Publications by authors named "L Niklason"

Disorders in pulmonary vascular integrity are a prominent feature in many lung diseases. Paracrine signaling is highly enriched in the lung and plays a crucial role in regulating vascular homeostasis. However, the specific local cell-cell crosstalk signals that maintain pulmonary microvascular stability in adult animals and humans remain largely unexplored.

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Tissue-engineered vascular conduits (TEVCs), often made by seeding autologous bone marrow cells onto biodegradable polymeric scaffolds, hold promise toward treating single-ventricle congenital heart defects (SVCHDs). However, the clinical adoption of TEVCs has been hindered by a high incidence of graft stenosis in prior TEVC clinical trials. Herein, we developed endothelialized TEVCs by coating the luminal surface of decellularized human umbilical arteries with human induced pluripotent stem cell (hiPSC)-derived endothelial cells (ECs), followed by shear stress training, in flow bioreactors.

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Importance: Vascular injuries require urgent repair to minimize loss of limb and life. Standard revascularization relies on autologous vein or synthetic grafts, but alternative options are needed when adequate vein is not feasible and when clinical conditions preclude safe use of synthetic materials.

Objective: To evaluate the performance of the acellular tissue engineered vessel (ATEV) in the repair of arterial injuries.

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Yang et al. generate tissue engineered blood vessels from hiPSC-derived smooth muscle cells harboring a mutation found in Loeys-Dietz syndrome. In vitro and in vivo data from these vessels provide new insight into the molecular physiology of aortic aneurysms and may create a paradigm for understanding a suite of vascular diseases.

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Article Synopsis
  • The Fas receptor interacts with its ligand, FasL, to trigger apoptosis, but many cancer cells have low Fas expression, making them resistant to this process.
  • Researchers found that blocking endocytosis increases Fas microaggregates on cancer cell membranes, making them more sensitive to Fas-induced apoptosis when treated with a Rho-kinase inhibitor called fasudil.
  • The combination of fasudil and soluble FasL effectively inhibited glioblastoma growth in lab models and mice, highlighting the potential of this approach for improving cancer treatments.
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