes. To overcome these challenges, we developed N201-gal, a novel β-galactosidase-reactive senolytic prodrug that self-assembles into stable nanoparticles, enabling oral administration and improved systemic bioavailability. Once internalized by senescent cells, N201-gal responds to β-galactosidase overexpression, triggering controlled drug release and inducing selective apoptosis in senescent cells while sparing normal cells. The nanoparticle formulation exhibited favorable physicochemical properties, including uniform particle size and pH stability suitable for gastrointestinal absorption. In vitro study shows that N201-gal demonstrated potent senolytic activity and reduced the expression of senescence-associated markers in retinal pigment epithelial (RPE) cells. In addition, in vivo study also shows that oral administration of N201-gal in a mouse model of doxorubicin-induced retinal senescence model significantly restored retinal tissue integrity and visual function through the targeted clearance of senescent cells. These findings highlight the potential of self-assembling senolytic prodrugs as a noninvasive and targeted therapeutic platform for age-related degenerative diseases.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0261"},"PeriodicalIF":9.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12484856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145214747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Peptide-Drug Conjugate M1pep-Tasquinimod Ameliorates Acute Pancreatitis via Selectively Clearing M1-like Macrophages. 肽-药物偶联物M1pep-Tasquinimod通过选择性清除m1样巨噬细胞改善急性胰腺炎。

IF 9.6

Biomaterials research Pub Date : 2025-09-24 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0250

Fangyue Guo, Xufeng Tao, Zhiwen Zhai, Xin Kong, Yunfei Dai, Yu Wu, Yao Xu, Xinya Zhao, Jing Lv, Dong Shang, Hong Xiang

{"title":"The Peptide-Drug Conjugate M1pep-Tasquinimod Ameliorates Acute Pancreatitis via Selectively Clearing M1-like Macrophages.","authors":"Fangyue Guo, Xufeng Tao, Zhiwen Zhai, Xin Kong, Yunfei Dai, Yu Wu, Yao Xu, Xinya Zhao, Jing Lv, Dong Shang, Hong Xiang","doi":"10.34133/bmr.0250","DOIUrl":"10.34133/bmr.0250","url":null,"abstract":"M1-like macrophages dominate local and systemic inflammatory response progression in acute pancreatitis (AP). The development of strategies to target pro-inflammatory M1-like macrophages in conjunction with primary pathophysiology-specific pharmacological therapy presents a challenge in the management of AP. Peptide-drug conjugates (PDCs), which are emerging second-generation conjugate drugs, have quickly become a new favorite in the field of targeted drug delivery due to their superior drug bioavailability, affinity, and stability. Tasquinimod (Tasq) is a specific inhibitor of S100A9 that is expressed mainly in M1-like macrophages during AP. Drug repositioning revealed that Tasq improved AP in a dose-dependent manner, but drug toxicity occurred at doses of 30 mg/kg. Therefore, we selected 2 specific M1-like macrophage-binding peptides (M1peps) by phage display technology and developed a novel PDC, M1pep-Tasq, by connecting M1peps to activated Tasq with a cleavable linker. Based on a mouse model of AP constructed by retrograde injection of sodium taurine cholate into the bile pancreatic duct and an M1-like macrophage polarization model induced by lipopolysaccharide + interferon-γ stimulation, we confirmed that M1pep-Tasq reduces the drug toxicity of Tasq and improves its efficacy by enhancing the targeting of Tasq to damaged organs in vivo and to M1-like macrophages in vitro. Furthermore, M1pep-Tasq effectively improves AP by inhibiting M1-like macrophage polarization by suppressing the S100A9-TLR4-MAPK pathway. Overall, we have developed a novel PDC, M1pep-Tasq, with promising applications in clinical settings to treat a range of inflammatory disorders by increasing the efficacy and reducing the toxicity of Tasq.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0250"},"PeriodicalIF":9.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enhancing Osteogenesis in Osteoporosis via Electromagnetized Gold Nanoparticles. 通过磁化金纳米颗粒促进骨质疏松症的成骨。

IF 9.6

Biomaterials research Pub Date : 2025-09-24 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0260

