Biomaterials research最新文献

{"title":"Amphiphilic Lipid-Single-Stranded DNA Conjugate-Mediated Cell Surface Engineering for Programmable Intercellular Tethering and Immune Synapse Formation.","authors":"Sungjun Kim, Chae Eun Lee, Ashok Kumar Jangid, Kyobum Kim","doi":"10.34133/bmr.0366","DOIUrl":"10.34133/bmr.0366","url":null,"abstract":"<p><p>Intercellular tethering and interface stability critically influence cellular activation, particularly in solid tumors where physical constraints limit sustained effector-target engagement. In particular, effective immune-synapse formation in natural killer cells requires stable cell-cell contact. However, most existing strategies rely on tumor-antigen-mediated recognition and are therefore vulnerable to antigen heterogeneity and immune escape. Here, we developed an amphiphilic single-stranded DNA (ssDNA)-based surface-engineering strategy that enables controllable and receptor-independent regulation of intercellular interfaces. Lipid-conjugated ssDNA constructs were designed to (a) anchor onto cell membranes, (b) induce sequence-specific association through DNA hybridization, and (c) enable thermally reversible dissociation of tethered cell pairs. This membrane modification was rapidly achieved, and complementary ssDNA pairing markedly increased effector-target tethering, cytotoxic granule and cytokine secretion, and elimination of triple-negative breast cancer cells. Importantly, this platform remained effective in 3-dimensional tumoroid models, where amphiphilic ssDNA enabled robust membrane localization and facilitated natural-killer-cell-mediated tumor disruption. Collectively, these results demonstrate that immune-synapse efficiency could be actively modulated by engineering the physical properties of intercellular interfaces. Moreover, this programmable ssDNA-based platform offers a versatile framework for regulating diverse cell-cell interfaces, with broad applicability across immunotherapy, tissue engineering, and cell-based therapeutic systems.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0366"},"PeriodicalIF":9.8,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13172579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147966019","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}

{"title":"A Peptide Inhibitor of Lymphocyte Activation Gene-3 Interaction with Fibrinogen-like Protein 1 Synergizes with Programmed Death-Ligand 1 Blockade to Restore T Cell Activity and Inhibit Tumor Growth.","authors":"Seok-Min Lee, Smriti Gurung, Min-Sung Park, Sri Murugan Poongkavithai Vadevoo, Gowri Rangaswamy Gunassekaran, Min-Jong Kim, Sang-Hyun Kim, Ha-Jeong Kim, Eun Jung Park, Sangmin Lee, Wonpil Im, Soyoun Kim, Byungheon Lee","doi":"10.34133/bmr.0364","DOIUrl":"10.34133/bmr.0364","url":null,"abstract":"<p><p>The immune checkpoint lymphocyte activation gene-3 (LAG-3) interacts with major histocompatibility complex class II and fibrinogen-like protein 1 (FGL-1) to suppress T cell activity, contributing to resistance against immunotherapies such as programmed death-ligand 1 (PD-L1) blockade. This study aimed to identify LAG-3-binding peptides capable of disrupting these immunosuppressive interactions. Using a phage-displayed peptide library, we identified 2 candidate peptides, LAG3pep-1 and LAG3pep-2, that preferentially bound to LAG-3-expressing cells and recombinant LAG-3 protein. A LAG-3 D1 domain-blocking antibody competitively inhibited the peptide binding to LAG-3-expressing cells, confirming target specificity. Among the 2 peptides, LAG3pep-2 demonstrated higher binding affinity and greater stability toward LAG-3. These findings were further supported by structural modeling and all-atom simulation of the LAG-3 and peptide complexes and in silico mutational analysis. Functionally, LAG3pep-2 restored interleukin-2 secretion in T cells suppressed by tumor-derived FGL-1 more effectively than LAG3pep-1. Furthermore, LAG3pep-2 synergized with a PD-L1-blocking antibody to rescue T cell cytotoxicity and cytokine production in tumor cell co-culture assays. In vivo, systemic administration of LAG3pep-2 in combination with PD-L1 blockade significantly suppressed syngeneic tumor growth, enhanced anti-tumor immunity, and exhibited no observable systemic toxicity, outperforming either monotherapy. Collectively, these findings identify LAG3pep-2 as a peptide inhibitor of LAG-3 interaction with FGL-1 and a promising combinatorial agent to potentiate PD-L1-targeted cancer immunotherapies.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0364"},"PeriodicalIF":9.8,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13172577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147965908","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}

