Tissue Engineering Part A最新文献

{"title":"Influencing Endothelial Cells' Roles in Inflammation and Wound Healing Through Nucleic Acid Delivery.","authors":"Valerie Lallo, Laura G Bracaglia","doi":"10.1089/ten.TEA.2023.0296","DOIUrl":"10.1089/ten.TEA.2023.0296","url":null,"abstract":"<p><p>Tissue engineering and wound-healing interventions are often designed for use in diseased and inflamed environments. In this space, endothelial cells (ECs) are crucial regulators of inflammation and healing, as they are the primary contact for recruitment of immune cells, as well as production of proinflammatory cytokines, which can stimulate or reduce inflammation. Alternatively, proliferation and spreading of ECs result in the formation of new vascular tissue or repair of damaged tissue, both critical for wound healing. Targeting ECs with specific nucleic acids could reduce unwanted inflammation or promote tissue regeneration as needed, which are two large issues involved in many regenerative medicine goals. Polymeric delivery systems are tools that can control the delivery of nucleic acids and prolong their effects. This review describes the use of polymeric vehicles for the delivery of nucleic acids to ECs for tissue engineering. Impact statement Tissue engineering is a rapidly growing field that has the potential to resolve many disease states and improve the quality of life of patients. In some applications, tissue-engineered strategies or constructs are developed to rebuild spaces damaged by disease or degeneration. To rebuild the native tissue, these constructs may need to interact with unwanted immune activity and cells. Various immune cells are often the focus of therapies as they are critical players in the inflammatory response; however, endothelial cells are also an extremely important and promising target in these cases. In addition, controlled delivery of specific-acting molecules, such as nucleic acids, is of growing interest for the regeneration and health of a variety of different tissues. It is important to understand what has been done and the potential of these targets and therapeutics for future investigation and advancements in tissue engineering.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11040193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139041024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"p53 Activation Facilitates Transdifferentiation of Human Cardiac Fibroblasts into Endothelial Cells.","authors":"Yu Zhang, Xuefeng Li, Hong Tian, Miaomiao Xi, Jinsong Zhou, Hai Li","doi":"10.1089/ten.TEA.2023.0146","DOIUrl":"10.1089/ten.TEA.2023.0146","url":null,"abstract":"<p><p>Vascular endothelial cells (ECs), locating at the inner side of vascular lumen, play critical roles in maintaining vascular function and participate in tissue repair and neovascularization. Although increasing studies have shown positive effects of transplantation of vascular ECs or their precursor cells on neovascularization and functional recovery of ischemic tissues, the quantity of <i>in vivo</i> ECs is limited and their quality is affected by age, gender, disease, and others, which hinder their clinical application and further study. Chemical transdifferentiation is a promising approach to generate patient-specific cells. In this process, somatic cells are directly converted into desired cell types without the risk of tumorigenicity by pluripotent cell transplantation and exogenous gene introduction by transgene technology. In the present study, we derived ECs from human cardiac fibroblasts (CFs) through an optimized chemical induction method. The derived ECs expressed endothelial specific markers, took up low-density lipoprotein, secreted angiogenic cytokines under hypoxic condition, and formed microvessels <i>in vitro</i> and <i>in vivo</i>. This CF-EC transition bypassed pluripotency and germ layer differentiation, but underwent a stage of endothelialization. Although p53 maintained the same level during the period of CF-EC transdifferentiation, we could modulate p53 transcriptional activity to further improve cell transition efficiency, which mainly functioned at the later stage of endothelialization. Optimization and exploring the regulatory mechanism of CF-EC transition complement each other, which not only broadens the sources of patient-specific ECs but also provides valuable references for the <i>in vivo</i> direct transdifferentiation study and the elucidation of endothelial development and dysfunction. Impact statement This study provides an optimized chemical induction method to derive endothelial cells (ECs) from human cardiac fibroblasts (CFs), which not only broadens the sources of patient-specific ECs but also provides a good research model of mesenchymal-endothelial transition. Studying the molecular process and regulatory mechanism of CF-EC transdifferentiation will provide valuable references for the <i>in vivo</i> direct transdifferentiation for clinical therapy and deepen the understanding of endothelial development and dysfunction.