Yang Liu, Yan Li, Xue Bai, Yu Gu

{"title":"Enhancing Osteogenesis in Osteoporosis via Electromagnetized Gold Nanoparticles.","authors":"Yang Liu, Yan Li, Xue Bai, Yu Gu","doi":"10.34133/bmr.0260","DOIUrl":"10.34133/bmr.0260","url":null,"abstract":"Osteoporosis (OP) is the most common bone metabolic disorder worldwide, markedly compromising patients' quality of life and imposing a substantial healthcare burden. However, current clinical treatments for OP are not able to provide satisfactory therapeutic outcomes, particularly in the presence of complex inflammatory conditions. The integration of noninvasive physical therapy and bionanotechnology has shown great promise in modulating cellular functions and optimizing the bone microenvironment. In this study, we demonstrated that electromagnetized gold nanoparticles (AuNPs) exhibited excellent biocompatibility at the cellular, vascular, and major organ levels. These electromagnetized AuNPs significantly enhanced the biological behaviors of osteoblasts, including proliferation, migration, colony formation, and osteogenic differentiation. Remarkably, RNA sequencing analysis revealed that electromagnetized AuNPs significantly activated the mitochondrial oxidative phosphorylation pathway while suppressing the interleukin-17 pro-inflammatory signaling pathway. Additionally, electromagnetized AuNPs stabilized mitochondrial membrane potential and boosted adenosine triphosphate (ATP) production while reducing cell apoptosis and oxidative stress, thereby promoting osteogenic differentiation under inflammatory conditions. Furthermore, in a mouse model of inflammation-induced OP, the electromagnetized AuNPs effectively restored bone mass and improved trabecular architecture. Collectively, our findings provide a proof-of-concept that electromagnetized AuNPs enhance osteogenesis by promoting osteogenic differentiation and optimizing the bone microenvironment, highlighting their potential as a promising therapeutic strategy for OP.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0260"},"PeriodicalIF":9.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12459909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nucleolin-Targeted DNA Nanoflowers Enable Multimodal Synergistic Cancer Therapy. 核蛋白靶向DNA纳米花可实现多模式协同癌症治疗。

IF 9.6

Biomaterials research Pub Date : 2025-09-23 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0254

Anwen Ren, Huan Liu, Zimei Tang, Peng Zheng, Qingyi Hu, Tao Huang

{"title":"Nucleolin-Targeted DNA Nanoflowers Enable Multimodal Synergistic Cancer Therapy.","authors":"Anwen Ren, Huan Liu, Zimei Tang, Peng Zheng, Qingyi Hu, Tao Huang","doi":"10.34133/bmr.0254","DOIUrl":"10.34133/bmr.0254","url":null,"abstract":"Copper plays multifunctional roles in both physical processes and cancer development. Since copper is an excellent candidate for Fenton-like reactions and the inducer of cuproptosis, copper-based antitumor drugs have attracted many researchers in recent years. However, there are still some barriers to their clinical application, such as leakage to normal tissues, excess of glutathione (GSH), and lack of H2O2 in the tumor microenvironment, indicating that copper alone is not enough for cancer therapy. Herein, we constructed a DNA-based nanodrug loaded with Cu2+ and glucose oxidase (GOx) for synergistic cancer therapy, namely, glucose oxidase-copper-DNA hybrid nanoflower (GCD). AS1411 aptamer, coded in the long single-stranded DNA sequence, provided GCD with tumor-targeting ability, enhancing its bio-safety. The addition of GOx not only provided adequate H2O2 but also helped deplete GSH. Besides, as it oxidated glucose to gluconic acid, the main energy source of tumor cells was cut off. The in vitro and in vivo antitumor ability of GCD was verified. We also examined immune cell death induction and the immune regulation role of GCD and found that the combination of anti-programmed death-1 antibody further enhanced its antitumor effect. These results contribute to the further study and application of copper-based drug development.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0254"},"PeriodicalIF":9.6,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12454938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mesenchymal Stem Cell-Derived Exosomes Inhibit Stim1-Orai1 Signaling and Calcium Overload-Induced Mitochondrial Damage of Follicular Helper T Cells in Lupus. 间充质干细胞来源的外泌体抑制刺激1- orai1信号和钙超载诱导的狼疮滤泡辅助性T细胞线粒体损伤

IF 9.6

Biomaterials research Pub Date : 2025-09-22 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0255

Yingyu Wang, Qingyong Xiang, Yueren Wu, Xiaoyun Zhang, Zhongzhou Huang, Yunxia Hou, Yan Wang, Ji Yang, Weiguo Wan, Hejian Zou, Xue Yang