{"title":"A Monolithic 3D-Printed Platform for Functional Maturation and In Situ Contractility Assessment of 3D Skeletal Muscle.","authors":"Jongwoo Ahn, Seonghun Mun, YoungWon Koo, Sangmin Lee, Seung-Hoon Yang, Seo Hyeon Choi, Jin Hong Mok, Jungho Ahn, Steve K Cho, Jihoon Ko, Seokyoung Bang","doi":"10.34133/bmr.0363","DOIUrl":"10.34133/bmr.0363","url":null,"abstract":"<p><p>Sarcopenia-a debilitating consequence of global population aging characterized by the loss of muscle mass and function-demands in vitro platforms that enable a rigorous and quantitative assessment of muscle contractility. Pillar-displacement-based microphysiological systems are promising for this purpose but suffer from tension loss as tissues compact, creating variable boundary conditions and undermining reliability. We developed a monolithic, 3-dimensional printed Fast-Optimizing and Regeneration/Contraction-Evaluating platform featuring a detachable polydimethylsiloxane spacer that maintains a constant interpillar distance during long-term culture. The monolithic structure, fabricated by stereolithography, ensures high architectural reproducibility. Under the fixed-length boundary conditions, engineered muscles exhibited improved cellular alignment, enhanced myogenic differentiation, and more advanced structural maturation, resulting in markedly higher twitch and tetanic forces upon electrical stimulation. Together, these results establish the Fast-Optimizing and Regeneration/Contraction-Evaluating platform as a robust and reproducible muscle microphysiological system with fixed-length boundary conditions, enabling reliable, long-term quantitative evaluation of morphological and functional changes for tissue-engineering, drug-screening, and muscular-disease-modeling applications.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0363"},"PeriodicalIF":9.8,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147944120","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}

{"title":"A \"One-Stone-Three-Birds\" Inspired Nanoplatform for Multitargeted Ulcerative Colitis Therapy via Combined Aryl Hydrocarbon Receptor Activation and Reactive Oxygen Species Scavenging.","authors":"Kai Dong, Zelin Guan, Danyang Wang, Jinyao Sun, Ying Zhang, Cuiyu You, Yuanming Xing","doi":"10.34133/bmr.0356","DOIUrl":"10.34133/bmr.0356","url":null,"abstract":"<p><p>In the pathogenesis of ulcerative colitis, inflammatory responses, mucosal injury, and gut dysbiosis form a mutually reinforcing network that perpetuates disease progression. Current clinical interventions can rarely modulate these pathological modules simultaneously, underscoring the urgent need for more effective therapeutic strategies. Here, we report a dual-functional nanotherapy that couples aryl hydrocarbon receptor (AhR) activation with on-site reactive oxygen species (ROS) scavenging. An amphiphilic copolymer, HA-TK-LA (HTL), was synthesized by grafting lipoic acid (LA) to hyaluronic acid (HA) via a ROS-cleavable thioketal (TK) linker. The copolymer self-assembles into ~130-nm nanoparticles that encapsulate the natural AhR ligand indole-3-acetic acid (IAA) with a high loading efficiency of 73%. The resulting IAA@HTL nanoparticles exhibit ROS/glutathione-triggered drug release and are actively taken up by inflamed intestinal epithelial cells and M1 macrophages through CD44-mediated endocytosis, leading to suppressed epithelial apoptosis and macrophage repolarization toward an anti-inflammatory phenotype. In dextran sulfate sodium-induced murine colitis, IAA@HTL specifically accumulates in the inflamed colon and markedly alleviates disease activity. Mechanistically, IAA and LA released from the nanoparticles synergistically activate aryl hydrocarbon receptor/cytochrome P450 family 1 subfamily A member 1 and nuclear factor erythroid 2-related factor 2/heme oxygenase-1 signaling, skew macrophages toward an anti-inflammatory state, dampen proinflammatory cytokine release, and reinforce the mucosal barrier by up-regulating tight-junction proteins and interleukin-22 secretion. As inflammation subsides and mucosal integrity is restored, the gut microbiota gradually returns to homeostasis. Collectively, this study establishes a ROS-scavenging and AhR-activating nanodelivery system that achieves a \"one-stone-three-birds\" outcome-attenuating inflammation, repairing mucosa, and rebalancing microbiota-providing new experimental evidence and theoretical support for ulcerative colitis therapy.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0356"},"PeriodicalIF":9.8,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13161534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147936170","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}

