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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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Proteomic Analysis of Tumor Necrosis Factor-Alpha (TNF-alpha)-Induced L6 Myotube Secretome Reveals Novel TNF-alpha-Dependent Myokines in Diabetic Skeletal Muscle

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Title
Proteomic Analysis of Tumor Necrosis Factor-Alpha (TNF-alpha)-Induced L6 Myotube Secretome Reveals Novel TNF-alpha-Dependent Myokines in Diabetic Skeletal Muscle
Author
Yoon, Jong HyukSong, ParkyongJang, Jin-HyeokKim, Dae-KyumChoi, SunkyuKim, JaeyoonGhim, JaewangKim, DayeaPark, SehoonLee, HyeongjiKwak, DongohYea, KyungmooHwang, DaeheeSuh, Pann-GhillRyu, Sung Ho
Issue Date
2011-12
Publisher
AMER CHEMICAL SOC
Citation
JOURNAL OF PROTEOME RESEARCH, v.10, no.12, pp.5315 - 5325
Abstract
There is a strong possibility that skeletal muscle can respond to irregular metabolic states by secreting specific cytokines. Obesity-related chronic inflammation, mediated by pro-inflammatory cytokines, is believed to be one of the causes of insulin resistance that results in type 2 diabetes. Here, we attempted to identify and characterize the members of the skeletal muscle secretome in response to tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance. To conduct this study, we comparatively analyzed the media levels of proteins released from L6 skeletal muscle cells. We found 28 TNF-a modulated secretory proteins by using separate filtering methods: Gene Ontology, SignalP, and SecretomeP, as well as the normalized Spectral Index for label-free quantification. Ten of these secretory proteins were increased and 18 secretory proteins were decreased by TNF-a treatment. Using microarray analysis of Zuker diabetic rat skeletal muscle combined with bioinformatics and QPCR, we found a correlation between TNF-alpha-mediated insulin resistance and type 2 diabetes. This novel approach combining analysis of the conditioned secretome and transcriptome has identified several previously unknown, TNF-alpha-dependent secretory proteins, which establish a foothold for research on the different causes of insulin resistance and their relationships with each other.
URI
https://scholarworks.unist.ac.kr/handle/201301/10093
URL
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=82755184961
DOI
10.1021/pr200573b
ISSN
1535-3893
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BIO_Journal Papers
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