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- W1988088971 abstract "Endothelin-1 (ET-1) expression is increased after lung transplantation in association with ischemia reperfusion injury and acute rejection. However, little is known of the role of ET-1 during the development of obliterative bronchiolitis. In this study, we investigated the biological significance of ET-1 in obliterative airway disease development using a rat tracheal allograft model. Immunoreactivity of ET-1 and its receptors ET-RA and ET-RB was increased four-fold in allografts compared with syngrafts and localized to mononuclear cells and smooth muscle cells of the myofibroproliferative lesion and airway wall, indicating that ET-1 may mediate its effects in both a paracrine and autocrine manner in smooth muscle cells. Inhibition of ET-1 action by a nonselective ET-1 receptor antagonist, bosentan, significantly decreased tracheal occlusion, which was linked to delayed epithelial necrosis, suppressed smooth muscle cell proliferation, and a marked reduction in the number of interleukin-1β and interleukin-2 immunoreactive cells. Our findings show that endogenous ET-1 activation is associated with obliteration of the airway wall, and blocking signaling downstream of ET-1 receptors leads to attenuation of obliterative airway disease. The results suggest that ET-1 has a proproliferative and proinflammatory role in the development of obliterative bronchiolitis." @default.
- W1988088971 created "2016-06-24" @default.
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- W1988088971 date "2004-05-01" @default.
- W1988088971 modified "2023-10-17" @default.
- W1988088971 title "Role of Endogenous Endothelin-1 in Transplant Obliterative Airway Disease in the Rat" @default.
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- W1988088971 doi "https://doi.org/10.1111/j.1600-6143.2004.00414.x" @default.
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