Hao Jia, Le Kang, Ben Huang, Shuyang Lu, Zhiwen Ding, Zhenhang Chen, Chunsheng Wang, Jiangping Song, Yunzeng Zou, Yongxin Sun
Venous graft decay (VGD) occurs in coronary artery bypass grafting (CABG), and ischemia-reperfusion oxidative stress injury during the operation is involved in VGD. To explore the cellular phenotypic changes during this process, a stable oxidative stress model of human saphenous vein endothelial cells (HSVECs) is constructed. Through proteomics and cell experiments, it is found that the expression of BCL2L13 is upregulated during oxidative stress of HSVECs, and BCL2L13 regulated mitophagy through receptor-mediated interaction with LC3 and plays a role in cell protection. During oxidative stress, intracellular o8G epigenetic modification occurs, and the o8G modification of miR-6513-5p causes this molecule to lose its targeted regulation of BCL2L13 and participates in the upregulation of BCL2L13. There is a regulatory pathway of o8G modification-BCL2L13-LC3-mitophagy when oxidative stress occurs in HSVECs.
{"title":"o<sup>8</sup>G-miR-6513-5p/BCL2L13 Axis Regulates Mitophagy during Oxidative Stress in the Human Saphenous Vein Endothelial Cells.","authors":"Hao Jia, Le Kang, Ben Huang, Shuyang Lu, Zhiwen Ding, Zhenhang Chen, Chunsheng Wang, Jiangping Song, Yunzeng Zou, Yongxin Sun","doi":"10.1002/adbi.202400218","DOIUrl":"https://doi.org/10.1002/adbi.202400218","url":null,"abstract":"<p><p>Venous graft decay (VGD) occurs in coronary artery bypass grafting (CABG), and ischemia-reperfusion oxidative stress injury during the operation is involved in VGD. To explore the cellular phenotypic changes during this process, a stable oxidative stress model of human saphenous vein endothelial cells (HSVECs) is constructed. Through proteomics and cell experiments, it is found that the expression of BCL2L13 is upregulated during oxidative stress of HSVECs, and BCL2L13 regulated mitophagy through receptor-mediated interaction with LC3 and plays a role in cell protection. During oxidative stress, intracellular o<sup>8</sup>G epigenetic modification occurs, and the o<sup>8</sup>G modification of miR-6513-5p causes this molecule to lose its targeted regulation of BCL2L13 and participates in the upregulation of BCL2L13. There is a regulatory pathway of o<sup>8</sup>G modification-BCL2L13-LC3-mitophagy when oxidative stress occurs in HSVECs.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dallas E Altamirano, Eszter Mihaly, Jalissa D Emmens, Warren L Grayson
Tissue-engineered muscle grafts (TEMGs) are a promising treatment for volumetric muscle loss (VML). In this study, human myogenic progenitors (hMPs) cultured on electrospun fibrin microfiber bundles and evaluated the therapeutic potential of engineered hMP TEMGs in the treatment of murine tibialis anterior (TA) VML injuries is employed. In vitro, the hMP TEMGs express mature muscle markers by 21 days. Upon implantation into VML injuries, the hMP TEMGs enable remarkable regeneration. To further promote wound healing and myogenesis, human adipose-derived stem/stromal cells (hASCs) as fibroadipogenic progenitor (FAP)-like cells with the potential to secrete pro-regenerative cytokines are incorporated. The impact of dose and timing of seeding the hASCs on in vitro myogenesis and VML recovery using hMP-hASC TEMGs are investigated. The hASCs increase myogenesis of hMPs when co-cultured at 5% hASCs: 95% hMPs and with delayed seeding. Upon implantation into immunocompromised mice, hMP-hASC TEMGs increase cell survival, collagen IV deposition, and pro-regenerative macrophage recruitment, but result in excessive adipose tissue growth after 28 days. These data demonstrate the interactions of hASCs and hMPs enhance myogenesis in vitro but there remains a need to optimize treatments to minimize adipogenesis and promote full therapeutic recovery following VML treatment.
{"title":"Adipogenic-Myogenic Signaling in Engineered Human Muscle Grafts used to Treat Volumetric Muscle Loss.","authors":"Dallas E Altamirano, Eszter Mihaly, Jalissa D Emmens, Warren L Grayson","doi":"10.1002/adbi.202400113","DOIUrl":"https://doi.org/10.1002/adbi.202400113","url":null,"abstract":"<p><p>Tissue-engineered muscle grafts (TEMGs) are a promising treatment for volumetric muscle loss (VML). In this study, human myogenic progenitors (hMPs) cultured on electrospun fibrin microfiber bundles and evaluated the therapeutic potential of engineered hMP TEMGs in the treatment of murine tibialis anterior (TA) VML injuries is employed. In vitro, the hMP TEMGs express mature muscle markers by 21 days. Upon implantation into VML injuries, the hMP TEMGs enable remarkable regeneration. To further promote wound healing and myogenesis, human adipose-derived stem/stromal cells (hASCs) as fibroadipogenic progenitor (FAP)-like cells with the potential to secrete pro-regenerative cytokines are incorporated. The impact of dose and timing of seeding the hASCs on in vitro myogenesis and VML recovery using hMP-hASC TEMGs are investigated. The hASCs increase myogenesis of hMPs when co-cultured at 5% hASCs: 95% hMPs and with delayed seeding. Upon implantation into immunocompromised mice, hMP-hASC TEMGs increase cell survival, collagen IV deposition, and pro-regenerative macrophage recruitment, but result in excessive adipose tissue growth after 28 days. These data demonstrate the interactions of hASCs and hMPs enhance myogenesis in vitro but there remains a need to optimize treatments to minimize adipogenesis and promote full therapeutic recovery following VML treatment.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Esra Türker, Mateo S. Andrade Mier, Jessica Faber, Selma J. Padilla Padilla, Nicoletta Murenu, Philipp Stahlhut, Gregor Lang, Zan Lamberger, Jeanette Weigelt, Natascha Schaefer, Jörg Tessmar, Pamela L. Strissel, Torsten Blunk, Silvia Budday, Reiner Strick, Carmen Villmann
Breast Tumor Cells
Triple-negative breast cancer (TNBC) is the most invasive type of breast cancer with a high risk of brain metastasis. In article number 2400184, Carmen Villmann and co-workers systematically set up a 3D cellular system to study TNBC in a biomimetic brain surrounding in terms of cell–cell and cell–matrix interactions. 3D disease model for breast tumor cells (green) attached to collagen (red, confocal image) grown in thiolated hyaluronic acid-based hydrogel (background image black). Icons represent MEW PCL scaffolds, PEGAcr crosslinker, different extracellular matrix (ECM) proteins (collagen, fibronectin, laminin). ECM supplementation is the key regulator of cellular morphology behaviour and survival. The original confocal image was modified using an art filter.