Source:http://linkedlifedata.com/resource/pubmed/id/19739097
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2009-12-1
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pubmed:abstractText |
IL-13 is a central mediator of allergic inflammation and secreted by Th2 and bronchial smooth muscle cells (BSMC). However, little is known about the regulation of IL-13 secretion. To address it, a cDNA library of BSMC was screened for the proteins interacted with IL-13 by yeast two-hybridization. Besides IL-13 receptors, human sulfatase modifying factor 2 (SUMF2) was interacted with IL-13. Furthermore, SUMF2 and IL-13 were co-immunoprecipitated from BSMC, which was independent of IL-13 glycosylation. Interestingly, high levels of SUMF2 were expressed by BSMC, accompanied by significantly higher levels of intracellular IL-13, but lower levels of IL-13 secretion from BSMC. In contrast, little of SUMF2 was detected in lymphocytes, accompanied by lower levels of intracellular IL-13, but significantly higher levels of 12 kDa form of IL-13 secretion. Moreover, knockdown of SUMF2 expression by transfection with SUMF2-specific siRNA did not alter IL-13 mRNA transcription, but significantly reduced intracellular IL-13 levels, associated with increased levels of IL-13 secretion from BSMC. While induction of transient SUMF2 expression in lymphocytes failed to modulate IL-13 mRNA transcription. It significantly increased the contents of 12 kDa form of intracellular IL-13, accompanied by significantly reduced levels of IL-13 in their supernatants. In addition, blockage of N-glycosylation by treatment with tunicamycin eliminated 17 kDa form of intracellular IL-13, but failed to promote IL-13 secretion in BSMC. Collectively, our novel data clearly indicated that SUMF2 interacted with IL-13 and inhibited IL-13 secretion in BSMC and lymphocytes, which was independent of IL-13 glycosylation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1097-4644
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
108
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1076-83
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pubmed:meshHeading |
pubmed-meshheading:19739097-Bronchi,
pubmed-meshheading:19739097-Cells, Cultured,
pubmed-meshheading:19739097-Gene Knockdown Techniques,
pubmed-meshheading:19739097-Glycosylation,
pubmed-meshheading:19739097-Humans,
pubmed-meshheading:19739097-Inflammation,
pubmed-meshheading:19739097-Interleukin-13,
pubmed-meshheading:19739097-Lymphocytes,
pubmed-meshheading:19739097-Myocytes, Smooth Muscle,
pubmed-meshheading:19739097-Protein Binding,
pubmed-meshheading:19739097-Sulfatases
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pubmed:year |
2009
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pubmed:articleTitle |
SUMF2 interacts with interleukin-13 and inhibits interleukin-13 secretion in bronchial smooth muscle cells.
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pubmed:affiliation |
Department of Clinical Laboratory, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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