{"title":"Mesenchymal Stem Cell-Derived Exosomes Inhibit Stim1-Orai1 Signaling and Calcium Overload-Induced Mitochondrial Damage of Follicular Helper T Cells in Lupus.","authors":"Yingyu Wang, Qingyong Xiang, Yueren Wu, Xiaoyun Zhang, Zhongzhou Huang, Yunxia Hou, Yan Wang, Ji Yang, Weiguo Wan, Hejian Zou, Xue Yang","doi":"10.34133/bmr.0255","DOIUrl":"10.34133/bmr.0255","url":null,"abstract":"Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by aberrant T cell activity and excessive autoantibody production. Follicular helper T cells (Tfh) play a pivotal role in promoting B cell-mediated autoantibody generation, contributing to SLE progression. Although mesenchymal stem cell-derived exosomes (MSC-Exos) exhibit immunomodulatory properties, their effects on Tfh in SLE and the underlying mechanisms remain unclear. To address this, we first analyzed sorted Tfh from an imiquimod-induced lupus murine model (IMQ-SLE) and found that MSC-Exos effectively suppressed Tfh function. Consistently, Tfh polarization assays demonstrated that MSC-Exos modulate Tfh differentiation in vitro. Subsequently, we evaluated the therapeutic potential of intravenous MSC-Exos administration and confirmed that MSC-Exos markedly inhibited Tfh expansion and function in vivo. Further RNA sequencing followed by validation experiments identified that MSC-Exos restore calcium homeostasis in Tfh. Mechanically, MSC-Exos down-regulate stromal interaction molecule 1 (Stim1) and Orai1 expression, inhibiting nuclear factor of activated T cells (NFAT) and nuclear factor κB (NF-κB) activation. In parallel, MSC-Exos mitigate calcium overload-induced mitochondrial damage by suppressing mitochondrial calcium uniporter (MCU) expression. Finally, we observed that MSC-Exos also promote the differentiation of follicular regulatory T cells (Tfr) both in vivo and in vitro. These findings suggest that MSC-Exos ameliorate SLE by correcting cellular calcium dysregulation and mitochondrial damage in Tfh while simultaneously restoring the Tfh/Tfr imbalance, highlighting their potential as a therapeutic strategy for SLE.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0255"},"PeriodicalIF":9.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12451110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145132995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decreasing Lamin A Triggers Cell Fate Transitions through Heterochromatin-Nuclear Periphery Detethering. 减少层粘胶蛋白A通过异染色质-核外周脱栓触发细胞命运转变。

IF 9.6

Biomaterials research Pub Date : 2025-09-18 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0256

Lijuan Sun, Yafan Xie, Zhaoyan Zuo, Jian Liu, Jiaqi Yang, Iqra Ali, Qin Peng, Juhui Qiu

{"title":"Decreasing Lamin A Triggers Cell Fate Transitions through Heterochromatin-Nuclear Periphery Detethering.","authors":"Lijuan Sun, Yafan Xie, Zhaoyan Zuo, Jian Liu, Jiaqi Yang, Iqra Ali, Qin Peng, Juhui Qiu","doi":"10.34133/bmr.0256","DOIUrl":"10.34133/bmr.0256","url":null,"abstract":"The interplay between nuclear architecture and extracellular matrix stiffness orchestrates cell fate decisions, yet the molecular mechanisms remain poorly defined. Here, we investigate the role of Lamin A (LMNA), a nuclear structural protein whose expression correlates with tissue stiffness, in regulating cellular differentiation and fate decision. Using myoblasts and fibroblasts as models, it was observed that cells with low LMNA expression showed that higher cell deformation elevated expression of neurological genes and exhibited potential for differentiation into a neural-like fate. CUT&Tag sequencing of LMNA-knockdown cells revealed a reduction in the size of Lamin B1-associated domains, with enhanced Lamin B1 binding at muscle-related genes (Myf5 and Myf6) and diminished binding at the neural gene Nes, suggesting that changes in gene expression are associated with alterations in chromatin structure. Further analysis identified the dissolution of H3K9me2/3-labeled heterochromatin regions and their redistribution in the nucleoplasm following LMNA inhibition. Soft substrates (0.2 kPa) amplify the neural differentiation capacity in LMNA-knockout cells. Additionally, retinoic acid was shown to enhance the expression of neurologically related genes by suppressing LMNA expression. These findings reveal a novel substrate stiffness-induced mechanism by which Lamin A regulates cell fate transitions and provide a new approach for neural cell generation.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0256"},"PeriodicalIF":9.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sustained-Release Spermidine Hydrogel Inhibits M1 Macrophage Polarization and Promotes Tissue Repair for Spinal Cord Injury Repair. 缓释亚精胺水凝胶抑制M1巨噬细胞极化促进脊髓损伤修复的组织修复。

IF 9.6

Biomaterials research Pub Date : 2025-09-11 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0247

Yongjun Luo, Xiao Zhang, Qian Luo, Liang Wu, Shubo Gu, Zuozhi Xie, Xiaolin Zeng, Yili Xu, Yao Wu, Hao Zhou, Tao Xu, Zheng Zhou

