APL Bioengineering最新文献_第2页

Formononetin suppresses osteosarcoma by targeting MYO1B and remodeling the tumor immune microenvironment. 刺芒柄花素通过靶向MYO1B和重塑肿瘤免疫微环境抑制骨肉瘤。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-12-31 eCollection Date: 2025-12-01 DOI: 10.1063/5.0284083

Yun Liu, Liang Xiong, Wenyu Feng, Tianyu Xie, Jiming Liang, Mingxiu Yang, Shanhang Li, Kai Luo, Feicui Li, Shengping Tang, Shangyu Liu, Qian Huang, Shijie Liao, Jianhong Liu, Yangjie Cai, Qingjun Wei, Haijun Tang, Fuxing Tang

{"title":"Formononetin suppresses osteosarcoma by targeting MYO1B and remodeling the tumor immune microenvironment.","authors":"Yun Liu, Liang Xiong, Wenyu Feng, Tianyu Xie, Jiming Liang, Mingxiu Yang, Shanhang Li, Kai Luo, Feicui Li, Shengping Tang, Shangyu Liu, Qian Huang, Shijie Liao, Jianhong Liu, Yangjie Cai, Qingjun Wei, Haijun Tang, Fuxing Tang","doi":"10.1063/5.0284083","DOIUrl":"10.1063/5.0284083","url":null,"abstract":"Resistance to and associated toxic side effects of neoadjuvant chemotherapy remain major obstacles to improving the prognosis of osteosarcoma patients. Consequently, there is an urgent need to discover effective therapeutic agents with lower toxicity. In this study, the patient-derived xenograft (PDX) model was established and single-cell multi-omics sequencing was performed to comprehensively analyze changes in cellular heterogeneity and gene expression patterns of under formononetin treatment. We found that formononetin can significantly inhibit tumor growth in the osteosarcoma PDX model, on which the single-cell sequencing identified MYO1B as a key target mediating the anti-osteosarcoma effects of formononetin. In vitro experiments demonstrated that MYO1B overexpression enhanced the proliferation, invasion, and migration of osteosarcoma cells, while MYO1B silencing exhibited the opposite effects. Further investigation revealed that formononetin treatment markedly downregulated MYO1B expression, effectively suppressing the proliferative, invasive, and migratory phenotypes of osteosarcoma cells. Moreover, single-cell transcriptomic analysis of murine-derived cells showed that formononetin enhanced the cytotoxic activity of NK cells, promoted M1 macrophage polarization and inhibited M2 polarization, and reduced the proportion of senescent neutrophils, thereby alleviating the immunosuppressive state of the tumor microenvironment. Overall, our findings provide a comprehensive single-cell-level elucidation of the molecular mechanisms underlying the anti-osteosarcoma effects of formononetin, primarily involving downregulating the expression of MYO1B and remodeling the tumor immune microenvironment.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"9 4","pages":"046116"},"PeriodicalIF":4.1,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12757119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145901216","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}

引用次数: 0

Prediction of chronic obstructive pulmonary disease based on multimodal data and deep learning. 基于多模态数据和深度学习的慢性阻塞性肺疾病预测。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-12-24 eCollection Date: 2025-12-01 DOI: 10.1063/5.0289414

Haoran Deng, Xuchun Ding, Shiping Zhu, Xue Song, Yufei Guo

{"title":"Prediction of chronic obstructive pulmonary disease based on multimodal data and deep learning.","authors":"Haoran Deng, Xuchun Ding, Shiping Zhu, Xue Song, Yufei Guo","doi":"10.1063/5.0289414","DOIUrl":"10.1063/5.0289414","url":null,"abstract":"To address the issues of insufficient utilization of multimodal information, modal heterogeneity, and data gaps leading to poor model generalization in early prediction of chronic obstructive pulmonary disease (COPD), a deep learning-based multimodal dynamic fusion network (MMDF-Net) is proposed. This model integrates chest CT images, pulmonary function indicators, and environmental exposure data. It aligns image and non-image features via a dual-tower cross-modal contrastive learning module, mitigating semantic differences across modalities. A conditional generative adversarial network is used to generate high-fidelity environmental exposure data, reducing reliance on data completeness. A dynamic gating fusion mechanism adaptively adjusts multimodal weights based on patient smoking history, age, and other attributes to suppress noise. On the COPD Gene dataset, MMDF-Net achieves an area under the curve (AUC) of 0.92, a sensitivity of 92.3%, and a specificity of 88.7%, significantly outperforming single-modal models and dynamically adjusting weights according to disease stage. These results demonstrate that this multimodal dynamic fusion strategy can effectively address data heterogeneity and individual differences, providing technical support for precise early intervention in COPD.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"9 4","pages":"046115"},"PeriodicalIF":4.1,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12740421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145851166","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}

