Cellular and molecular bioengineering最新文献

{"title":"Neonatal and Adult Dermal Fibroblasts Remodel Hyaluronan Enriched Pericellular Matrix Differentially in Hyaluronic Acid Binding Peptide-Tethered Collagen Hydrogels.","authors":"Vanessa Christine Smith, Whitney Ann Ponwith, Steve Smith, Tugba Ozdemir","doi":"10.1007/s12195-026-00907-z","DOIUrl":"10.1007/s12195-026-00907-z","url":null,"abstract":"<p><strong>Purpose: </strong>The goal of this study was to evaluate the impact of hyaluronic acid binding peptide (HABP) on pericellular matrix remodeling and to determine whether this effect differs between adult and neonatal fibroblasts. Neonatal wound healing is characterized by minimal scarring compared to adult healing, which typically results in fibrotic scar formation. Hyaluronic acid (HA) plays an important role in extracellular matrix organization and collagen remodeling during scarless healing. We hypothesized that HABP would promote endogenous HA retention around the pericellular matrix and influence collagen remodeling in fibroblasts.</p><p><strong>Methods: </strong>Adult and neonatal human dermal fibroblasts were cultured in both two-dimensional and three-dimensional environments. HABP-tethered surfaces were used to promote HA retention around cells. Pericellular matrix formation and cell morphology were assessed in two-dimensional culture, while collagen contraction and collagen fibril morphology were evaluated in three-dimensional collagen gel systems.</p><p><strong>Results: </strong>Adult fibroblasts cultured on HABP surfaces appeared similar in shape to neonatal fibroblasts, suggesting that HABP could promote a more regenerative phenotype. Collagen contraction was steeper in peptide-tethered conditions than in control samples for both cell types. The presence of HABP increased contraction significantly in the presence of Hyaluronidase (HAdase). Collagen fibers exhibited altered width and organization in the presence of HABP and Scr-HABP compared with control samples.</p><p><strong>Conclusions: </strong>These findings suggest that HABP enhances HA retention and alters collagen remodeling, supporting a pro-regenerative fibroblast remodeling response.</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 3","pages":"269-282"},"PeriodicalIF":3.5,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13365068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Publisher Correction: Multiscale ECM Stiffness Characterization and Quantitative Single-Cell Analysis Reveal ITGA3-Mediated Stiffness-Responsive Subpopulation Dynamics in Papillary Thyroid Carcinoma.","authors":"Shengnan Tang, Yihong Huang, Xueyang Huang, Ling Chen, Xuegang Xin","doi":"10.1007/s12195-026-00904-2","DOIUrl":"10.1007/s12195-026-00904-2","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s12195-026-00895-0.].</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"205"},"PeriodicalIF":5.0,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Cardiac Fibrosis: Mechanobiology, Epigenetics, and the Path to Precision Therapy.","authors":"Mohammad Hamouz, Raneem Y Hammouz, Christine Caruana, Denise Micallef, Andrzej K Bednarek, Philip Dingli","doi":"10.1007/s12195-026-00903-3","DOIUrl":"10.1007/s12195-026-00903-3","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s12195-026-00896-z.].</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"161"},"PeriodicalIF":5.0,"publicationDate":"2026-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Publisher Correction: Assessing the Relationship Between Bladder Cancer Cell Contractile Phenotypes and Their Invasive Properties.","authors":"Laurence Carignan, Reza Alavi, Martial Millet, Mathilde Lavigne, Stéphane Chabaud, Marc-Étienne Huot, Stéphane Bolduc, François Bordeleau","doi":"10.1007/s12195-026-00905-1","DOIUrl":"10.1007/s12195-026-00905-1","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s12195-026-00897-y.].</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"223"},"PeriodicalIF":5.0,"publicationDate":"2026-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Nanoparticle-Host Interactions: The Impact of Physiological and Pathological Factors on Biodistribution, Immune Processes, and Translational Challenges.","authors":"Louay Abo Qoura, Dmitry Kostyushev, Alessandro Parodi, Daniel I Boyarintsev, Vladimir Chulanov, Vadim S Pokrovsky","doi":"10.1007/s12195-026-00901-5","DOIUrl":"https://doi.org/10.1007/s12195-026-00901-5","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s12195-026-00888-z.].</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"249"},"PeriodicalIF":5.0,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Publisher Correction: FGF-2-Overexpressing Adipose-Derived Stem Cells as a Paracrine Platform for Angiogenesis-Driven Tissue Regeneration.","authors":"Daisuke Seki, Michiyo Honda","doi":"10.1007/s12195-026-00902-4","DOIUrl":"https://doi.org/10.1007/s12195-026-00902-4","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s12195-025-00883-w.].