{"title":"Mesothelin-Binding Peptide Inhibits Cell Migration and Enables Targeted Delivery of a Mitochondrial-Membrane-Damaging Peptide to Pancreatic Tumors.","authors":"Min-Sung Park, Gowri Rangaswamy Gunassekaran, Seok-Min Lee, Sri Murugan Poongkavithai Vadevoo, Dong-Gyun Jo, Soyoun Kim, Eunji Ha, Sang-Kyun Kim, Hyejin Ahn, Sang-Jeon Chung, Gyeongmin Kang, Mi Rim Lee, Sang Myung Woo, Yun-Hee Kim, Byungheon Lee","doi":"10.34133/bmr.0361","DOIUrl":"10.34133/bmr.0361","url":null,"abstract":"<p><p>Mesothelin (MSLN) is up-regulated in many tumors, including pancreatic tumors, making it a promising therapeutic target. We used a phage-displayed peptide library to identify an MSLN-binding peptide. CTILWSLTC, synthesized in cyclic form (MSLNpep), was selected from the library. MSLNpep bound preferentially to MSLN-high versus MSLN-low cells, internalized efficiently, and bound recombinant MSLN more strongly than a control peptide. MSLNpep treatment reduced migration and invasion in MSLN-high tumor cells. To enable targeted cytotoxicity, we generated chimeras linking MSLNpep to L-form or D-form mitochondrial-membrane-damaging peptides (MSLNpep-KLA and MSLNpep-kla, respectively). MSLNpep-kla-and, to a lesser extent, MSLNpep-KLA-exhibited selective cytotoxicity toward MSLN-high versus MSLN-low cells. Systemic MSLNpep-kla, but not MSLNpep-KLA, suppressed orthotopic pancreatic tumor growth, increased survival, and produced no detectable hepatic or renal toxicity in mice. MSLNpep-kla also induced cytotoxicity in patient-derived pancreatic cancer organoids proportionate to MSLN expression. Analysis of a public single-cell RNA-sequencing dataset of human pancreatic cancer tissues revealed that <i>MSLN</i> was predominantly expressed in malignant ductal cells while showing negligible expression in normal ductal cells and stromal cells. These findings demonstrate that MSLNpep inhibits tumor-cell migration and enables targeted delivery of therapeutic payloads to MSLN-high pancreatic tumors, supporting its use as a peptide ligand for cancer therapy.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0361"},"PeriodicalIF":9.8,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13158456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147936133","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}

{"title":"Nervonic Acid from <i>Malania oleifera</i> Reverses Parkinson's Disease by Regulating Oxidative Stress, Neuroinflammation, and Gut Microbiota.","authors":"Yuwen Li, Xiao Peng, Yang Xu, Jingyu Zhao, Yong Chen, Xuesong Liu, Lihua Peng","doi":"10.34133/bmr.0349","DOIUrl":"10.34133/bmr.0349","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a neurodegenerative disease characterized by the progressive loss of dopaminergic neurons in the substantia nigra, accompanied by oxidative stress and neuroinflammation. While nervonic acid (NA) is recognized as an essential component of myelin sphingolipids, its specific therapeutic mechanisms in PD have not been thoroughly elucidated. In this study, we investigated the neuroprotective potential of NA derived from <i>Malania oleifera</i> and elucidated its underlying multimechanistic effect. We demonstrated that NA targets the core drivers of neuronal injury by restoring PTEN-induced kinase 1-Parkin-mediated mitophagy to alleviate mitochondrial dysfunction and oxidative stress. Concurrently, NA reprograms microglia from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype, thereby inhibiting cytokine secretion and resolving neuroinflammation. Beyond these central protective effects, metabolomics analysis revealed that NA serves as a direct biosynthetic precursor for long-chain ceramides, facilitating myelin regeneration. In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced PD mice, these synergistic mechanisms collectively preserved dopaminergic neurons and improved motor function substantially. Furthermore, 16S ribosomal RNA amplicon sequencing revealed an associative remodeling of the gut microbiota, specifically enriching beneficial genera such as <i>Akkermansia</i>. Collectively, this study establishes NA as a potent multitarget therapeutic that concurrently regulates oxidative stress, neuroinflammation, and myelin regeneration to alleviate PD pathology.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0349"},"PeriodicalIF":9.8,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147870715","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}

