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Endothelin-1 stimulates resistin gene expression.

Ya-Chu Tang1, Chi-Wei Liu, Hsin-Huei Chang

  • 1Department of Life Sciences (Y.-C.T., C.-W.L., H.-H.C., Y.-H.K.), National Central University, Jhongli, Taoyuan 32001, Taiwan; Department and Institute of Physiology (C.-C.J.), National Yang Ming University, Taipei 11221, Taiwan; Division of Gastroenterology (Y.-C.K.), Department of Internal Medicine, Taiwan Landseed Hospital, Taoyuan 32449, Taiwan; and Department of Emergency (C.-C.K., Y.-M.H.), Armed Forces Taoyuan General Hospital, Taoyuan 32551, Taiwan.

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Summary

Endothelin-1 (ET-1) upregulates resistin gene expression via the ET type-A receptor, activating ERK1/2, JNKs, AKT, and JAK2/STAT3 pathways in adipocytes. This study elucidates the signaling cascade linking ET-1 to resistin production.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Signaling

Background:

  • Resistin and endothelin-1 (ET-1) are implicated in adipocyte function and insulin resistance.
  • The precise signaling mechanism by which ET-1 influences resistin gene expression remains unclear.

Purpose of the Study:

  • To investigate the signaling pathways mediating ET-1-stimulated resistin gene expression in 3T3-L1 adipocytes.
  • To identify key molecular players involved in the ET-1-resistin axis.

Main Methods:

  • 3T3-L1 adipocytes were treated with ET-1 and various receptor antagonists and kinase inhibitors.
  • Resistin mRNA levels were quantified using quantitative real-time PCR.
  • Protein phosphorylation of downstream signaling molecules (ERK1/2, JNKs, AKT, STAT3) was assessed via Western blotting.
  • In vivo studies examined resistin mRNA and protein levels in adipose tissue.

Main Results:

  • ET-1 dose-dependently and time-dependently increased resistin mRNA levels, requiring new mRNA synthesis.
  • The ET type-A receptor antagonist BQ610, but not the ET type-B receptor antagonist BQ788, blocked ET-1-induced resistin mRNA expression and downstream signaling.
  • Inhibitors of ERK1/2, JNKs, AKT, and JAK2/STAT3 pathways abrogated ET-1-stimulated resistin mRNA levels and phosphorylation.
  • p38 kinase inhibition did not affect ET-1's action on resistin expression.

Conclusions:

  • ET-1 stimulates resistin gene expression through the ET type-A receptor.
  • The signaling cascade involves ERK1/2, JNKs, AKT, and JAK2/STAT3 pathways.
  • These findings provide crucial insights into the molecular regulation of resistin by ET-1 in adipose tissue.