</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"251"},"PeriodicalIF":5.0,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the Relationship Between Bladder Cancer cell Contractile Phenotypes and their Invasive Properties.","authors":"Laurence Carignan, Reza Alavi, Martial Millet, Mathilde Lavigne, Stéphane Chabaud, Marc-Étienne Huot, Stéphane Bolduc, François Bordeleau","doi":"10.1007/s12195-026-00897-y","DOIUrl":"10.1007/s12195-026-00897-y","url":null,"abstract":"<p><strong>Purpose: </strong>Increased cell contractility is considered a hallmark of highly aggressive tumor cells in several cancers. However, the relationship between cell contractility and cancer invasiveness in bladder cancer (BLCA) remains understudied, despite the fact that BLCA is the 6th most prevalent cancer with high risk of recurrence. Here, we explore the relationship between the contractile phenotype of cancer cells and their invasiveness.</p><p><strong>Methods: </strong>The invasive potential of five BLCA cell lines (RT4, SW-780, SW-1710, MGH-U3 and T24) was investigated using transwell and 3D spheroid invasion assays. Cell contractility was measured using traction force microscopy, 3D collagen gel compaction and quantitative polarized light microscopy of spheroids. Mechanotransduction was measured by YAP nuclear translocation and stiffness-mediated cell migration was investigated on stiffness-gradient substrates.</p><p><strong>Results: </strong>We found that the T24 and MGH-U3 cell lines were capable of invasion, while SW-780, RT4, and SW-1710 were non-invasive. The invasive cell lines exerted higher traction forces on their surrounding environment compared to their non-invasive counterparts. Furthermore, the invasive cell lines exhibited increased YAP nuclear translocation on stiffer substrate. When seeded on a stiffness-gradient substrate, invasive cell lines preferred high stiffnesses, whereas non-invasive cell lines migrated towards low-to-mid stiffness substrates.</p><p><strong>Conclusion: </strong>Our findings uncover the relationship between the invasiveness of BLCA cell lines and their contractile phenotypes. We also show that a single assay is not sufficient to infer on a given aggressive phenotype. Furthermore, this study provides a comparative baseline for these cell lines to expand mechanobiology-related investigation in BLCA.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s12195-026-00897-y.</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"207-221"},"PeriodicalIF":5.0,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13128998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Graphene Nanoplatelets Suppress Foam Cell Formation and Atherogenic Inflammation in Macrophages.","authors":"Farizah Hanim Lat, Ahmad Naqib Shuid, Mohd Yusmaidie Aziz, Muhammad Azrul Zabidi, Muhammad Mahyiddin Ramli, Rafeezul Mohamed","doi":"10.1007/s12195-026-00899-w","DOIUrl":"10.1007/s12195-026-00899-w","url":null,"abstract":"<p><strong>Scope: </strong>Foam cell formation is a hallmark of early atherosclerosis, driving plaque development and chronic vascular inflammation. These lipid-engorged macrophages form through excessive uptake of oxidised low-density lipoprotein (oxLDL) and play a central role in disease progression. Graphene nanoplatelets (GNPs), known for their high surface area and biocompatibility, have emerged as promising nanomaterials for biomedical intervention. This study evaluates the potential of GNPs to prevent atherosclerosis by targeting foam cell formation.</p><p><strong>Methods: </strong>Computational analyses, including molecular docking and dynamics simulations, were used to assess the binding affinity of GNPs with key atherogenic proteins such as apolipoprotein B and the LDL receptor. GNPs were structurally characterised using Raman spectroscopy, X-ray diffraction, and Fourier-transform infrared spectroscopy. In vitro assays were conducted on RAW264.7 macrophages to assess cytotoxicity, lipid accumulation, cholesterol levels, cytokine production, and gene expression after treatment with GNPs (1 μg/mL) and oxLDL.</p><p><strong>Results: </strong>GNPs exhibited strong binding affinity to apoB and the LDL receptor, suggesting potential interference with lipid uptake. Structural analyses confirmed the integrity and purity of the GNPs. In vitro, GNPs showed no cytotoxic effects and significantly reduced lipid accumulation and intracellular cholesterol levels in oxLDL-treated macrophages. They also suppressed the secretion of pro-inflammatory cytokines (IFNγ, IL-6, IL-1β) and downregulated genes associated with foam cell formation (IL-1β, ACAT-1, CD36), while upregulating ABCA1, a key gene involved in cholesterol efflux.