In vivo effects of vitamin D on the proliferation and differentiation of rat keratinocytes

Abstract

The hormonal form of vitamin D appears to be a physiological regulator of the epidermogenesis. While its differentiation-promoting effect is well accepted, there are conflicting reports of its action on keratinocyte proliferation. This study evaluates the specific changes induced by vitamin D treatment in the epidermis of rats nutritionally deprived of vitamin D by cell size analysis, acridine orange flowcytometry, and the immunohistochemical detection of proteins related to the different stages of differentiation (epidermal calcium binding protein and suprabasal keratins recognized by KL1 antibody) The total keratinocyte and isolated keratinocyte subpopulations were studied. Vitamin D deficiency was associated in the total population with a lower percentage of actively proliferating cells and with a lack of differentiation markers. Study of the isolated cell populations demonstrated, however, that small cells were actively proliferating, whereas they were mainly in the resting stage in the normal epidermis. Treatment with vitamin D dramatically increased cell proliferation and stimulated the appearance of differentiation markers. Some of the observed effects, such as an increase in proliferation and the appearance of epidermal calcium binding protein, were due to the normalisation of the vitamin D deficiency-induced hypocalcemia, whereas the expression of suprabasal keratins was directly dependent on vitamin D. We conclude that the action of vitamin D on the epidermis is associated with increases in both proliferation and differentiation of keratinocytes. Vitamin D itself and its resulting action on calcium homeostasis appear to contribute to the observed effects.

Smads mediate signaling of the TGFβ superfamily in normal keratinocytes but are lost during skin chemical carcinogenesis

“…In addition, Smads may aect epidermal dierentiation via TGFb-independent pathways. Potential candidates for these TGFb-independent genes include calmodulin, NF-kB, and the vitamin D receptor, all of which have been shown to play an important role in epidermal dierentiation (Bikle and Pillai, 1988;Hu et al, 1999;Li et al, 1999;Ma et al, 1997;Roop et al, 1987;Rougui et al, 1996;Takeda et al, 1999), and to interact directly with Smads (Kon et al, 1999;Yanagisawa et al, 1999;Zimmerman et al, 1998). Therefore, it will be worthwhile to further determine the exact role of Smads in epidermal dierentiation in the future.…”

Vitamins and photoaging: Do scientific data support their use?

“…Vitamin D has become a standard treatment in psoriasis for its ability to inhibit epidermal keratinocyte hyperproliferation. [122][123][124] The critical contribution of vitamin D to the skin's innate immune system through the induction of the antimicrobial peptide cathelicidin was also recently elucidated. 113 As a steroid hormone, vitamin D exerts its effects by activating the nuclear vitamin D receptor.…”

Ergocalciferol promotes in vivo differentiation of keratinocytes and reduces photodamage caused by ultraviolet irradiation in hairless mice

“…T he active form of vitamin D is known as a physiological regulator of the differentiation and proliferation of skin cells including keratinocytes, fibroblasts, and adipocytes (1)(2)(3)(4)(5). In particular, active vitamin D 3 and its analogues have been reported to be effective in patients with skin diseases associated with abnormal proliferation of keratinocytes such as psoriasis (6,7).…”