Proteomic analysis of tumor necrosis factor-alpha (TNF-α)-induced L6 myotube secretome reveals novel TNF-α-dependent myokines in diabetic skeletal muscle

J Proteome Res. 2011 Dec 2;10(12):5315-25. doi: 10.1021/pr200573b. Epub 2011 Nov 11.

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-α)-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-α 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-α treatment. Using microarray analysis of Zuker diabetic rat skeletal muscle combined with bioinformatics and Q-PCR, we found a correlation between TNF-α-mediated insulin resistance and type 2 diabetes. This novel approach combining analysis of the conditioned secretome and transcriptome has identified several previously unknown, TNF-α-dependent secretory proteins, which establish a foothold for research on the different causes of insulin resistance and their relationships with each other.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Cells, Cultured
  • Computational Biology
  • Culture Media, Conditioned
  • Cytokines / analysis
  • Cytokines / metabolism*
  • Databases, Protein
  • Diabetes Mellitus, Type 2 / metabolism
  • Gene Expression Profiling / methods
  • Glucose Transporter Type 4 / metabolism
  • Insulin / pharmacology
  • Insulin Resistance
  • Male
  • Mass Spectrometry / methods
  • Muscle Fibers, Skeletal / drug effects*
  • Muscle Fibers, Skeletal / metabolism
  • Muscle Fibers, Skeletal / pathology
  • Muscle Proteins / analysis
  • Muscle Proteins / metabolism*
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / metabolism*
  • Muscle, Skeletal / pathology
  • Proteomics / methods*
  • Rats
  • Real-Time Polymerase Chain Reaction
  • Transcriptome
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Culture Media, Conditioned
  • Cytokines
  • Glucose Transporter Type 4
  • Insulin
  • Muscle Proteins
  • Slc2a4 protein, rat
  • Tumor Necrosis Factor-alpha