Vitamin D and calcium play major roles in our bone health in addition to roles in tissues and cells. These roles in tissues and cells are associated with some cancers. The purpose of this study was to determine attitudes of cancer patients towards their dietary intakes of vitamin D and calcium. A questionnaire was completed by 128 volunteers (mean age=53.5 years±16.6, 94 women, 34 men) from the Montgomery Cancer Clinic in Montgomery, Alabama. Cancer-reporting participants (n=59) were likely to agree more (p=0.048) to the statement, “I try to eat healthy every day” compared to non-cancer reporting participants (n=69) on a 5-point Likert scale; similar results occurred for the statement, “I have a healthy diet” (p=0.050). Participants without cancer consumed more fish (salmon, tuna, halibut, etc.) than cancer-reporting participants (p=.035). Women and cancer-reporting participants were more concerned with eating healthy and obtaining vitamin D and calcium than non-cancer participants and men.

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Die Arbeit stellt mögliche Einflüsse durch 1,25- Dihydroxy-Vitamin D3 (1,25-VitD3) und Retinsäure (RA) in humanen mesenchymalen Stammzellen (hMSC) sowohl während der adipogenen und osteogenen Differenzierung als auch während der Kurzzeit- und Langzeitstimulation auf das Mikromilieu dar. Die Stimulation mit 1,25-VitD3 und RA verlangsamt das Wachstumsverhalten und verändert die Zellmorphologie von hMSC. Effekte auf die Genexpression werden auf mRNA-Ebene mittels RT-PCR dargestellt. Der Phänotyp als auch teilweise die Genexpression der osteogenen und adipogenen Differenzierung wird durch 1,25-VitD3 induziert und durch RA inhibiert. Zudem wird sowohl die „Mikromilieu-Zusammensetzung“ als auch das „Transkriptionssignal“ von 1,25-VitD3 und RA gegenseitig beeinflusst. / The paper reports about possible effects of 1,25-dihydroxy-vitamin D3 (1,25-VitD3) und retinoic acid (RA) in human mesenchymal stem cells (hMSC) during adipogenic and osteogenic differentiation as well as effects on the microenvironment during a short and long time stimulation. Stimulation with 1,25-VitD3 and RA slows down the growth rate and alters cell morphology of hMSC. Effects on gene expression are shown at the mRNA level by means of RT-PCR. The phenotype and partly the gene expression of adipogenic and osteogenic differentiation are stimulated by 1,25-VitD3 and are inhibited by RA. In addition, both the “microenvironment composition” and the “transcription signal” of 1,25-VitD3 and RA are mutually influenced.

In humans, the epidermis is the main site for the synthesis of Vitamin D3 (cholecalciferol) from 7-dehydrocholesterol. Cholecalciferol undergoes further hydroxylation in the liver and kidney to produce the active form of the circulating hormone 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3). In target cells, 1,25(OH)2D3 interacts with the specific intracellular vitamin D receptor (VDR), a member of the nuclear receptor superfamily. However, epidermal keratinocytes, in addition to being target cells, have enzymes required for autocrine production of 1,25(OH)2D3. They can convert cholecalciferol to 1,25(OH)2D3 via 25-hydroxylase (CYP2R1) and 1α-hydroxylase (CYP27B1). Another enzyme, 24-hydroxylase (CYP24A1), regulates local levels by inactivating 1,25(OH)2D3. While recent studies have shown that absence of VDR or 1,25(OH)2D3 impairs formation of granulation tissue during wound healing in mice, little is known about the autocrine and paracrine regulation of biologically active vitamin D3 by human dermal fibroblasts during cutaneous wound healing. Primary cultures of human keratinocytes and fibroblasts expressed VDR and all the cytochrome enzymes necessary for autocrine production of vitamin D. The relative expression of VDR mRNA was higher in dermal fibroblasts than donor-matched keratinocytes. In contrast, epidermal keratinocytes had a higher mRNA expression of vitamin D3 metabolising enzymes. A scratch wound assay confirmed that 1,25(OH)2D3 stimulated keratinocyte migration, but paradoxically inhibited fibroblast migration as early as 4h, yet neither cholecalciferol nor 25-hydroxyvitamin D3 had any effect. VDR knockdown using small interfering RNA (siRNA) abolished the inhibitory effect of 1,25(OH)2D3 on fibroblast migration, demonstrating the requirement for the VDR in this response. Immunofluorescent staining revealed that 1,25(OH)2D3 increased nuclear VDR protein expression, without a corresponding increase in VDR mRNA transcription only in mechanically wounded dermal fibroblasts, indicating activation of the receptors. Incubation with either 1,25(OH)2D3, cholecalciferol or 25(OH)D3 up-regulated CYP24A1 transcription. This response was most pronounced with 1,25(OH)2D3, suggesting a tightly regulated feedback control on 1,25(OH)2D3 bioavailability within the dermis. In addition, cholecalciferol also increased CYP2R1 and CYP27B1 mRNA expression in scratched dermal fibroblasts, providing evidence for autocrine regulation of 1,25(OH)2D3 by dermal fibroblasts. Expression of α-SMA protein was up-regulated in cultured dermal fibroblasts following scratching, which was down-regulated in the presence of 1,25(OH)2D3. These observations suggest that 1,25(OH)2D3 may restrict differentiation of wounded dermal fibroblasts into pro-fibrotic myofibroblasts. 1,25(OH)2D3 also down-regulated MMP-2 secretion and collagen type I to III ratio in scratched dermal fibroblasts. Using a human ex vivo wound healing model, it was demonstrated that 1,25(OH)2D3, but not cholecalciferol, stimulated the rate of wound closure. In summary, this study has confirmed that human dermal fibroblasts express the transcriptional machinery for autocrine production of 1,25(OH)2D3, and a higher VDR expression suggests they are more responsive than keratinocytes. Changes in CYP and VDR expression in the presence of cholecalciferol, 25-hydroxyvitamin D3 or 1,25(OH)2D3 indicate fine-tuning of the bioavailability of vitamin D in the dermis after wounding. Down-regulation of α-SMA, MMP-2 secretion and the collagen type I to III ratio by 1,25(OH)2D3 highlight an important role for 1,25(OH)2D3 in modulating wound healing and the scarring process.

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