JAK and STAT members of yellow catfish Pelteobagrus fulvidraco and their roles in leptin affecting lipid metabolism

Gen Comp Endocrinol. 2016 Jan 15:226:14-26. doi: 10.1016/j.ygcen.2015.12.014. Epub 2015 Dec 15.

Abstract

The present study clones and characterizes the full-length cDNA sequences of members in JAK-STAT pathway, explores their mRNA tissue expression and the biological role in leptin influencing lipid metabolism in yellow catfish Pelteobagrus fulvidraco. Full-length cDNA sequences of five JAKs and seven STAT members, including some splicing variants, were obtained from yellow catfish. Compared to mammals, more members of the JAKs and STATs family were found in yellow catfish, which provided evidence that the JAK and STAT family members had arisen by the whole genome duplications during vertebrate evolution. All of these members were widely expressed across the eleven tissues (liver, white muscle, spleen, brain, gill, mesenteric fat, anterior intestine, heart, mid-kidney, testis and ovary) but at the variable levels. Intraperitoneal injection in vivo and incubation in vitro of recombinant human leptin changed triglyceride content and mRNA expression of several JAKs and STATs members, and genes involved in lipid metabolism. AG490, a specific inhibitor of JAK2-STAT pathway, partially reversed leptin-induced effects, indicating that the JAK2a/b-STAT3 pathway exerts main regulating actions of leptin on lipid metabolism at transcriptional level. Meanwhile, the different splicing variants were differentially regulated by leptin incubation. Thus, our data suggest that leptin activated the JAK/STAT pathway and increases the expression of target genes, which partially accounts for the leptin-induced changes in lipid metabolism in yellow catfish.

Keywords: JAK–STAT pathway; Leptin; Lipid metabolism; Pelteobagrus fulvidraco.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Catfishes / genetics
  • Catfishes / metabolism*
  • Janus Kinases / genetics
  • Janus Kinases / metabolism*
  • Leptin / pharmacology*
  • Lipid Metabolism / drug effects*
  • Lipid Metabolism / physiology
  • Liver / metabolism*
  • Phosphorylation / drug effects
  • STAT Transcription Factors / genetics
  • STAT Transcription Factors / metabolism*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Triglycerides / metabolism

Substances

  • Leptin
  • STAT Transcription Factors
  • Triglycerides
  • Janus Kinases