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41221486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Porous Precision-Templated 40 μm Pore Scaffolds Promote Healing through Synergy in Macrophage Receptor with Collagenous Structure and Toll-Like Receptor Signaling.","authors":"Nathan R Chan, Billanna Hwang, Michael S Mulligan, Buddy D Ratner, James D Bryers","doi":"10.1089/ten.TEA.2023.0144","DOIUrl":"10.1089/ten.TEA.2023.0144","url":null,"abstract":"<p><p>Porous precision-templated scaffolds (PTS) with uniform, interconnected, 40 μm pores have shown favorable healing outcomes and a reduced foreign body reaction (FBR). Macrophage receptor with collagenous structure (MARCO) and toll-like receptors (TLRs) have been identified as key surface receptors in the initial inflammatory phase of wound healing. However, the role of MARCO and TLRs in modulating monocyte and macrophage phenotypes within PTS remains uncharacterized. In this study, we demonstrate a synergetic relationship between MARCO and TLR signaling in cells inhabiting PTS, where induction with TLR3 or TLR4 agonists to 40 μm scaffold-resident cells upregulates the transcription of MARCO. Upon deletion of MARCO, the prohealing phenotype within 40 μm PTS polarizes to a proinflammatory and profibrotic phenotype. Analysis of downstream TLR signaling shows that MARCO is required to attenuate nuclear factor kappa B (NF-κB) inflammation in 40 μm PTS by regulating the transcription of inhibitory NFKB inhibitor alpha (<i>NFKBIA</i>) and interleukin-1 receptor-associated kinase 3 (<i>IRAK-M</i>), primarily through a <i>MyD88</i>-dependent signaling pathway. Investigation of implant outcome in the absence of MARCO demonstrates an increase in collagen deposition within the scaffold and the development of tissue fibrosis. Overall, these results further our understanding of the molecular mechanisms underlying MARCO and TLR signaling within PTS. Impact statement Monocyte and macrophage phenotypes in the foreign body reaction (FBR) are essential for the development of a proinflammatory, prohealing, or profibrotic response to implanted biomaterials. Identification of key surface receptors and signaling mechanisms that give rise to these phenotypes remain to be elucidated. In this study, we report a synergistic relationship between macrophage receptor with collagenous structure (MARCO) and toll-like receptor (TLR) signaling in scaffold-resident cells inhabiting porous precision-templated 40 μm pore scaffolds through a <i>MyD88</i>-dependent pathway that promotes healing. These findings advance our understanding of the FBR and provide further evidence that suggests MARCO, TLRs, and fibrosis may be interconnected.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11040183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139418732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunomodulatory Strategies for Cartilage Regeneration in Osteoarthritis.","authors":"Orlaith Kennedy, Andrew Kitson, Chiebuka Okpara, Lesley W Chow, Tomas Gonzalez-Fernandez","doi":"10.1089/ten.TEA.2023.0255","DOIUrl":"10.1089/ten.TEA.2023.0255","url":null,"abstract":"<p><p>Osteoarthritis (OA) is the most prevalent musculoskeletal disorder and a leading cause of disability globally. Although many efforts have been made to treat this condition, current tissue engineering (TE) and regenerative medicine strategies fail to address the inflammatory tissue environment that leads to the rapid progression of the disease and prevents cartilage tissue formation. First, this review addresses in detail the current anti-inflammatory therapies for OA with a special emphasis on pharmacological approaches, gene therapy, and mesenchymal stromal cell (MSC) intra-articular administration, and discusses the reasons behind the limited clinical success of these approaches at enabling cartilage regeneration. Then, we analyze the state-of-the-art TE strategies and how they can be improved by incorporating immunomodulatory capabilities such as the optimization of biomaterial composition, porosity and geometry, and the loading of anti-inflammatory molecules within an engineered structure. Finally, the