ChloroquineV1, Main, Exploration, bibRecord, 000952

Clinical and genetic spectrum of interstitial lung disease in Chinese children associated with surfactant protein C mutations

Identifieur interne : 000952 ( Main/Exploration ); précédent : 000951; suivant : 000953

Clinical and genetic spectrum of interstitial lung disease in Chinese children associated with surfactant protein C mutations

Auteurs : Da Hong [République populaire de Chine] ; Dan Dai [République populaire de Chine] ; Jing Liu [République populaire de Chine] ; Congcong Zhang [République populaire de Chine] ; Tingting Jin [République populaire de Chine] ; Yanyan Shi [République populaire de Chine] ; Gaoli Jiang [République populaire de Chine] ; Mei Mei [République populaire de Chine] ; Libo Wang [République populaire de Chine] ; Liling Qian [République populaire de Chine]

Source :

Italian Journal of Pediatrics [ 1824-7288 ] ; 2019.

RBID : PMC:6714457

Abstract

Background

Mutations in the surfactant protein C gene (SFTPC) result in interstitial lung disease (ILD). Our objective was to characterize clinical and genetic spectrum of ILD in Chinese children associated with SFTPC mutations.

Methods

Six Chinese children with ILD heterozygous for SFTPC mutations were included. Candidate genes responsible for surfactant dysfunction were sequenced by next-generation sequencing. Subclones of SFTPC with novel mutations were generated and transiently transfected into A549 cells. The functional characterization of mutant surfactant protein C (SP-C) was evaluated by Western blotting and immunofluorescence.

Results

The age of onset ranged from 7 days to 15 months. All cases required supplemental oxygen. Failure to thrive (5/6) was the most significant extra-pulmonary manifestation. Hydroxychloroquine was given as the long-term treatment of lung disease in four patients and two of them responded well. Three mutations were identified in six patients: four with I73T, one with D105G, one with Y113H. Mutations in three patients were inherited and three arised de novo. Western blotting revealed totally different band patterns between mutant SP-C (D105G and Y113H) and the wildtype. Immunofluorescence showed mutant SP-C (D105G) was scarcely trafficked to lamellar bodies but localized well to early endosomes, which was in marked contrast to the wildtype protein.

Conclusion

SFTPC mutations were an important cause of childhood ILD in Chinese population. I73T was a common SFTPC mutation in Chinese ILD children associated with surfactant protein C mutations.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6714457

DOI: 10.1186/s13052-019-0710-2
PubMed: 31462320
PubMed Central: 6714457

Affiliations:

République populaire de Chine

Le document en format XML

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<author><name sortKey="Jin, Tingting" sort="Jin, Tingting" uniqKey="Jin T" first="Tingting" last="Jin">Tingting Jin</name>
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<author><name sortKey="Shi, Yanyan" sort="Shi, Yanyan" uniqKey="Shi Y" first="Yanyan" last="Shi">Yanyan Shi</name>
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<author><name sortKey="Jiang, Gaoli" sort="Jiang, Gaoli" uniqKey="Jiang G" first="Gaoli" last="Jiang">Gaoli Jiang</name>
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<author><name sortKey="Wang, Libo" sort="Wang, Libo" uniqKey="Wang L" first="Libo" last="Wang">Libo Wang</name>
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<author><name sortKey="Qian, Liling" sort="Qian, Liling" uniqKey="Qian L" first="Liling" last="Qian">Liling Qian</name>
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<series><title level="j">Italian Journal of Pediatrics</title>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p id="Par1">Mutations in the surfactant protein C gene (<italic>SFTPC</italic>
) result in interstitial lung disease (ILD). Our objective was to characterize clinical and genetic spectrum of ILD in Chinese children associated with <italic>SFTPC</italic>
 mutations.</p>
</sec>
<sec><title>Methods</title>
<p id="Par2">Six Chinese children with ILD heterozygous for <italic>SFTPC</italic>
 mutations were included. Candidate genes responsible for surfactant dysfunction were sequenced by next-generation sequencing. Subclones of <italic>SFTPC</italic>
 with novel mutations were generated and transiently transfected into A549 cells. The functional characterization of mutant surfactant protein C (SP-C) was evaluated by Western blotting and immunofluorescence.</p>
</sec>
<sec><title>Results</title>
<p id="Par3">The age of onset ranged from 7 days to 15 months. All cases required supplemental oxygen. Failure to thrive (5/6) was the most significant extra-pulmonary manifestation. Hydroxychloroquine was given as the long-term treatment of lung disease in four patients and two of them responded well. Three mutations were identified in six patients: four with I73T, one with D105G, one with Y113H. Mutations in three patients were inherited and three arised de novo. Western blotting revealed totally different band patterns between mutant SP-C (D105G and Y113H) and the wildtype. Immunofluorescence showed mutant SP-C (D105G) was scarcely trafficked to lamellar bodies but localized well to early endosomes, which was in marked contrast to the wildtype protein.</p>
</sec>
<sec><title>Conclusion</title>
<p id="Par4"><italic>SFTPC</italic>
 mutations were an important cause of childhood ILD in Chinese population. I73T was a common <italic>SFTPC</italic>
 mutation in Chinese ILD children associated with surfactant protein C mutations.</p>
</sec>
</div>
</front>
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</author>
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<author><name sortKey="Lane, K" uniqKey="Lane K">K Lane</name>
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Serveur d'exploration Chloroquine

Clinical and genetic spectrum of interstitial lung disease in Chinese children associated with surfactant protein C mutations

Clinical and genetic spectrum of interstitial lung disease in Chinese children associated with surfactant protein C mutations

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