</p><p><strong>Conclusion: </strong>These findings demonstrate that GNPs effectively inhibit foam cell formation, reduce atherogenic inflammation, and enhance lipid clearance in macrophages. GNPs represent a promising nanotherapeutic strategy for the prevention of atherosclerosis.</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"225-248"},"PeriodicalIF":3.5,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac Fibrosis: Mechanobiology, Epigenetics, and the Path to Precision Therapy.","authors":"Mohammad Hamouz, Raneem Y Hammouz, Christine Caruana, Denise Micallef, Andrzej K Bednarek, Philip Dingli","doi":"10.1007/s12195-026-00896-z","DOIUrl":"10.1007/s12195-026-00896-z","url":null,"abstract":"<p><p>Cardiac fibrosis represents a complex pathological process driven by persistent fibroblast activation, dysregulated cardiomyocyte-ECM crosstalk, and maladaptive mechanotransduction, ultimately resulting in myocardial stiffening and progressive heart failure. This review integrates insights from single-cell and spatial transcriptomics, biomechanical studies, and epigenetic profiling to illuminate the cellular heterogeneity and molecular circuits underlying fibrotic remodelling. We highlight emerging therapies including CRISPR-based gene editing, FAP-targeted CAR-T immunotherapy, nanomedicine for selective RNA delivery, and patient-derived cardiac organoids; that collectively position fibrosis as a reversible and actionable target. Finally, we discuss precision medicine strategies leveraging genomics, circulating biomarkers, artificial intelligence, and environmental risk assessment to deliver personalized anti-fibrotic interventions. By uniting mechanobiology, molecular engineering, and clinical innovation, this review charts a translational roadmap toward durable reversal of cardiac fibrosis.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"129-159"},"PeriodicalIF":5.0,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiscale ECM Stiffness Characterization and Quantitative Single-Cell Analysis Reveal ITGA3-Mediated Stiffness-Responsive Subpopulation Dynamics in Papillary Thyroid Carcinoma.","authors":"Shengnan Tang, Yihong Huang, Xueyang Huang, Ling Chen, Xuegang Xin","doi":"10.1007/s12195-026-00895-0","DOIUrl":"10.1007/s12195-026-00895-0","url":null,"abstract":"<p><strong>Purpose: </strong>Extracellular matrix (ECM) stiffening is a defining feature of papillary thyroid carcinoma (PTC) and influences the emergence of cancer cell subpopulations with distinct behaviors. While tissue-scale measurements provide important insights, they do not capture the local stiffness at the cellular scale, which defines the microenvironment that guides subpopulation organization through integrin-dependent mechanotransduction. This study aimed to quantitatively assess ECM stiffness across tissue and cellular scales and investigate how it shapes PTC subpopulation composition, focusing on integrin α3 (ITGA3) as a key mediator of stiffness-responsive cellular remodeling.</p><p><strong>Methods: </strong>Human PTC tissues were examined to assess ECM stiffness at multiple scales and to evaluate ITGA3 expression. A stiffness-mimicking hydrogel system was used to investigate how modulation of ITGA3 influences cellular responses to matrix rigidity. Single-cell imaging and computational analyses were applied to resolve stiffness-responsive cell-state patterns, and additional experiments were performed to further examine adhesion-associated functional effects.</p><p><strong>Results: </strong>ECM stiffness was elevated at both tissue and cellular scales in human PTC. Experimental models reproducing these stiffness conditions revealed that ITGA3 is required for cells to properly respond to a stiff mechanical environment. Single-cell analyses identified distinct stiffness-responsive subpopulations, and loss of ITGA3 disrupted their redistribution across different mechanical conditions. Additional perturbation experiments further supported a central role for ITGA3 in stiffness-responsive remodeling of cell states.</p><p><strong>Conclusion: </strong>This study integrates multi-scale stiffness measurements with single-cell analysis to reveal how ECM mechanics influence phenotypic heterogeneity in PTC. By identifying ITGA3 as a key mediator of stiffness-responsive remodeling, our findings link matrix stiffness with the organization of distinct cellular subpopulations. Together, these results provide conceptual insight into how the mechanical microenvironment shapes cell behavior in PTC.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s12195-026-00895-0.</p>","PeriodicalId":9687,"journal":{"name":"Cellular and molecular bioengineering","volume":"19 2","pages":"191-203"},"PeriodicalIF":5.0,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}