引用次数: 0

Stiffness-mediated paracrine signaling enhances induction of EMT in oral squamous cell carcinoma. 刚度介导的旁分泌信号增强了口腔鳞状细胞癌中EMT的诱导。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-12-23 eCollection Date: 2025-12-01 DOI: 10.1063/5.0299456

So Youn Moon, Marcelo Lazzaron Lamers, Adam J Engler

{"title":"Stiffness-mediated paracrine signaling enhances induction of EMT in oral squamous cell carcinoma.","authors":"So Youn Moon, Marcelo Lazzaron Lamers, Adam J Engler","doi":"10.1063/5.0299456","DOIUrl":"10.1063/5.0299456","url":null,"abstract":"Oral Squamous Cell Carcinoma (OSCC) contains diverse communities of cells within the oral mucosa. A subset of the epithelia is highly responsive to changing niche conditions, resulting in their loss of polarity, epithelial-to-mesenchymal transition (EMT), and invasion in tumor-adjacent stroma. Given the range of cell states, we sought to understand how cytokine-mediated signaling from mesenchymal SCC25 cells or stiffness-induced mesenchymal (simCal27) cells caused EMT in naïve Cal27 epithelial cells. Media conditioned by SCC25 enhanced Cal27 cell migration, nuclear localization of EMT markers, and caused transcriptomic changes related to cytokine response ontological terms. SCC and simCal27 cells have unique cytokine profiles, which when regressed against transcriptomic changes, suggested that higher expression of IL-1a, IL-6, IL-8, Angiogenin, and PAI-1 in conditioned media could drive EMT; upregulation of these cytokines also appears impactful for overall survival and progression-free interval. However, depletion and supplementation assays clearly show that the presence of these specific cytokines is critical to induce a migratory phenotype and that naïve Cal27's motility is regulated by MAPK and AKT signaling pathways; loss or inhibition of these pathways reduced migration. These data suggest that paracrine signals from stiffness-induced mesenchymal cells act via distinct kinase pathways and may be necessary for cooperative dissemination of OSCC.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"9 4","pages":"046114"},"PeriodicalIF":4.1,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12737868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145835023","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}

引用次数: 0

Tissue regenerative medicine: Clinical advances, challenges, and opportunities. 组织再生医学：临床进展、挑战和机遇。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-12-18 eCollection Date: 2025-12-01 DOI: 10.1063/5.0296897

Seleem Badawy, Varshiny Gopinath, Ana M Diaz Espinosa, Kasinan Suthiwanich, Ethan C Kelmser, Victoria Duke, Veda Kamaraju, Karina Nakayama, Manoj Manna, Julianne J-Y Liu, Sara S Nunes, Keyue Shen, Ngan F Huang

引用次数: 0

Cell-mediated matrix deformations and cell-cell adhesions determine epithelial collective cell migration phenotypes. 细胞介导的基质变形和细胞-细胞粘附决定上皮集体细胞迁移表型。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-12-17 eCollection Date: 2025-12-01 DOI: 10.1063/5.0295506

Corinne E Leonard, Jessanne Y Lichtenberg, Hazel R Sterling, Jesse Rolston, Sydnie K Tran, Priscilla Y Hwang

