TGF-β1-induced Chloride Channel Activity and Migration of Human Eosinophils
type: CreativeWork
description: Asthma is a chronic disease of the airways characterized by airway hyperresponsiveness, airway inflammation, and airway remodeling. Eosinophils migrate to the airways and play a significant role in the pathogenesis of asthma, particularly through their release of mediators and cytokines. Transforming growth factor (TGF)-β also induces asthmatic features in the lungs, especially airway remodeling. Eosinophils and TGF-β are closely linked to each other in the induction of airway remodeling. TGF-β activity also affects chloride channel activity, which can regulate mediator release and cell migration. Therefore,the role that TGF-β1 stimulation of eosinophils has on chloride channel activity and migration of eosinophils and the underlying mechanisms involved in this process were examined.|Human blood eosinophils were stimulated with TGF-β1, the tyrosine kinase inhibitor genistein, the protein kinase C (PKC)-δ/ε inhibitor rottlerin, the general PKC inhibitor staurosporine, and the chloride channel inhibitors 4,4’-diisothiocyanatostilbene-2,2’-disulfonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB). Protein expression of the chloride channel (CLC) family of chloride channels, PKC isozymes, and Smad transcription factors was determined using western blot, and mRNA expression of CLC was examined using RT-PCR. Chloride channel activity was measured by patch clamping, and eosinophil chemotaxis was assessed using a Boyden microchemotaxis chamber. Flow cytometry was used to determine shape change.|The results showed that TGF-β1 stimulation increased protein expression of ClC-3. There was also more CLC-3 protein expression in asthmatic eosinophils than normal eosinophils. TGF-β1 increased protein expression of PKC-β1, PKC-δ, and phospho-Smad3. TGF-β1 increased the chloride channel activity of the eosinophils, which was blocked by rottlerin. TGF-β1 induced chemotaxis of eosinophils, which was blocked by rottlerin, DIDS and NPPB. Eosinophil shape change occurr…
abstract: Asthma is a chronic disease of the airways characterized by airway hyperresponsiveness, airway inflammation, and airway remodeling. Eosinophils migrate to the airways and play a significant role in the pathogenesis of asthma, particularly through their release of mediators and cytokines. Transforming growth factor (TGF)-β also induces asthmatic features in the lungs, especially airway remodeling. Eosinophils and TGF-β are closely linked to each other in the induction of airway remodeling. TGF-β activity also affects chloride channel activity, which can regulate mediator release and cell migration. Therefore,the role that TGF-β1 stimulation of eosinophils has on chloride channel activity and migration of eosinophils and the underlying mechanisms involved in this process were examined.|Human blood eosinophils were stimulated with TGF-β1, the tyrosine kinase inhibitor genistein, the protein kinase C (PKC)-δ/ε inhibitor rottlerin, the general PKC inhibitor staurosporine, and the chloride channel inhibitors 4,4’-diisothiocyanatostilbene-2,2’-disulfonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB). Protein expression of the chloride channel (CLC) family of chloride channels, PKC isozymes, and Smad transcription factors was determined using western blot, and mRNA expression of CLC was examined using RT-PCR. Chloride channel activity was measured by patch clamping, and eosinophil chemotaxis was assessed using a Boyden microchemotaxis chamber. Flow cytometry was used to determine shape change.|The results showed that TGF-β1 stimulation increased protein expression of ClC-3. There was also more CLC-3 protein expression in asthmatic eosinophils than normal eosinophils. TGF-β1 increased protein expression of PKC-β1, PKC-δ, and phospho-Smad3. TGF-β1 increased the chloride channel activity of the eosinophils, which was blocked by rottlerin. TGF-β1 induced chemotaxis of eosinophils, which was blocked by rottlerin, DIDS and NPPB. Eosinophil shape change occurr…
author: Moore, Benjamin
language: en_US
date published: 2009-05
date modified: 2026-07-24T01:50:57Z
provider: Creighton University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Creighton University

PropertyValue
property ID: Handle
value: http://hdl.handle.net/10504/232