Vitamin D target proteins: Function and regulation

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Abstract
Recent findings have indicated that calbindin‐D28k, the first known target of vitamin D action, is present in osteoblasts and protects against TNF and glucocorticoid induced apoptosis of osteoblastic cells. Cytokine mediated destruction of pancreatic β cells, a cause of insulin dependent diabetes, is also inhibited by calbindin‐D28k. In calbindin‐D28k transfected pancreatic β cells free radical formation by cytokines is inhibited by calbindin. Thus, besides its role as a facilitator of calcium diffusion, calbindin has a major role in protecting against cellular degeneration in different cell types. Besides calbindin, the other known pronounced effect of 1,25(OH)2D3 in intestine and kidney is increased synthesis of 25(OH)D3 24‐hydroxylase (24(OH)ase) which is involved in the catabolism of 1,25(OH)2D3. We have noted that CCAAT enhancer binding protein β (C/EBPβ) is induced by 1,25(OH)2D3 in kidney and osteoblastic cells and can enhance the transcriptional response of 24(OH)ase to 1,25(OH)2D3. These studies establish C/EBPβ as a novel 1,25(OH)2D3 target gene and indicate a role for C/EBPβ in 24(OH)ase transcription. These studies extend our previous studies related to factors that affect vitamin D receptor (VDR) mediated 24(OH)ase transcription (YY1, TFIIB, CBP) and the effect of signaling pathways on 24(OH)ase transcription and cofactor recruitment. J. Cell. Biochem. 88: 238–244, 2003.
Funding Information
  • NIH(to S.C.) (DK38961)