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Medical & Biological Engineering & Computing

Erschienen in:

01.05.2008 | Special Issue

Endothelial cytoskeletal elements are critical for flow-mediated dilation in human coronary arterioles

verfasst von: Yanping Liu, Hongwei Li, Aaron H. Bubolz, David X. Zhang, David D. Gutterman

Erschienen in: Medical & Biological Engineering & Computing | Ausgabe 5/2008

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Abstract

Mitochondrial H₂O₂ contributes to flow-mediated dilation (FMD) in human coronary arterioles (HCA). We examined the hypothesis that the endothelial cytoskeleton plays a critical role in transducing endothelial wall shear stress into a stimulus for releasing mitochondrial ROS. Phallacidin together with α-, β-tubulin antibodies and Mito-Tracker Red showed the proximity of F-actin, microtubules and mitochondria in endothelial cells. Cytochalasin D (CytoD) and nocodazole (Noc) disrupted endothelial F-actin and microtubules in HCA, respectively, concurrent with a reduction in the generation of cytosolic O₂ ^•− and H₂O₂ (hydroethidine and dichlorodihydrofluorescein fluorescence) and mitochondrial superoxide (mitoSox) during flow (control: 3.5 ± 1.6, Cyto D: 0.51 ± 0.2, Noc: 0.81 ± 0.6). FMD, but not the dilation to bradykinin or papaverine, was reduced by Cyto D (26 ± 10% vs. 56 ± 3%) or Noc (26 ± 11% vs. 58 ± 7%). These results suggest that cytoskeletal elements are a critical component of the signaling mechanism linking endothelial shear stress and mitochondrial release of ROS in the human coronary microcirculation.

Vorheriger Artikel Small artery remodelling in hypertension: causes, consequences and therapeutic implications

Nächster Artikel The development of the heart and microcirculation: role of shear stress

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Titel: Endothelial cytoskeletal elements are critical for flow-mediated dilation in human coronary arterioles
verfasst von: Yanping Liu
Hongwei Li
Aaron H. Bubolz
David X. Zhang
David D. Gutterman
Publikationsdatum: 01.05.2008
Verlag: Springer Berlin Heidelberg
Erschienen in: Medical & Biological Engineering & Computing / Ausgabe 5/2008
Print ISSN: 0140-0118
Elektronische ISSN: 1741-0444
DOI: https://doi.org/10.1007/s11517-008-0331-1

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