Homo sapiens Raw sequence reads

We have recently shown that fluoxetine (FX) exerted potent anti-inflammatory action on cultured human epidermal keratinocytes, and it also suppressed the toll-like receptor 3 activator polyinosinic:polycytidylic acid (p(I:C))-induced release of the itch-mediator endothelins via the indirect inhibition of the phosphoinositide 3-kinase (PI3K) pathway. Importantly, besides its role in shaping immune, PI3K pathway is a positive regulator of proliferation in epidermal keratinocytes. Moreover, it has already been shown to play an important role in promoting proliferation of lesional keratinocytes in psoriasis. Thus, within the confines of the current, highly focused follow-up study, we aimed to assess whether potent anti-inflammatory concentration (14 mikorM) of FX influences proliferation and/or differentiation of human epidermal keratinocytes

本团队此前已证实，氟西汀（fluoxetine，FX）对体外培养的人表皮角质形成细胞具有强效抗炎活性，同时还可通过间接抑制磷脂酰肌醇3-激酶（phosphoinositide 3-kinase，PI3K）通路，减少toll样受体3（toll-like receptor 3）激活剂聚肌苷酸-聚胞苷酸（polyinosinic:polycytidylic acid，p(I:C)）诱导的瘙痒介质内皮素释放。
值得注意的是，PI3K通路不仅参与免疫调控，同时也是表皮角质形成细胞增殖的正向调节因子。此外，已有研究表明，该通路在促进银屑病皮损处角质形成细胞增殖过程中发挥关键作用。
因此，在本项针对性极强的后续聚焦研究中，我们旨在评估14 μM浓度的氟西汀是否会对人表皮角质形成细胞的增殖及/或分化产生影响。