{"title":"Visible-Light-Curable Catechol-Reinforced Gelatin Bioglue for Rapid Hemostasis and Engineered Tissue Assembly.","authors":"Ashfaq Ahmad, Jian Shin, Jaylord M Pioquinto, Se Eun Kim, Yong Sook Kim, Jessie S Jeon, Yeong-Jin Choi, Hee-Gyeong Yi","doi":"10.34133/bmr.0360","DOIUrl":"10.34133/bmr.0360","url":null,"abstract":"<p><p>Hydrogel-based tissue adhesives hold promise for diverse biomedical applications, yet achieving strong, durable adhesion to wet, dynamic biological surfaces remains challenging. The catechol-containing amino acid 3,4-dihydroxy-l-phenylalanine (DOPA) is a crucial functional motif in mussel-inspired adhesives and has been extensively investigated for incorporation into various biomaterials. However, conventional approaches of DOPA incorporation and subsequent crosslinking have shown limited potential for clinical translation. We developed a bioinspired strategy involving pH-controlled enzymatic conversion of tyrosine residues in porcine gelatin into DOPA. The resulting catechol-functionalized gelatin was blended with native tyrosine-rich gelatin to form a hybrid adhesive hydrogel, termed DOPA-tyrosine gelatin (DTG) bioglue. DTG was designed to achieve (a) rapid visible-light-driven ruthenium-based crosslinking for structural integrity and (b) enhanced interfacial adhesion via DOPA-mediated interactions with tissue surface. Its shear-thinning and fast-curing properties enable its use as a bioink for both extrusion-based and digital-light-processing 3-dimensional bioprinting. We demonstrated the DTG-assisted tissue-tissue integration for large-area construct assembly, addressing current volumetric fabrication limitations in microextrusion bioprinting. Moreover, it demonstrated superior hemostatic performance in rat liver and vascular injury models. Collectively, DTG bioglue is a promising candidate for next-generation adhesive biomaterial for regenerative medicine and surgical applications.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0360"},"PeriodicalIF":9.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13150077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147870705","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}

{"title":"PD-L1/Lag3 Bispecific Immune Checkpoint Blocking Nanocage Exhibits Potent Antitumor Activity beyond Dual Blockade of PD-L1 and Lag3.","authors":"Seok-Min Lee, Minseong Kim, Chanju Lee, Minah Lee, Hee Jung Yoon, Byungheon Lee, Eun Jung Park, Soyoun Kim","doi":"10.34133/bmr.0362","DOIUrl":"10.34133/bmr.0362","url":null,"abstract":"<p><p>The therapeutic efficacy of blocking programmed cell death protein 1 and programmed cell death ligand 1 (PD-L1) can be augmented through combination with additional immune checkpoint inhibitors. Lymphocyte-activation gene 3 (Lag3) is an inhibitory checkpoint receptor that contributes to T-cell exhaustion and tumor immune evasion. We hypothesized that cotargeting PD-L1 and Lag3 using a human ferritin nanocage platform could provide an alternative therapeutic strategy to monoclonal antibodies (mAbs) against PD-L1 or Lag3 in modulating antitumor immune responses. Here, we describe a PD-L1/Lag3 bispecific immune checkpoint-blocking ferritin nanocage (P1L2) displaying 24 PD-L1 binding peptides and 24 Lag3 binding peptides on its surface. P1L2 demonstrated simultaneous binding to both PD-L1 and Lag3 and exhibited stronger immune-stimulatory activity than either parent nanocage or mAbs against PD-L1 or Lag3. In a syngeneic mouse colon cancer model, P1L2 specifically targeted tumors and substantially suppressed tumor growth compared with each parent nanocage alone or in combination. Moreover, P1L2 showed more potent antitumor activity than a mAb against PD-L1 or Lag3 alone or in combination. These findings demonstrate that the PD-L1/Lag3 bispecific immune checkpoint-blocking ferritin nanocage is a promising nanomedicine for cancer immunotherapy and has potential applications against various solid tumors.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0362"},"PeriodicalIF":9.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13150080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147870724","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}

