This record provides bibliographic details and links to the original research. An editorial study breakdown is not available.
What the researchers found
1α,25-dihydroxyvitamin D3 (1,25D3) significantly upregulates the CAMP gene and LL-37 protein expression in human keratinocytes, and this effect requires retinoid X receptor alpha (RXRα) but is independent of vitamin D receptor (VDR) upregulation.
Why it matters
Understanding how vitamin D regulates antimicrobial peptides via RXRα can inform new strategies to boost skin immunity and develop treatments for infections or skin disorders.
How the study worked
The study analyzed gene and protein expression in human skin and gingival biopsies and in cultured human keratinocyte (HaCaT) cells treated with 1,25D3. RXRα involvement was tested using short interfering RNA to knock down RXRα expression.
What this study cannot tell us
The study was conducted primarily in cell cultures and tissue biopsies, which may not fully replicate in vivo skin conditions; the exact signaling pathways downstream of RXRα were not fully elucidated.
Read the original research
Vitamin D-induced up-regulation of human keratinocyte cathelicidin anti-microbial peptide expression involves retinoid X receptor α.
Cell and tissue research, 366(2), 353-362
Citation
Svensson, Daniel; Nebel, Daniel; Voss, Ulrikke; Ekblad, Eva; Nilsson, Bengt-Olof. (2016). Vitamin D-induced up-regulation of human keratinocyte cathelicidin anti-microbial peptide expression involves retinoid X receptor α.. Cell and tissue research, 366(2), 353-362. https://doi.org/10.1007/s00441-016-2449-z