{"title":"Cell-mediated matrix deformations and cell-cell adhesions determine epithelial collective cell migration phenotypes.","authors":"Corinne E Leonard, Jessanne Y Lichtenberg, Hazel R Sterling, Jesse Rolston, Sydnie K Tran, Priscilla Y Hwang","doi":"10.1063/5.0295506","DOIUrl":"10.1063/5.0295506","url":null,"abstract":"Successful development of tissue structures requires different collective cell migration patterns or phenotypes. Two examples of collective migration phenotypes in epithelial morphogenic processes, such as tubulogenesis, are rotational and invasive. Rotational collective migration phenotypes (RCM) typically lead to acinar structures, and invasive collective migration (ICM) phenotypes lead to duct-like structures. How cells adopt these different phenotypes is still largely unknown. Here, we investigate how cell-cell adhesion marker P-cadherin (CDH3) and mechanical cell-matrix interactions, including matrix deformations, protrusions, and focal adhesions, control rotational or invasive phenotypes during tubulogenesis. To accomplish our objective, we created a custom 3D microfluidic assay to perform live-cell imaging of epithelial clusters or cysts [wild-type (WT) and CDH3-depleted (CDH3-/-)] undergoing tubulogenesis, while simultaneously measuring matrix deformation rates. Our findings reveal WT epithelial cysts maintain rotational phenotypes, but transition to an invasive phenotype to undergo tubulogenesis. Furthermore, we demonstrate ICM phenotypes correlate with higher matrix deformation rates compared to rotational phenotypes. Our studies reveal CDH3 is required for epithelial cysts to transition from rotational to ICM phenotypes, associated with decreased matrix deformation rates. Without CDH3, epithelial cysts lose their ability to adopt ICM phenotypes, which can be rescued by RhoA activation. Finally, we demonstrate that the RhoA-rescued ICM phenotype is mediated, in part, by increased matrix deformation rates and vinculin recruitment to focal adhesion sites.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"9 4","pages":"046113"},"PeriodicalIF":4.1,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12714399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145805897","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}

引用次数: 0

Microfluidic lung cancer models: Bridging clinical treatment strategies and tumor microenvironment recapitulation. 微流控肺癌模型：连接临床治疗策略和肿瘤微环境概述。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-12-16 eCollection Date: 2025-12-01 DOI: 10.1063/5.0282002

Zhiyun Yu, Arsalan A Khan, Wara Naeem, Jeffrey A Borgia, Michael J Liptay, Christopher W Seder, Jian Zhou

{"title":"Microfluidic lung cancer models: Bridging clinical treatment strategies and tumor microenvironment recapitulation.","authors":"Zhiyun Yu, Arsalan A Khan, Wara Naeem, Jeffrey A Borgia, Michael J Liptay, Christopher W Seder, Jian Zhou","doi":"10.1063/5.0282002","DOIUrl":"10.1063/5.0282002","url":null,"abstract":"Lung cancer remains the leading cause of cancer-related mortality worldwide, with non-small cell lung cancer accounting for a majority of cases. Despite advances in targeted therapies and immunotherapy, challenges such as tumor heterogeneity, resistance mechanisms, and limited preclinical models hinder treatment efficacy. Traditional cancer models, including 2D cell cultures and animal models, often fail to accurately replicate the lung's complex architecture, microenvironment, and biomechanical cues, leading to poor predictive performance in drug development. Microfluidic-based organ-on-a-chip technology offers a promising alternative by integrating human-derived cells with precisely controlled perfusion, mechanical cues, and tumor-stroma interactions in physiologically relevant 3D models. These platforms enable the study of lung cancer biology, drug responses, and patient-specific therapeutic outcomes with improved accuracy. In this review, we discuss recent advancements in microfluidic systems for recapitulating normal lung physiology and 3D lung cancer microenvironment, covering various microfluidic platforms with applications in disease modeling and drug testing. Unlike other review articles, we bring first-hand insights from clinicians about the current treatment practice for lung cancer and the clinical utilities of lung cancer-on-a-chip models, which bioengineers have been seeking. We also highlight the translational potential of these systems in personalized oncology and the need for interdisciplinary collaborations, particularly with clinicians, to enhance their clinical impact.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"9 4","pages":"041505"},"PeriodicalIF":4.1,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12711315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145783199","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}

