期刊
NANOMEDICINE-NANOTECHNOLOGY BIOLOGY AND MEDICINE
卷 5, 期 1, 页码 30-41出版社
ELSEVIER
DOI: 10.1016/j.nano.2008.07.002
关键词
Pulmonary endothelium; Permeability; Agonists; Actin cytoskeleton; Force mapping
资金
- NHLBI NIH HHS [R01 HL087823-02, HL58064, HL076259, P01 HL058064, HL075349, R01 HL075349, R01 HL076259, R01 HL087823, P01 HL058064-140008, R01 HL076259-06A2] Funding Source: Medline
Actomyosin contraction directly regulates endothelial cell (EC) permeability, but intracellular redistribution of cytoskeletal tension associated with EC permeability is poorly understood. We used atomic force microscopy (AFM), EC permeability assays, and fluorescence microscopy to link barrier regulation, cell remodeling, and cytoskeletal mechanical properties in EC treated with barrier-protective as well as barrier-disruptive agonists. Thrombin, vascular endothelial growth factor, and hydrogen peroxide increased EC permeability, disrupted cell junctions, and induced stress fiber formation. Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine, hepatocyte growth factor, and iloprost tightened EC barriers, enhanced peripheral actin cytoskeleton and adherens junctions, and abolished thrombin-induced permeability and EC remodeling. AFM force mapping and imaging showed differential distribution of cell stiffness: barrier-disruptive agonists increased stiffness in the central region, and barrier-protective agents decreased stiffness in the center and increased it at the periphery. Attenuation of thrombin-induced permeability correlates well with stiffness changes from the cell center to periphery. These results directly link for the first time the patterns of cell stiffness with specific EC permeability responses. (C) 2009 Elsevier Inc. All rights reserved.
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