review discusses the future directions for the new generation of TE strategies for OA treatment, specifically focusing on the spatiotemporal modulation of anti-inflammatory agent presentation to allow for tailored patient-specific therapies. Impact statement Osteoarthritis (OA) is a prevalent and debilitating musculoskeletal disorder affecting millions worldwide. Despite significant advancements in regenerative medicine and tissue engineering (TE), mitigating inflammation while simultaneously promoting cartilage tissue regeneration in OA remains elusive. In this review article, we discuss current anti-inflammatory therapies and explore their potential synergy with cutting-edge cartilage TE strategies, with a special focus on novel spatiotemporal and patient-specific anti-inflammatory strategies.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138833216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Modulation of the Immune System to Improve Tissue Regeneration Strategies.","authors":"Laura G Bracaglia, Themis R Kyriakides","doi":"10.1089/ten.tea.2024.29055.editorial","DOIUrl":"10.1089/ten.tea.2024.29055.editorial","url":null,"abstract":"","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140051149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bending the Rules: Amplifying PD-L1 Immunoregulatory Function Through Flexible Polyethylene Glycol Synthetic Linkers.","authors":"Nicole M Racca, Alexander Dontu, Kayle Riley, Esma S Yolcu, Haval Shirwan, María M Coronel","doi":"10.1089/ten.TEA.2023.0274","DOIUrl":"10.1089/ten.TEA.2023.0274","url":null,"abstract":"<p><p>Immune checkpoint signaling, such as programmed cell death protein-1 (PD-1), is a key target for immunotherapy due to its role in dampening immune responses. PD-1 signaling in T cells is regulated by complex physicochemical and mechanical cues. However, how these mechanical forces are integrated with biochemical responses remains poorly understood. Our previous work demonstrated that the use of an immobilizing polyethylene glycol (PEG) linker on synthetic microgels for the presentation of a chimeric form of PD-L1, SA-PD-L1, lead to local regulatory responses capable of abrogating allograft rejection in a model of cell-based transplantation. We herein provide evidence that enhanced immune regulating function can be obtained when presentation of SA-PD-L1 is achieved through a longer more flexible PEG chain. Presentation of SA-PD-L1 through a linker of high molecular weight, and thus longer length (10 kDa, 60 nm in length), led to enhance conversion of naive T cells into T regulatory cells (Tregs) <i>in vitro</i>. In addition, using a subcutaneous implant model and protein tethered through three different linker sizes (6, 30, and 60 nm) to the surface of PEG hydrogels, we demonstrated that longer linkers promoted PD-1 immunomodulatory role <i>in vivo</i> through three main functions: (1) augmenting immune cell recruitment at the transplant site; (2) promoting the accumulation of naive Tregs expressing migratory markers; and (3) dampening CD8⁺ cytolytic molecule production while augmenting expression of exhaustion phenotypes locally. Notably, accumulation of Treg cells at the implant site persisted for over 30 days postimplantation, an effect not observed when protein was presented with the shorter version of the linkers (6 and 30 nm). Collectively, these studies reveal a facile approach by which PD-L1 function can be modulated through external tuning of synthetic presenting linkers. Impact statement Recently, there has been a growing interest in immune checkpoint molecules as potential targets for tolerance induction, including programmed cell death protein-1 (PD-1). However, how the mechanics of ligand binding to PD-1 receptor affect downstream activation signaling pathways remains unresolved. By taking advantage of the effect of polyethylene glycol chain length on molecule kinetics in an aqueous solution, we herein show that PD-L1 function can be amplified by adjusting the length of the grafting linker. Our results uncover a potential facile mechanism that can be exploited to advance the role of immune checkpoint ligands, in particular PD-L1, in tolerance induction for immunosuppression-free cell-based therapies.