@article{TomaschMaleinerHromadaetal.,
  author    = {Tomasch, Janine and Maleiner, Babette and Hromada, Carina and Szwarc-Hofbauer, Dorota and Teuschl-Woller, Andreas},
  title     = {Cyclic Tensile Stress Induces Skeletal Muscle Hypertrophy and Myonuclear Accretion in a 3D Model},
  series = {Tissue Eng. Part A.},
  volume    = {2023},
  journal   = {Tissue Eng. Part A.},
  number    = {Mar},
  pages     = {257 -- 268},
  abstract  = {Skeletal muscle is highly adaptive to mechanical stress due to its resident stem cells and the pronounced level of myotube plasticity. Herein, we study the adaptation to mechanical stress and its underlying molecular mechanisms in a tissue-engineered skeletal muscle model. We subjected differentiated 3D skeletal muscle-like constructs to cyclic tensile stress using a custom-made bioreactor system, which resulted in immediate activation of stress-related signal transducers (Erk1/2, p38). Cell cycle re-entry, increased proliferation, and onset of myogenesis indicated subsequent myoblast activation. Furthermore, elevated focal adhesion kinase and β-catenin activity in mechanically stressed constructs suggested increased cell adhesion and migration. After 3 days of mechanical stress, gene expression of the fusogenic markers MyoMaker and MyoMixer, myotube diameter, myonuclear accretion, as well as S6 activation, were significantly increased. Our results highlight that we established a promising tool to study sustained adaptation to mechanical stress in healthy, hypertrophic, or regenerating skeletal muscle.},
  subject      = {fibrin},
  language  = {en}
}
@misc{HromadaTomaschWeihsetal.,
  author    = {Hromada, Carina and Tomasch, Janine and Weihs, Anna and R{\"u}nzler, Dominik and Teuschl, Andreas},
  title     = {Engineering of 3D Tissue Constructs Using our Novel MagneTissue Bioreactor as Alternatives to Animal Models},
  subject      = {Bioreactor},
  language  = {en}
}
@article{HromadaHartmannOesterreicheretal.,
  author    = {Hromada, Carina and Hartmann, Jaana and Oesterreicher, Johannes and Stoiber, Anton and Daerr, Anna and Sch{\"a}dl, Barbara and Priglinger, Eleni and Teuschl-Woller, Andreas H. and Holnthoner, Wolfgang and Heinzel, Johannes Christoph and Hercher, David},
  title     = {Occurrence of Lymphangiogenesis in Peripheral Nerve Autografts Contrasts Schwann Cell-Induced Apoptosis of Lymphatic Endothelial Cells In Vitro},
  series = {Biomolecules},
  volume    = {2022},
  journal   = {Biomolecules},
  number    = {12, 6},
  pages     = {820},
  abstract  = {Peripheral nerve injuries pose a major clinical concern world-wide, and functional recovery after segmental peripheral nerve injury is often unsatisfactory, even in cases of autografting. Although it is well established that angiogenesis plays a pivotal role during nerve regeneration, the influence of lymphangiogenesis is strongly under-investigated. In this study, we analyzed the presence of lymphatic vasculature in healthy and regenerated murine peripheral nerves, revealing that nerve autografts contained increased numbers of lymphatic vessels after segmental damage. This led us to elucidate the interaction between lymphatic endothelial cells (LECs) and Schwann cells (SCs) in vitro. We show that SC and LEC secretomes did not influence the respective other cell types' migration and proliferation in 2D scratch assay experiments. Furthermore, we successfully created lymphatic microvascular structures in SC-embedded 3D fibrin hydrogels, in the presence of supporting cells; whereas SCs seemed to exert anti-lymphangiogenic effects when cultured with LECs alone. Here, we describe, for the first time, increased lymphangiogenesis after peripheral nerve injury and repair. Furthermore, our findings indicate a potential lymph-repellent property of SCs, thereby providing a possible explanation for the lack of lymphatic vessels in the healthy endoneurium. Our results highlight the importance of elucidating the molecular mechanisms of SC-LEC interaction.},
  subject      = {Tissue Engineering},
  language  = {en}
}