Byssinosis: Role of Polymer Length on the Effect of Tannin on the Airway β-Adrenergic Receptor |
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Authors: | M M Cloutier L Guernsey |
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Institution: | (1) University of Connecticut Health Center, Farmington, CT 06030 USA, US |
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Abstract: | Tannin, isolated from cotton bracts and implicated in the pathogenesis of byssinosis, inhibits isoproterenol and forskolin-stimulated
cAMP release from airway cells in part by decreasing cell surface β-adrenergic receptor number and uncoupling the β-adrenergic
receptor from its stimulatory G-protein (Gs) and in part by inhibiting adenylyl cyclase activity. We have hypothesized that cotton tannin, because of its long polymer
length, interacts with the hydrophobic binding pocket of the β-adrenergic receptor and alters β-adrenergic receptor binding
and Gs coupling. In these studies, tannins of three different polymer lengths and molecular masses were isolated from cotton bracts
using sequential Amicon ultrafiltration molecular mass > 10,000 (YM10 retentate), 1,000–10,000 (YM10 filtrate), and 1,000–5,000
Da (YM2 retentate)]. The YM10 retentate (25 μg/ml) decreased chloride secretion (Jnet = 1.11 ± 0.28 (control) to 0.59 ± 0.18
μEq/cm2·h, p < 0.05, n= 6), decreased cell surface β-adrenergic receptor number (18.0 ± 1.8 (control) to 10.6 ± 0.9 fmol/mg protein, p < 0.02, n= 4), and inhibited forskolin-stimulated cAMP release (5,254 ± 1,290 (control) to 2,968 ± 620 pmol/mg protein, p < 0.01, n= 8). In contrast, neither the YM10 filtrate nor the YM2 retentate had any effect on net chloride secretion, β-adrenergic
cell surface receptor number, or forskolin-stimulated cAMP release. We conclude that polymer length is essential for the effect
of tannin on the β-adrenergic receptor and on adenylyl cyclase.
Accepted for publication: 28 June 1998 |
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Keywords: | : Chloride secretion— Adenylyl cyclase— Cotton bracts extract— Occupational lung disease |
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