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139693651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Cell Density of a Methacrylic Acid-Based Hydrogel Implant on Embedded Islet Function and Viability.","authors":"Krystal Ortaleza, Michael V Sefton","doi":"10.1089/ten.TEA.2023.0155","DOIUrl":"10.1089/ten.TEA.2023.0155","url":null,"abstract":"<p><p>Subcutaneous delivery of islets in a methacrylic acid-based hydrogel may offer a functional cure for type 1 diabetes. Here we show in mice that the hydrogel is able to provide sufficient vasculature to support islet function and viability, when islets are used at a low islet volume fraction (i.e., cell density). The Krogh cylinder model was used to mathematically estimate the effect of implant volume, for a fixed islet dose (600 islet equivalents [IEQ]), on the minimum vessel density required to maintain sufficient pO₂ within the graft. Modeling suggested that 200 μL implants would have low enough islet densities and enough vessels to have islets remain viable, but that 50 μL implants would not; this was confirmed experimentally through measurement of glucose level in streptozotocin-induced diabetic severe combined immunodeficiency disease (SCID/bg) mice, comparing 200 and 50 μL implants, both with 600 IEQ. Vessel densities were ∼20-30 vessels/mm² independent of implant volume and vessels were sufficient to increase subcutaneous oxygen tension, as measured with microcapsules containing oxygen sensitive material (a platinum [Pt] porphyrin); both these results were determined without cells. These results are useful in thinking about the scale-up of this system to humans: to maintain a low islet density (∼0.5%), many more islets will require attention to the subcutaneous implant configuration to satisfy the oxygen needs of the cells.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92157560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spontaneous Alignment of Myotubes Through Myogenic Progenitor Cell Migration.","authors":"Lauren E Mehanna, Adrianna R Osborne, Charlotte A Peterson, Brad J Berron","doi":"10.1089/ten.TEA.2023.0177","DOIUrl":"10.1089/ten.TEA.2023.0177","url":null,"abstract":"<p><p>In large-volume muscle injuries, widespread damage to muscle fibers and the surrounding connective tissue prevents myogenic progenitor cells (MPCs) from initiating repair. There is a clinical need to rapidly fabricate large muscle tissue constructs for integration at the site of large volume muscle injuries. Most strategies for myotube alignment require microfabricated structures or prolonged orientation times. We utilize the MPC's natural propensity to close gaps across an injury site to guide alignment on collagen I. When MPCs are exposed to an open boundary free of cells, they migrate unidirectionally into the cell-free region and align perpendicular to the original boundary direction. We study the utility of this phenomenon with biotin-streptavidin adhesion to position the cells on the substrate, and then demonstrate the robustness of this strategy with unmodified cells, creating a promising tool for MPC patterning without interrupting their natural function. We preposition MPCs in straight-line patterns separated with small gaps. This temporary positioning initiates the migratory nature of the MPCs to align and form myotubes across the gaps, similar to how they migrate and align with a single open boundary. There is a directional component to the MPC migration perpendicular (90°) to the original biotin-streptavidin surface patterns. The expression of myosin heavy chain, the motor protein of muscle thick filaments, is confirmed through immunocytochemistry in myotubes generated from MPCs in our patterning process, acting as a marker of skeletal muscle differentiation. The rapid and highly specific binding of biotin-streptavidin allows for quick formation of temporary patterns, with MPC alignment based on natural regenerative behavior rather than complex fabrication techniques.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138453223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Hybrid Electrospun-Extruded Polydioxanone Suture for Tendon Tissue Regeneration.","authors":"Roxanna E Abhari, Sarah J B Snelling, Edyta Augustynak, Simon Davis, Roman Fischer, Andrew J Carr, Pierre-Alexis Mouthuy","doi":"10.1089/ten.TEA.2023.0273","DOIUrl":"10.1089/ten.TEA.2023.0273","url":null,"abstract":"<p><p>Many surgical tendon repairs fail despite advances in surgical materials and techniques. Tendon repair failure can be partially attributed to the tendon's poor intrinsic healing capacity and the repurposing of sutures from other clinical applications. Electrospun materials show promise as a biological scaffold to support endogenous tendon repair, but their relatively low tensile strength has limited their clinical translation. It is hypothesized that combining electrospun fibers with a material with increased tensile strength