FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2003669122> ?p ?o ?g. }

• W2003669122 endingPage "237.e4" @default.
• W2003669122 startingPage "230" @default.
• W2003669122 abstract "BackgroundThe adipokine leptin is a potential new mediator for bronchial epithelial homeostasis. Asthma is a chronic inflammatory disease characterized by airway remodeling that might affect disease chronicity and severity. TGF-β is a tissue growth factor the dysregulation of which is associated with airway remodeling.ObjectiveWe sought to determine whether a bronchial epithelial dysfunction of the leptin/leptin receptor pathway contributes to asthma pathogenesis and severity.MethodsWe investigated in vitro the presence of leptin/leptin receptor on human bronchial epithelial cells. Then we studied the effect of TGF-β and fluticasone propionate on leptin receptor expression. Finally, the role of leptin on TGF-β release and cell proliferation was analyzed. Ex vivo we investigated the presence of leptin/leptin receptor in the epithelium of bronchial biopsy specimens from subjects with asthma of various severities and from healthy volunteers, and some features of airway remodeling, such as reticular basement membrane (RBM) thickness and TGF-β expression in the epithelium, were assessed.ResultsIn vitro bronchial epithelial cells express leptin/leptin receptor. TGF-β decreased and fluticasone propionate increased leptin receptor expression, and leptin decreased the spontaneous release of TGF-β and increased cell proliferation. Ex vivo the bronchial epithelium of subjects with mild, uncontrolled, untreated asthma showed a decrease expression of leptin and its receptor and an increased RBM thickness and TGF-β expression when compared with values seen in healthy volunteers. Furthermore, severe asthma was associated with a reduced expression of leptin and its receptor and an increased RBM thickness with unaltered TGF-β expression.ConclusionsDecreased expression of leptin/leptin receptor characterizes severe asthma and is associated with airway remodeling features. The adipokine leptin is a potential new mediator for bronchial epithelial homeostasis. Asthma is a chronic inflammatory disease characterized by airway remodeling that might affect disease chronicity and severity. TGF-β is a tissue growth factor the dysregulation of which is associated with airway remodeling. We sought to determine whether a bronchial epithelial dysfunction of the leptin/leptin receptor pathway contributes to asthma pathogenesis and severity. We investigated in vitro the presence of leptin/leptin receptor on human bronchial epithelial cells. Then we studied the effect of TGF-β and fluticasone propionate on leptin receptor expression. Finally, the role of leptin on TGF-β release and cell proliferation was analyzed. Ex vivo we investigated the presence of leptin/leptin receptor in the epithelium of bronchial biopsy specimens from subjects with asthma of various severities and from healthy volunteers, and some features of airway remodeling, such as reticular basement membrane (RBM) thickness and TGF-β expression in the epithelium, were assessed. In vitro bronchial epithelial cells express leptin/leptin receptor. TGF-β decreased and fluticasone propionate increased leptin receptor expression, and leptin decreased the spontaneous release of TGF-β and increased cell proliferation. Ex vivo the bronchial epithelium of subjects with mild, uncontrolled, untreated asthma showed a decrease expression of leptin and its receptor and an increased RBM thickness and TGF-β expression when compared with values seen in healthy volunteers. Furthermore, severe asthma was associated with a reduced expression of leptin and its receptor and an increased RBM thickness with unaltered TGF-β expression. Decreased expression of leptin/leptin receptor characterizes severe asthma and is associated with airway remodeling features." @default.
• W2003669122 created "2016-06-24" @default.
• W2003669122 creator A5007373159 @default.
• W2003669122 creator A5026139034 @default.
• W2003669122 creator A5026715859 @default.
• W2003669122 creator A5062951393 @default.
• W2003669122 creator A5064642801 @default.
• W2003669122 creator A5065733629 @default.
• W2003669122 creator A5066244090 @default.
• W2003669122 creator A5073019940 @default.
• W2003669122 creator A5078289429 @default.
• W2003669122 creator A5090527489 @default.
• W2003669122 date "2009-08-01" @default.
• W2003669122 modified "2023-10-15" @default.
• W2003669122 title "Leptin and leptin receptor expression in asthma" @default.
• W2003669122 cites W1498451757 @default.
• W2003669122 cites W1907072707 @default.
• W2003669122 cites W1963513289 @default.
• W2003669122 cites W1979081669 @default.
• W2003669122 cites W2002284972 @default.
