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- W4235652893 abstract "BackgroundAn increase in airway smooth muscle (ASM) cell proliferation leads to an increase in the bulk of the ASM, one of the characteristic features of asthma. We have previously shown that ASM cells from asthmatic individuals proliferate more than those from nonasthmatic subjects. This increased growth might be due to compromised inhibitory mechanisms within the ASM of asthmatic subjects.ObjectiveThe purpose of this study was to determine whether the proliferative control exerted by prostaglandin E2 (PGE2) was altered in the asthmatic ASM cells.MethodsWe used tritated thymidine uptake to measure cell proliferation and cell-surface ELISAs to detect the presence of cell-surface receptors on ASM cells isolated from asthmatic and nonasthmatic individuals.ResultsThe asthmatic ASM cells were significantly more sensitive to proliferation inhibition by PGE2 than the nonasthmatic cells (P<.02). The PGE2 (E-prostanoid [EP]) receptors EP2 and EP3 were detected on asthmatic and nonasthmatic smooth muscle cells in culture. There were significantly more receptors on the asthmatic cells. The asthmatic cells also had increased sensitivity to proliferation inhibition by EP2-specific agonists but not by EP3-specific agonists.ConclusionThe increased growth observed in asthmatic ASM cells is not the result of impaired responsiveness to PGE2. In contrast, these cells have increased sensitivity. This increased sensitivity might be mediated by the increased numbers of EP2 receptors on the surface." @default.
- W4235652893 created "2022-05-12" @default.
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- W4235652893 date "2004-05-01" @default.
- W4235652893 modified "2023-09-26" @default.
- W4235652893 title "Increased sensitivity of asthmatic airway smooth muscle cells to prostaglandin E2 might be mediated by increased numbers of E-prostanoid receptors*1" @default.
- W4235652893 doi "https://doi.org/10.1016/s0091-6749(04)01060-7" @default.
- W4235652893 hasPublicationYear "2004" @default.
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