Prof. Grant J. Anhalt

隆, 橋本

doi:10.2336/nishinihonhifu.62.403

Cited by 2 publications

(2 citation statements)

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“…Instead of enhancing the proliferative rate of primary keratinocytes, purified forskolin consistently inhibited keratinocyte thymidine incorporation (Fig. 3a), unlike the positive control epidermal growth factor (EGF) (37). Thus, we concluded that cAMP stimulation does not directly increase the proliferation of purified primary murine keratinocytes.…”

Section: Resultsmentioning

confidence: 75%

Pigment‐independent cAMP‐mediated epidermal thickening protects against cutaneous UV injury by keratinocyte proliferation

Scott

Christian

Kesler

et al. 2012

Experimental Dermatology

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The epidermis increases pigmentation and epidermal thickness in response to ultraviolet exposure to protect against UV-associated carcinogenesis; however, the contribution of epidermal thickness has been debated. In a humanized skin mouse model that maintains interfollicular epidermal melanocytes, we found that forskolin, a small molecule that directly activates adenylyl cyclase and promotes cAMP generation, up-regulated epidermal eumelanin accumulation in fair-skinned melanocortin-1-receptor (Mc1r)-defective animals. Forskolin-induced pigmentation was associated with a reproducible expansion of epidermal thickness irrespective of melanization or the presence of epidermal melanocytes. Rather, forskolin-enhanced epidermal thickening was mediated through increased keratinocyte proliferation, indirectly through secreted factor(s) from cutaneous fibroblasts. We identified keratinocyte growth factor (Kgf) as a forskolin-induced fibroblast-derived cytokine that promoted keratinocyte proliferation, as forskolin induced Kgf expression both in the skin and in primary fibroblasts. Lastly, we found that even in the absence of pigmentation, forskolin-induced epidermal thickening significantly diminished the amount of UVA and UVB that passed through whole skin and reduced the amount of UVB-associated epidermal sunburn cells. These findings suggest the possibility of pharmacologic-induced epidermal thickening as a novel UV-protective therapeutic intervention, particularly for individuals with defects in pigmentation and adaptive melanization.

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Section: Resultsmentioning

confidence: 75%

Pigment‐independent cAMP‐mediated epidermal thickening protects against cutaneous UV injury by keratinocyte proliferation

Scott

Christian

Kesler

et al. 2012

Experimental Dermatology

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“…EPR stimulates the proliferation of gastric cells [4] and human keratinocytes [5,6], and it is a factor a¡ecting pancreatic cancer and in£ammatory disease [7,8]. Therefore, EPR plays a critical role in regulating several biological activities.…”

Section: Introductionmentioning

confidence: 99%

Solution structure of epiregulin and the effect of its C‐terminal domain for receptor binding affinity

et al. 2003

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Epiregulin (EPR), a novel member of epidermal growth factor (EGF) family, is a ligand for ErbB-1 and ErbB-4 receptors. The binding a⁄nity of EPR for the receptors is lower than those of other EGF-family ligands. The solution structure of EPR was determined using two-dimensional nuclear magnetic resonance spectroscopy. The secondary structure in the C-terminal domain of EPR is di¡erent from other EGFfamily ligands because of the lack of hydrogen bonds. The structural di¡erence in the C-terminal domain may provide an explanation for the reduced binding a⁄nity of EPR to the ErbB receptors.

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Prof. Grant J. Anhalt

Cited by 2 publications

References 0 publications

Pigment‐independent cAMP‐mediated epidermal thickening protects against cutaneous UV injury by keratinocyte proliferation

Pigment‐independent cAMP‐mediated epidermal thickening protects against cutaneous UV injury by keratinocyte proliferation

Solution structure of epiregulin and the effect of its C‐terminal domain for receptor binding affinity

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