Ultraviolet B irradiation reduces the expression of adiponectin in ovarial adipose tissues through endocrine actions of calcitonin gene-related peptide-induced serum amyloid A

PLoS One. 2014 May 20;9(5):e98040. doi: 10.1371/journal.pone.0098040. eCollection 2014.

Abstract

Ultraviolet (UV) B irradiation decreases blood adiponectin levels, but the mechanism is not well understood. This study investigated how UVB irradiation reduces adiponectin expression in ovarial adipose tissues. Female Hos:HR-1 hairless mice were exposed to UVB (1.6 J/cm(2)) irradiation and were killed 24 h later. UVB irradiation decreased the adiponectin protein level in the serum and the adiponectin mRNA level in ovarial adipose tissues. UVB irradiation also decreased the mRNA levels of peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer binding protein (C/EBP) α, C/EBPβ, and fatty acid binding protein 4 (aP2) in ovarial adipose tissues. In contrast, UVB irradiation increased the mRNA levels of interleukin (IL)-6 and monocyte chemoattractant protein (MCP)-1 in ovarial adipose tissues. In the serum and liver, the levels of serum amyloid A (SAA), involved in PPARγ, C/EBPα, C/EBPβ, aP2, IL-6, and MCP-1 regulation, increased after UVB irradiation. The SAA gene is regulated by IL-1β, IL-6, and tumor necrosis factor-α, but only IL-6 expression increased in the liver after UVB irradiation. Additionally, in the liver, hypothalamus, and epidermis, UVB irradiation increased the expression of calcitonin gene-related peptide (CGRP), which upregulates SAA in the liver. Collectively, our results suggest that the CGRP signal induced by skin exposure to UVB transfers to the liver, possibly through the brain, and increases SAA production via IL-6 in the liver. In turn, serum SAA acts in an endocrine manner to decreases the serum adiponectin level by downregulating factors that regulate adiponectin expression in adipose tissues.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin / blood
  • Adiponectin / genetics*
  • Adiponectin / metabolism
  • Adipose Tissue / metabolism*
  • Adipose Tissue / radiation effects*
  • Animals
  • CCAAT-Enhancer-Binding Protein-alpha / genetics
  • CCAAT-Enhancer-Binding Protein-alpha / metabolism
  • CCAAT-Enhancer-Binding Protein-beta / genetics
  • CCAAT-Enhancer-Binding Protein-beta / metabolism
  • Calcitonin Gene-Related Peptide / blood
  • Calcitonin Gene-Related Peptide / metabolism*
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Fatty Acid-Binding Proteins / genetics
  • Fatty Acid-Binding Proteins / metabolism
  • Female
  • Gene Expression Regulation / radiation effects*
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Liver / metabolism
  • Mice
  • Organ Specificity / genetics
  • Ovary / metabolism*
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Serum Amyloid A Protein / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism
  • Ultraviolet Rays*

Substances

  • Adiponectin
  • CCAAT-Enhancer-Binding Protein-alpha
  • CCAAT-Enhancer-Binding Protein-beta
  • Chemokine CCL2
  • Fabp4 protein, mouse
  • Fatty Acid-Binding Proteins
  • Interleukin-1beta
  • Interleukin-6
  • PPAR gamma
  • Serum Amyloid A Protein
  • Tumor Necrosis Factor-alpha
  • Calcitonin Gene-Related Peptide

Grant support

This work was supported by JSPS KAKENHI (grant numbers 24580199). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.