{"title":"Genetically Engineered Cell Membrane-Coated Nanodrug for Targeted Treatment of Thyroid Cancer.","authors":"Shaojie Xu, Xingyin Li, Youyun Peng, Xue Yang, Yuhang Su, Hanning Li, Sining Wang, Xin Huang, Xingrui Li, Yaying Du","doi":"10.34133/bmr.0358","DOIUrl":"10.34133/bmr.0358","url":null,"abstract":"<p><p>Thyroid cancer is the most common endocrine malignancy, particularly in patients with radioactive iodine-refractory differentiated thyroid cancer (RAIR-DTC), who have limited treatment options and poor clinical prognosis. In this study, doxorubicin and sorafenib were loaded into the photothermal conversion agent mesoporous polydopamine, forming mPDS. Tumor cell membrane coating engineering resulted in the formation of mPDS@CAR-M, significantly improving tumor targeting. After internalization by tumor cells, the loaded drugs are rapidly released under near-infrared laser irradiation. mPDS@CAR-M effectively inhibits tumor cell proliferation by enhancing oxidative stress, suppressing the PI3K-AKT-mTOR signaling pathway, and inducing cytotoxic autophagy. By activating harmful autophagy, mPDS@CAR-M further inhibits the epithelial-mesenchymal transition process, reducing tumor cell migration capacity. In vivo experiments showed that mPDS@CAR-M significantly reduced tumor volume, with its therapeutic efficacy closely related to the expression level of the targeted surface antigen. Therefore, mPDS@CAR-M demonstrates significant potential in the treatment of RAIR-DTC, providing a novel direction for further clinical exploration.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0358"},"PeriodicalIF":9.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13150073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147870700","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}

{"title":"Oxygen Permeable Dextran Nanogels as a Hemoglobin-Based Oxygen Carrier.","authors":"Jaeeun Oh, Hyemin Cho, Kidong Kim, Young-Joon Park, Yun Suk Huh, Sejin Son","doi":"10.34133/bmr.0355","DOIUrl":"10.34133/bmr.0355","url":null,"abstract":"<p><p>Hemoglobin-based oxygen carriers have been extensively explored as oxygen delivery platform. Among them, encapsulation-based hemoglobin-based oxygen carriers face a key limitation: Dense matrices surrounding hemoglobin hinder the precise control of oxygen binding and release, thereby reducing oxygen delivery efficiency to target tissues. In this study, we developed a hemoglobin-loaded dextran-based nanogel (Hb@Dex-NG) via Schiff base cross-linking between oxidized dextran and 4-arm polyethylene glycol (PEG)-NH₂ to address these limitations. This nanogel system constructed via cross-linking of oxidized dextran and PEG features a permeable internal structure that enables efficient oxygen exchange. Ultraviolet-visible spectroscopy and oxygen dissociation analyses confirmed that the encapsulated hemoglobin retained oxygen-binding capacity. Notably, increasing the PEG content during synthesis led to denser internal structure, which, in turn, slowed oxygen release rates-demonstrating the modulability of this system as a controllable oxygen delivery carrier. Moreover, Hb@Dex-NG exhibited markedly reduced nitric oxide scavenging activity and suppressed autoxidation, suggesting enhanced vascular compatibility and oxidative stability. Overall, Hb@Dex-NG offers a structurally adjustable and biocompatible platform that overcomes major challenges associated with encapsulation strategy of oxygen delivery carrier, presenting a promising candidate for safe and effective oxygen delivery platforms.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0355"},"PeriodicalIF":9.8,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13113307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147792084","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}