Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2012
Clara cell protein expression in human neonates during respiratory distress syndrome.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Arias-Martínez Joel, Palacios-Sánchez Miguel, Delgado-Franco Dagoberto, Guzmán-Bárcenas José, García-Latorre Ethel, Zhang Limei, Irles Claudine
Аннотация
BACKGROUND/AIMS: Clara cell protein (cc-10) has been shown to negatively regulate inflammation, protect pulmonary surfactant from degradation in the lung, and administration of this recombinant protein improves the condition of infant respiratory distress syndrome (iRDS), a disease that occurred mainly in preterm infants. In view of the possibility that altered expression of cc-10 might regulate its protective function, we attempted to characterize this protein in infants with iRDS.
METHODS: Using bronchotraqueal aspirates from human infants, we analyzed cc-10 in two-dimensional gel electrophoresis (2-DE) by combining immunoprecipitation, carbonyl groups and total protein immunoblotting.
RESULTS: Seven forms of cc-10 were detected with western immunoblots in infants with iRDS while only four forms were present in neonates who needed mechanical ventilation for other reasons without any lung disease (control group). The overall levels of cc-10 in iRDS were lower and differences were seen in isoform pattern and distribution.
CONCLUSION: Our demonstration that cc-10 is differentially expressed in infants with iRDS may point the way towards one possible mechanism that potentially involves modifications of the protein structure with its anti-inflammatory and surfactant protective function and could be detrimental for this airway disorder.
METHODS: Using bronchotraqueal aspirates from human infants, we analyzed cc-10 in two-dimensional gel electrophoresis (2-DE) by combining immunoprecipitation, carbonyl groups and total protein immunoblotting.
RESULTS: Seven forms of cc-10 were detected with western immunoblots in infants with iRDS while only four forms were present in neonates who needed mechanical ventilation for other reasons without any lung disease (control group). The overall levels of cc-10 in iRDS were lower and differences were seen in isoform pattern and distribution.
CONCLUSION: Our demonstration that cc-10 is differentially expressed in infants with iRDS may point the way towards one possible mechanism that potentially involves modifications of the protein structure with its anti-inflammatory and surfactant protective function and could be detrimental for this airway disorder.