Effects of vitamin D3 on the expression of growth-related oncogene-α in THP-1 cells and human primary monocytes

J Food Sci. 2012 Feb;77(2):H47-52. doi: 10.1111/j.1750-3841.2011.02532.x. Epub 2012 Jan 17.


Asthma and many autoimmune diseases, such as systemic lupus erythematosus, have been reported to associate with vitamin D deficiency recently. Growth-related oncogene-α (GRO-α)/CXCL1, a neutrophil-related chemokine, have an important influence on the chronic inflammation of these diseases. It is unknown whether vitamin D has regulatory effects on GRO-α expression in human monocytes. To this end, the human monocytic leukemia cell line, THP-1, and human primary monocytes were pretreated with 1α, 25-(OH)(2)D(3), and was stimulated with lipopolysaccharide (LPS). Supernatants were collected to determine GRO-α level by ELISA. The intracellular signaling was investigated by nuclear factor (NF)-κB inhibitor, the mitogen-activated protein kinase (MAPK) inhibitors, and Western blot. In our studies, LPS-induced GRO-α was significantly enhanced in THP-1 cells, but suppressed in human primary monocytes by 1α, 25-(OH)(2)D(3). Western blotting revealed that 1α, 25-(OH)(2)D(3) increased LPS-stimulated pp38 expression in THP-1 cells, but suppressed LPS-stimulated pMEK1/2-pERK and pJNK in human primary monocytes. In conclusion, the opposite effects of 1α, 25-(OH)(2)D(3) on GRO-α expression in THP-1 cells and human primary monocytes indicated that the data from THP-1 cells should be further confirmed by human primary monocytes. Moreover, vitamin D3 may have potentiality in treating GRO-α-related chronic inflammatory diseases, like asthma and autoimmune diseases.

MeSH terms

  • Blotting, Western
  • Cell Line, Tumor
  • Chemokine CXCL1 / genetics*
  • Chemokine CXCL1 / metabolism
  • Cholecalciferol / pharmacology*
  • Humans
  • I-kappa B Proteins / genetics
  • I-kappa B Proteins / metabolism
  • Lipopolysaccharides / metabolism
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinases / genetics
  • Mitogen-Activated Protein Kinases / metabolism
  • Monocytes / drug effects*
  • Monocytes / metabolism
  • NF-KappaB Inhibitor alpha
  • Signal Transduction


  • CXCL1 protein, human
  • Chemokine CXCL1
  • I-kappa B Proteins
  • Lipopolysaccharides
  • NFKBIA protein, human
  • NF-KappaB Inhibitor alpha
  • Cholecalciferol
  • Mitogen-Activated Protein Kinases