Experimental dermatology · 2018
FoxO1 enhances differentiation and apoptosis in human primary keratinocytes.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Shi Ge, Liao Pei-Yu, Cai Xiao-Lin, Pi Xiao-Xue, Zhang Man-Feng, Li Shi-Jie, Quan Juan-Hua, Fan Yi-Ming
Аннотация
Forkhead box-O1 (FoxO1) is a key nutrient- and growth factor-dependent regulator of metabolism, but its functional role in human primary keratinocytes (HPKs) is less known. To investigate the role of FoxO1 in HPKs and effect of insulin-like growth factor 1 (IGF-1) and isotretinoin on FoxO1 expression, HPKs were treated with 1.2 mmol/L calcium chloride, 1-20 ng/mL IGF-1 and 0.1-10 μmol/L isotretinoin. Recombinant adenovirus expressing FoxO1 or FKHR shRNA lentivirus transfection was introduced to upregulate or silence FoxO1 expression. Epidermal FoxO1 immunostaining was lower in acne lesion than in normal skin. FoxO1 overexpression induced involucrin expression, G2/M arrest and apoptosis but suppressed proliferation, while FoxO1 silencing decreased involucrin expression but increased proliferation, S phase and viable cells in HPKs. IGF-1 downregulated FoxO1 and involucrin but upregulated p-Akt expression in HPKs, which was blocked by pretreatment with LY294002. Isotretinoin enhanced FoxO1, p53 and p21 but inhibited p-FoxO1 and involucrin expression in HPKs. These results demonstrate that FoxO1 promotes differentiation and apoptosis in HPKs. IGF-1 may reduce keratinocyte differentiation through PI3K/Akt/FoxO1 pathway, while isotretinoin can reinforce FoxO1 expression. FoxO1 may be involved in acne pathogenesis and could serve as a potential therapeutic target.
Предметные рубрики MeSH
Acne VulgarisApoptosisCell Cycle CheckpointsCell DifferentiationCell ProliferationCell SurvivalCells, CulturedChromonesDermatologic AgentsEnzyme InhibitorsForkhead Box Protein O1Gene ExpressionGene SilencingHumansInsulin-Like Growth Factor IIsotretinoinKeratinocytesMorpholinesPhosphorylationPrimary Cell CultureProtein PrecursorsProto-Oncogene Proteins c-aktSignal TransductionTransfectionTumor Suppressor Protein p53Up-Regulation