{"title":"Sustained-Release Spermidine Hydrogel Inhibits M1 Macrophage Polarization and Promotes Tissue Repair for Spinal Cord Injury Repair.","authors":"Yongjun Luo, Xiao Zhang, Qian Luo, Liang Wu, Shubo Gu, Zuozhi Xie, Xiaolin Zeng, Yili Xu, Yao Wu, Hao Zhou, Tao Xu, Zheng Zhou","doi":"10.34133/bmr.0247","DOIUrl":"10.34133/bmr.0247","url":null,"abstract":"The use of injectable hydrogels represents a viable approach for enhancing neural repair and promoting functional restoration after spinal cord trauma. Nevertheless, the current performance of these materials is not yet optimal and further optimization is necessary. Engineering a cell-free hydrogel delivery system with sustained anti-inflammatory capacity is of great relevance for advancing therapeutic strategies in spinal cord injury (SCI). Here, we fabricated a biomimetic hydrogel incorporating spermidine to modulate the post-injury immune microenvironment. The material was constructed by photocrosslinking aldehyde-modified methacrylated hyaluronic acid (AHAMA) through dynamic Schiff base chemistry, enabling controlled and prolonged spermidine release. This hydrogel demonstrated expedited gelation kinetics coupled with stable and exceptional mechanical properties. In addition, the cell-free AHAMA hydrogels have substantially enhanced the cellular-matrix interactions and facilitated neuronal integration. Furthermore, the spermidine-loaded hydrogel exerted potent immunomodulatory effects by suppressing M1 macrophage (classically activated macrophage) polarization through activation of STAT1 (signal transducer and activator of transcription 1) signaling axis. In vivo assessments demonstrated enhanced neuroregeneration and axonal elongation at the lesion site, which translated into marked improvements in locomotor function in the murine SCI model. Collectively, the combination of sustained spermidine release with a bioinspired, cell-free AHAMA hydrogel scaffold offers an effective therapeutic approach to modulate inflammation and enhance tissue repair in the injured spinal cord environment.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0247"},"PeriodicalIF":9.6,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12423504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145066673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Mesoporous Silica-Based Naringenin Delivery System Promoting Macrophage M2 Polarization in Atherosclerosis. 基于二氧化硅的中孔柚皮素递送系统促进动脉粥样硬化中巨噬细胞M2极化。

IF 9.6

Biomaterials research Pub Date : 2025-09-08 eCollection Date: 2025-01-01 DOI: 10.34133/bmr.0248

Shenhui Ren, Junchao Liu, Hongji Pu, Penghui Wang, Xiaodong Wu, Jinbao Qin, Xiaobing Liu, Minyi Yin, Xinwu Lu, Bo Li, Zhen Zhao

{"title":"A Mesoporous Silica-Based Naringenin Delivery System Promoting Macrophage M2 Polarization in Atherosclerosis.","authors":"Shenhui Ren, Junchao Liu, Hongji Pu, Penghui Wang, Xiaodong Wu, Jinbao Qin, Xiaobing Liu, Minyi Yin, Xinwu Lu, Bo Li, Zhen Zhao","doi":"10.34133/bmr.0248","DOIUrl":"10.34133/bmr.0248","url":null,"abstract":"Atherosclerosis is the leading cause of global cardiovascular morbidity and mortality associated with inflammatory and immunological mechanisms. Immunotherapy has demonstrated promising efficacy in the management of atherosclerosis. Nevertheless, certain immunotherapeutic approaches are associated with limitations, including suboptimal efficacy and non-negligible adverse effects. Upon the pivotal role of macrophage phenotypes in atherosclerosis progression, naringenin-loaded manganese-doped mesoporous silica nanoparticles (MMSN@NAR) were designed and synthesized to reprogram M1 macrophages toward the M2 phenotype, thereby offering a potential therapeutic strategy for atherosclerosis treatment. High loading capacity of naringenin was achieved in MMSN carriers, with superior biocompatibility profiles compared to naringenin dissolved in dimethyl sulfoxide, while maintaining pH-dependent release behavior as demonstrated by dialysis assays. MMSN@NAR is preferentially phagocytosed by M1 macrophages, attenuates inflammatory responses, protects against oxidative stress, and promotes M2 polarization via the AMP-activated protein kinase (AMPK) pathway in vitro. In the ApoE-/- mouse unilateral carotid artery ligation model of atherosclerosis, MMSN@NAR demonstrated marked accumulation in plaques and excellent biocompatibility. Compared to using naringenin or MMSN alone, it could further reduce plaque area by approximately 40% or 60% by inducing macrophage phenotype transformation, which was confirmed by section staining and immunofluorescence. Collectively, this study highlights enhanced macrophage M2 polarization inhibiting atherosclerosis by MMSN@NAR as a promising nanoplatform, offering a novel therapeutic approach based on anti-inflammatory immune regulation.","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"29 ","pages":"0248"},"PeriodicalIF":9.6,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12415335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0