Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells
Identifieur interne : 000044 ( PascalFrancis/Checkpoint ); précédent : 000043; suivant : 000045Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells
Auteurs : Elizabeth A. Perkett [États-Unis] ; Wojclech Ornatowski [États-Unis] ; Jens F. Poschet [États-Unis] ; Vojo Deretic [États-Unis]Source :
- Pediatric pulmonology [ 8755-6863 ] ; 2006.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Pédiatrie.
English descriptors
- KwdEn :
Abstract
Cystic fibrosis (CF) remains a fatal progressive disease in spite of the discovery and characterization of the CFTR gene. Transforming growth factor beta (TGF-p) has been implicated in pathophysiology of CF Previous reports have shown the trans-Golgi network (TGN) is hyperacdified in CF epithelial cells in culture and that this hyperacidification can be corrected with the membrane permeant weak base, chloroquine. In this study bioactive TGF-p produced by CF and normal cells was measured using a reporter cell line with a TGF-p responsive promoter linked to luciferase. Increased levels of TGF-β were detected in the conditioned media from CF epithelial cells compared to their matched controls-(IB3-1 vs. S9; pCEP-R vs. pCEP, CuFi-4 vs. NuLi-1). Levels of TGF-β were normalized with chloroquine indicating that the hyperacidification of the TGN of CF cells is responsible for the altered TGF-p levels.
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Pascal:06-0360316Le document en format XML
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<term>Anomaly</term>
<term>Antimalarial</term>
<term>Bronchus</term>
<term>Chloroquine</term>
<term>Chronic</term>
<term>Cystic fibrosis</term>
<term>Epithelial cell</term>
<term>Fibrosis</term>
<term>Furin</term>
<term>Golgi apparatus</term>
<term>Inflammation</term>
<term>Lung</term>
<term>Parasiticide</term>
<term>Pediatrics</term>
<term>Respiratory disease</term>
<term>Transforming growth factor β</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Mucoviscidose</term>
<term>Appareil respiratoire pathologie</term>
<term>Chloroquine</term>
<term>Anomalie</term>
<term>Facteur croissance transformant β</term>
<term>Activité</term>
<term>Bronche</term>
<term>Cellule épithéliale</term>
<term>Poumon</term>
<term>Fibrose</term>
<term>Chronique</term>
<term>Inflammation</term>
<term>Furin</term>
<term>Appareil Golgi</term>
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<front><div type="abstract" xml:lang="en">Cystic fibrosis (CF) remains a fatal progressive disease in spite of the discovery and characterization of the CFTR gene. Transforming growth factor beta (TGF-p) has been implicated in pathophysiology of CF Previous reports have shown the trans-Golgi network (TGN) is hyperacdified in CF epithelial cells in culture and that this hyperacidification can be corrected with the membrane permeant weak base, chloroquine. In this study bioactive TGF-p produced by CF and normal cells was measured using a reporter cell line with a TGF-p responsive promoter linked to luciferase. Increased levels of TGF-β were detected in the conditioned media from CF epithelial cells compared to their matched controls-(IB3-1 vs. S9; pCEP-R vs. pCEP, CuFi-4 vs. NuLi-1). Levels of TGF-β were normalized with chloroquine indicating that the hyperacidification of the TGN of CF cells is responsible for the altered TGF-p levels.</div>
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<fC07 i1="04" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Appareil digestif pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Digestive diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Aparato digestivo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Genetic disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Métabolisme pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Metabolic diseases</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Metabolismo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Pancréas pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Pancreatic disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Páncreas patología</s0>
<s5>40</s5>
</fC07>
<fN21><s1>240</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Nouveau-Mexique</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Nouveau-Mexique"><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A." last="Perkett">Elizabeth A. Perkett</name>
</region>
<name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name>
<name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name>
<name sortKey="Ornatowski, Wojclech" sort="Ornatowski, Wojclech" uniqKey="Ornatowski W" first="Wojclech" last="Ornatowski">Wojclech Ornatowski</name>
<name sortKey="Poschet, Jens F" sort="Poschet, Jens F" uniqKey="Poschet J" first="Jens F." last="Poschet">Jens F. Poschet</name>
</country>
</tree>
</affiliations>
</record>
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