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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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CXCL3 positively regulates adipogenic differentiation.

Joji Kusuyama1, Anna Komorizono1, Kenjiro Bandow2

  • 1Department of Oral Biochemistry, Field of Developmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.

Journal of Lipid Research
|August 12, 2016
PubMed
Summary

Chemokine ligand 3 (CXCL3) promotes adipogenesis, the development of fat cells. This study identifies CXCL3 as a novel adipokine that enhances fat cell differentiation via ERK and JNK signaling pathways.

Keywords:
C-X-C motif chemokine ligand 3adipocyteschemokinecytokinesinflammationperoxisome proliferator-activated receptorsprotein kinases/mitogen-activated protein kinase

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Area of Science:

  • Cell Biology
  • Endocrinology
  • Molecular Biology

Background:

  • Chemokines are cytokines that regulate cell migration and inflammation.
  • Emerging evidence suggests chemokines play roles in cell differentiation.
  • The specific functions of chemokines in adipocytes remain largely unexplored.

Purpose of the Study:

  • To investigate the expression of chemokines and their receptors during adipogenic differentiation.
  • To elucidate the role of specific chemokines, particularly CXCL3, in the process of adipogenesis.
  • To identify the signaling pathways and molecular mechanisms by which CXCL3 influences adipocyte development.

Main Methods:

  • Gene expression analysis of chemokines and receptors in adipocytes.
  • Stimulation of adipogenic differentiation in cell lines (3T3-L1, ST2) with CXCL3 and CXCL13.
  • Gene knockdown studies using siRNA targeting CXCL3 and its receptor CXCR2.
  • Western blot analysis to assess protein phosphorylation (ERK, JNK).
  • Chromatin immunoprecipitation (ChIP) assay to determine transcription factor binding.

Main Results:

  • CXCL3 and its receptor CXCR2 were highly expressed in mature adipocytes.
  • CXCL3 significantly promoted adipogenic differentiation, indicated by increased lipid droplet accumulation and adipogenic marker expression.
  • Knockdown of CXCL3 or CXCR2 inhibited adipogenesis.
  • CXCL3 induced ERK and JNK phosphorylation, and this effect was blocked by specific inhibitors.
  • CXCL3-induced expression of C/EBPβ and C/EBPδ was dependent on ERK and JNK signaling.
  • PPARγ2 was found to bind to the cxcl3 promoter region.

Conclusions:

  • CXCL3 is identified as a novel adipokine that enhances adipogenesis.
  • CXCL3 acts through autocrine and/or paracrine mechanisms to promote fat cell differentiation.
  • The signaling pathway involves CXCL3-induced activation of ERK and JNK, leading to the upregulation of C/EBPβ and C/EBPδ.
  • PPARγ2 plays a role in regulating CXCL3 expression during adipogenesis.