may improve the suture's mechanical properties while retaining biophysical cues necessary to encourage cell-mediated repair. This article describes the production of a hybrid electrospun-extruded suture with a sheath of submicron electrospun fibers and a core of melt-extruded fibers. The porosity and tensile strength of this hybrid suture is compared with an electrospun-only braided suture and clinically used sutures Vicryl and polydioxanone (PDS). Bioactivity is assessed by measuring the adsorbed serum proteins on electrospun and melt-extruded filaments using mass spectrometry. Human hamstring tendon fibroblast attachment and proliferation were quantified and compared between the hybrid and control sutures. Combining an electrospun sheath with melt-extruded cores created a hybrid braid with increased tensile strength (70.1 ± 0.3N) compared with an electrospun only suture (12.9 ± 1 N, <i>p</i> < 0.0001). The hybrid suture had a similar force at break to clinical sutures, but lower stiffness and stress. The Young's modulus was 772.6 ± 32 MPa for the hybrid suture, 1693.0 ± 69 MPa for PDS, and 3838.0 ± 132 MPa for Vicryl, <i>p</i> < 0.0001. Hybrid sutures had lower overall porosity than electrospun-only sutures (40 ± 4% and 60 ± 7%, respectively, <i>p</i> = 0.0018) but had a significantly larger overall porosity and average pore diameter compared with surgical sutures. There were similar clusters of adsorbed proteins on electrospun and melt-extruded filaments, which were distinct from PDS. Tendon fibroblast attachment and cell proliferation on hybrid and electrospun sutures were significantly higher than on clinical sutures. This study demonstrated that a bioactive suture with increased tensile strength and lower stiffness could be produced by adding a core of 10 μm melt-extruded fibers to a sheath of electrospun fibers. In contrast to currently used sutures, the hybrid sutures promoted a bioactive response: serum proteins adsorbed, and fibroblasts attached, survived, grew along the sutures, and adopted appropriate morphologies.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10954604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138833215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell-Derived Extracellular Matrix Fiber Scaffolds Improve Recovery from Volumetric Muscle Loss.","authors":"Cassandra Reed, Tai Huynh, Jacob Schluns, Payton Phelps, Jamie Hestekin, Jeffrey C Wolchok","doi":"10.1089/ten.TEA.2022.0227","DOIUrl":"10.1089/ten.TEA.2022.0227","url":null,"abstract":"<p><p>There are currently no surgical procedures that effectively address the treatment of volumetric muscle loss (VML) injuries that has motivated the development of implantable scaffolding. In this study, the effectiveness of an allogenic scaffold fabricated using fibers built from the extracellular matrix (ECM) collected from muscle fibroblast cells during growth in culture was explored using a hindlimb VML injury (tibialis anterior muscle) in a rat model. Recovery outcomes (8 weeks) were explored in comparison with unrepaired controls as well previously examined allogenic scaffolds prepared from decellularized skeletal muscle (DSM) tissue (<i>n</i> = 9/sample group). At 8-week follow-up, we found that the repair of VML injuries using ECM fiber scaffolds in combination with an autogenic mince muscle (MM) paste significantly improved the recovery of peak contractile torque (79% ± 13% of uninjured contralateral muscle) when compared with unrepaired VML controls (57% ± 13%). Similar significant improvements were measured for muscle mass restoration (93% ± 10%) in response to ECM fiber+MM repair when compared with unrepaired VML controls (73% ± 13%). Of note, mass and contractile strength recovery outcomes for ECM fiber scaffolds were not significantly different from DSM+MM repair controls. These <i>in vivo</i> findings support the further exploration of cell-derived ECM fiber scaffolds as a promising strategy for the repair of VML injury with recovery outcomes that compare favorably with current tissue-sourced ECM scaffolds. Furthermore, although the therapeutic potential of ECM fibers as a treatment strategy for muscle injury was explored in this study, they could be adapted for high-throughput fabrication methods developed and routinely used by the textile industry to create a broad range of woven implants (e.g., hernia meshes) for even greater clinical impact.</p>","PeriodicalId":56375,"journal":{"name":"Tissue Engineering Part A","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10136247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}