引用次数: 0

Integration of single-cell and bulk transcriptomics uncovers CHST6 as a shared pathogenic driver in idiopathic pulmonary fibrosis and lung cancer. 单细胞和整体转录组学的整合揭示了CHST6是特发性肺纤维化和肺癌的共同致病驱动因素。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-12-16 eCollection Date: 2025-12-01 DOI: 10.1063/5.0289275

Shengqiang Mao, Jiayi Jiang, Zhiqiang Liu, Yi Li

{"title":"Integration of single-cell and bulk transcriptomics uncovers CHST6 as a shared pathogenic driver in idiopathic pulmonary fibrosis and lung cancer.","authors":"Shengqiang Mao, Jiayi Jiang, Zhiqiang Liu, Yi Li","doi":"10.1063/5.0289275","DOIUrl":"10.1063/5.0289275","url":null,"abstract":"Idiopathic pulmonary fibrosis (IPF), a progressive and fatal lung disease, significantly increases the risk of lung cancer, particularly lung adenocarcinoma (LUAD). However, the shared genetic mechanisms driving IPF and LUAD comorbidities remain poorly understood, necessitating integrated multi-omics investigations. Through bulk and single-cell transcriptomic analyses, we identified 308 shared differentially expressed genes enriched in lipid metabolism and immune-inflammatory processes. Additionally, single-cell profiling revealed significant alterations in epithelial cells and macrophage populations between LUAD and IPF tissues, underscoring their role in disease progression. Furthermore, the copy number variation profiling identified a premalignant epithelial subpopulation in IPF exhibiting transcriptional signatures resembling LUAD malignant epithelial cells, and trajectory analysis illustrated a potential temporal progression toward malignancy. To identify co-causal genes, we performed weighted gene coexpression network analysis, defining modules associated with key cell types involved in comorbidities. Moreover, leveraging 101 algorithm combinations across ten machine learning approaches, we constructed a robust prognostic model, pinpointing CHST6 as a top prognostic gene consistently upregulated in both LUAD and IPF. Functional validation confirmed that CHST6 promotes lung cancer cell proliferation, migration, and invasion. In conclusion, our findings elucidate the shared molecular landscape of LUAD and IPF and propose that CHST6 is a promising co-disease therapeutic target.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"9 4","pages":"046112"},"PeriodicalIF":4.1,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12711314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145783180","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}

引用次数: 0

Mechanomedicine: Translating mechanical forces into therapeutic strategies. 机械医学：将机械力转化为治疗策略。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-12-03 eCollection Date: 2025-12-01 DOI: 10.1063/5.0307361

Geraldine M O'Neill, Cheng Zhu, Dong-Hwee Kim, Jennifer Shin

引用次数: 0

Rules of life at the interface of calcium signaling and mechanobiology. 钙信号和机械生物学界面的生命规则。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-11-26 eCollection Date: 2025-12-01 DOI: 10.1063/5.0284022

Linlin Li, David Gazzo, Shams Mowafak Saad, Nissa J Larson, Eugene S Kim, Nilay Kumar, Mayesha Sahir Mim, Mothishwar Jayaraman Krishnan, Benjamin Speybroeck, Chang Ding, Shulan Xiao, Mary C Mullins, Anjali S Iyer-Pascuzzi, Qing Deng, Elsje Pienaar, Janice P Evans, David M Umulis, Jeremiah J Zartman