• W2003669122 cites W2005644246 @default.
• W2003669122 cites W2006174105 @default.
• W2003669122 cites W2013361230 @default.
• W2003669122 cites W2015677100 @default.
• W2003669122 cites W2028630600 @default.
• W2003669122 cites W2030916726 @default.
• W2003669122 cites W2041550275 @default.
• W2003669122 cites W2048327405 @default.
• W2003669122 cites W2077332632 @default.
• W2003669122 cites W2080165206 @default.
• W2003669122 cites W2084074153 @default.
• W2003669122 cites W2085600133 @default.
• W2003669122 cites W2090307028 @default.
• W2003669122 cites W2092067512 @default.
• W2003669122 cites W2094193490 @default.
• W2003669122 cites W2096242114 @default.
• W2003669122 cites W2105812200 @default.
• W2003669122 cites W2107731865 @default.
• W2003669122 cites W2107792698 @default.
• W2003669122 cites W2111609315 @default.
• W2003669122 cites W2113706105 @default.
• W2003669122 cites W2117265380 @default.
• W2003669122 cites W2117691369 @default.
• W2003669122 cites W2125245491 @default.
• W2003669122 cites W2135980864 @default.
• W2003669122 cites W2138713289 @default.
• W2003669122 cites W2142460886 @default.
• W2003669122 cites W2145320611 @default.
• W2003669122 cites W2146358096 @default.
• W2003669122 cites W2151379408 @default.
• W2003669122 cites W2157880621 @default.
• W2003669122 cites W2170428651 @default.
• W2003669122 cites W2171390260 @default.
• W2003669122 cites W2331287401 @default.
• W2003669122 doi "https://doi.org/10.1016/j.jaci.2009.04.032" @default.
• W2003669122 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19539983" @default.
• W2003669122 hasPublicationYear "2009" @default.
• W2003669122 type Work @default.
• W2003669122 sameAs 2003669122 @default.
• W2003669122 citedByCount "104" @default.
• W2003669122 countsByYear W20036691222012 @default.
• W2003669122 countsByYear W20036691222013 @default.
• W2003669122 countsByYear W20036691222014 @default.
• W2003669122 countsByYear W20036691222015 @default.
• W2003669122 countsByYear W20036691222016 @default.
• W2003669122 countsByYear W20036691222017 @default.
• W2003669122 countsByYear W20036691222018 @default.
• W2003669122 countsByYear W20036691222019 @default.
• W2003669122 countsByYear W20036691222020 @default.
• W2003669122 countsByYear W20036691222021 @default.
• W2003669122 countsByYear W20036691222022 @default.
• W2003669122 countsByYear W20036691222023 @default.
• W2003669122 crossrefType "journal-article" @default.
• W2003669122 hasAuthorship W2003669122A5007373159 @default.
• W2003669122 hasAuthorship W2003669122A5026139034 @default.
• W2003669122 hasAuthorship W2003669122A5026715859 @default.
• W2003669122 hasAuthorship W2003669122A5062951393 @default.
• W2003669122 hasAuthorship W2003669122A5064642801 @default.
• W2003669122 hasAuthorship W2003669122A5065733629 @default.
• W2003669122 hasAuthorship W2003669122A5066244090 @default.
• W2003669122 hasAuthorship W2003669122A5073019940 @default.
• W2003669122 hasAuthorship W2003669122A5078289429 @default.
• W2003669122 hasAuthorship W2003669122A5090527489 @default.
• W2003669122 hasBestOaLocation W20036691222 @default.
• W2003669122 hasConcept C126322002 @default.
• W2003669122 hasConcept C134018914 @default.
• W2003669122 hasConcept C14372207 @default.
• W2003669122 hasConcept C170493617 @default.
• W2003669122 hasConcept C194832188 @default.
• W2003669122 hasConcept C2776042228 @default.
• W2003669122 hasConcept C2780613262 @default.
• W2003669122 hasConcept C511355011 @default.
• W2003669122 hasConcept C71924100 @default.
• W2003669122 hasConceptScore W2003669122C126322002 @default.
• W2003669122 hasConceptScore W2003669122C134018914 @default.
• W2003669122 hasConceptScore W2003669122C14372207 @default.
• W2003669122 hasConceptScore W2003669122C170493617 @default.
• W2003669122 hasConceptScore W2003669122C194832188 @default.

• next