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Relaxation of human airway smooth muscle cells (1174.1)
Author(s) -
Fitzgerald Robert,
Lee Danielle,
Panettieri Reynold,
Wang Rui,
An Steven
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1174.1
Subject(s) - muscle relaxation , chemistry , contraction (grammar) , vascular smooth muscle , smooth muscle , cell , airway , biophysics , myocyte , relaxation (psychology) , flow cytometry , medicine , biology , biochemistry , immunology , anesthesia
The purpose of this study was to determine if H 2 S relaxed human airway smooth muscle cells. If so, we explored the mechanisms responsible for the phenomenon. Human airway smooth muscle cells (HASM) were prepared from human bronchi obtained from lungs unsuitable for transplantation. Dynamic changes in stiffness were measured as an indicator of contraction and relaxation of isolated HASM, using Magnetic Twisting Cytometry (MTC). Acute exposure of the cells to two agents capable of generating H 2 S, Na 2 S and GYY4137, decreased cell stiffness in a dose‐dependent fashion, with maximal relaxation at 10mM and 5mM, respectively. In addition, cells exposed to varying doses of GYY4137 for 24 hours exhibited dose‐dependent decreases in cell stiffness that were substantially greater than acute responses (21% relaxation at 300s vs 50% relaxation at 24h). We further determined that, like vascular smooth muscle, HASM exhibited the presence of ATP‐sensitive K channels and the H 2 S synthesizing enzyme, cystathionine‐g‐lyase. These findings demonstrated that smooth muscle in the airways react to H 2 S quite similarly to that in the vasculature, and suggest, thereby, this class of small gas molecules can be exploited for treating constricted human airways, such as found is asthma. Grant Funding Source : HL50712‐13 HL107361

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