{"title":"Rules of life at the interface of calcium signaling and mechanobiology.","authors":"Linlin Li, David Gazzo, Shams Mowafak Saad, Nissa J Larson, Eugene S Kim, Nilay Kumar, Mayesha Sahir Mim, Mothishwar Jayaraman Krishnan, Benjamin Speybroeck, Chang Ding, Shulan Xiao, Mary C Mullins, Anjali S Iyer-Pascuzzi, Qing Deng, Elsje Pienaar, Janice P Evans, David M Umulis, Jeremiah J Zartman","doi":"10.1063/5.0284022","DOIUrl":"10.1063/5.0284022","url":null,"abstract":"Living systems process a broad range of internal and external stimuli, respond to environmental constraints, and adapt to various conditions through tight coordination between signaling networks and cellular mechanics. Among these, calcium signaling and cytoskeletal regulation form an essential interplay that spans multiple scales of biological organization-from ion-protein interactions to intercellular communication and tissue-level behaviors. Calcium ions (Ca2+) act as universal messengers, integrating a wide range of cellular signaling inputs to modulate a broad range of cellular structures and functions through the spatiotemporal dynamics of their concentration changes. Ca2+ signals follow conserved principles, despite their diverse roles, that define regulatory \"Rules of Life\" (RoLs)-generalized mechanisms that operate across biological contexts. This review focuses on how Ca2+ regulates and is regulated by cytoskeletal dynamics, with a particular emphasis on computational modeling for predictive simulations. As key examples, we highlight three specific RoLs: (1) Ca2+ dynamics facilitate cytoskeletal reorganization following stress and damage, (2) Ca2+ regulates actin dynamics to control synapse processes supporting both synapse formation and exocytosis, and (3) reciprocal coupling of spatiotemporal Ca2+ signaling and cellular dynamics defines distinct cellular roles in emergent multicellular behavior. Finally, we outline future directions toward developing multimodal computational simulations for identifying new RoLs, integrating them into multi-scale computational frameworks, and applications in bioengineering, pharmacology, and regenerative medicine.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"9 4","pages":"041504"},"PeriodicalIF":4.1,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12659936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649605","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}

引用次数: 0

Digital light processing of hydrogel molds to guide cell mechanosensing and the fabrication of meniscal tissue constructs. 数字光处理的水凝胶模具，以指导细胞力学传感和制造半月板组织结构。

IF 4.1 3区医学

APL Bioengineering Pub Date : 2025-11-07 eCollection Date: 2025-12-01 DOI: 10.1063/5.0289256

Alysse DeFoe, Joshua Toth, Abhishek P Dhand, Lovie Deloney, Mackenzie Obenreder, Vivek B Shenoy, Jason A Burdick

{"title":"Digital light processing of hydrogel molds to guide cell mechanosensing and the fabrication of meniscal tissue constructs.","authors":"Alysse DeFoe, Joshua Toth, Abhishek P Dhand, Lovie Deloney, Mackenzie Obenreder, Vivek B Shenoy, Jason A Burdick","doi":"10.1063/5.0289256","DOIUrl":"10.1063/5.0289256","url":null,"abstract":"The organization of cells and extracellular matrix (ECM) informs tissue function. This structure/function relationship is especially evident in musculoskeletal (MSK) tissues in which a specific ECM organization (e.g., anisotropy) guides directional properties under load. Injury disrupts the ECM structure, and new methods are needed to recapitulate the organization of cells and ECM within MSK tissue constructs to improve tissue models as well as to fabricate implants for repair. To address this, we use digital light processing (DLP) to rapidly 3D print custom molds that support large (centimeter-scale) meniscal tissue construct formation from meniscal fibrochondrocytes embedded within collagen gels. Importantly, these hydrogel molds include multiple pillars designed to anchor the tissue constructs and provide biophysical cues to direct tissue organization. Here, the effect of pillar spacing aspect ratio, mold size, and mold curvature on tissue contraction and cellular organization is investigated both experimentally and in silico. Pillar placement results in either disorganized (1:1 pillar spacing) or anisotropic (1:2 or 1:4 pillar spacing) cell spreading, with anisotropy observed in molds ranging from 6 mm to 2.4 cm in length. The introduction of mold curvature does not impact final construct width but does increase cellular anisotropy relative to molds without curvature. Furthermore, culture in the presence of the contractility inhibitor Cytochalasin D reduces construct contraction. These observations of cell behavior and construct compaction based on mold design are supported by coarse-grain simulations. Overall, this work establishes an adaptable DLP-based platform to grow custom MSK constructs for tissue models or repair.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":"9 4","pages":"046111"},"PeriodicalIF":4.1,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12596089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145483447","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}

引用次数: 0