Abstract：
BACKGROUND: Keratinocyte dysdifferentiation and proinflammatory cytokine production play a central role in psoriatic inflammation. According to recent studies, the Rh family C glycoprotein (RHCG) enhances cell proliferation and disrupts cell differentiation. However, the specific role of RHCG psoriasis development remains unclear.
OBJECTIVE: We here explored the effect of RHCG on keratinocytes under psoriatic inflammation.
METHODS: The cell counting kit‑8 assay was conducted to assess proliferation. RHCG protein expression was assessed through western blotting and enzyme-linked immunosorbent assays. The expression of proinflammatory cytokines and differentiation markers was analyzed through a quantitative reverse-transcription polymerase chain reaction.
RESULTS: Both RHCG mRNA and protein levels increased in psoriatic skin. Notably, cultured keratinocytes treated with an M5 cocktail, which mimics psoriatic inflammation, exhibited higher RHCG expression. Furthermore, RHCG overexpression promoted keratinocyte proliferation, accompanied by an increase in the production of interleukin (IL)-1β, IL-6, and IL-8, and tumor necrosis factor-α. RHCG overexpression also resulted in higher expression of keratin 17, a differentiation marker. Conversely, RHCG gene knockdown reduced keratinocyte proliferation and cytokine secretion. RHCG inhibition in cells recovered both keratin 1 and loricrin expression. Additionally, RHCG overexpression facilitated the phosphorylation of nuclear factor-kappa B and extracellular signal-regulated protein kinase signaling pathways. Importantly, when these signaling pathways were inhibited, the effect of RHCG on keratinocytes was attenuated.
CONCLUSIONS: These findings support the substantial role of RHCG in psoriatic inflammation development and suggest that RHCG serves as a potential target for psoriasis treatment.
OBJECTIVE: We here explored the effect of RHCG on keratinocytes under psoriatic inflammation.
METHODS: The cell counting kit‑8 assay was conducted to assess proliferation. RHCG protein expression was assessed through western blotting and enzyme-linked immunosorbent assays. The expression of proinflammatory cytokines and differentiation markers was analyzed through a quantitative reverse-transcription polymerase chain reaction.
RESULTS: Both RHCG mRNA and protein levels increased in psoriatic skin. Notably, cultured keratinocytes treated with an M5 cocktail, which mimics psoriatic inflammation, exhibited higher RHCG expression. Furthermore, RHCG overexpression promoted keratinocyte proliferation, accompanied by an increase in the production of interleukin (IL)-1β, IL-6, and IL-8, and tumor necrosis factor-α. RHCG overexpression also resulted in higher expression of keratin 17, a differentiation marker. Conversely, RHCG gene knockdown reduced keratinocyte proliferation and cytokine secretion. RHCG inhibition in cells recovered both keratin 1 and loricrin expression. Additionally, RHCG overexpression facilitated the phosphorylation of nuclear factor-kappa B and extracellular signal-regulated protein kinase signaling pathways. Importantly, when these signaling pathways were inhibited, the effect of RHCG on keratinocytes was attenuated.
CONCLUSIONS: These findings support the substantial role of RHCG in psoriatic inflammation development and suggest that RHCG serves as a potential target for psoriasis treatment.
摘要：
背景：角质形成细胞分化异常和促炎细胞因子的产生在银屑病炎症中起重要作用。根据最近的研究，Rh家族C糖蛋白（RHCG）增强细胞增殖并破坏细胞分化。然而,RHCG在银屑病发病中的具体作用尚不清楚.
目的：我们在此探讨RHCG对银屑病炎症下角质形成细胞的影响。
方法：进行细胞计数试剂盒-8测定以评估增殖。通过蛋白质印迹和酶联免疫吸附测定评估RHCG蛋白表达。通过定量逆转录聚合酶链反应分析促炎细胞因子和分化标志物的表达。
结果：银屑病皮肤中RHCGmRNA和蛋白水平均升高。值得注意的是,用M5鸡尾酒处理的培养的角质形成细胞，模仿银屑病炎症，表现出较高的RHCG表达。此外，RHCG过表达促进角质形成细胞增殖，伴随着白细胞介素（IL）-1β的产生增加，IL-6、IL-8和肿瘤坏死因子-α。RHCG过表达还导致分化标志物角蛋白17的更高表达。相反，RHCG基因敲低减少角质形成细胞增殖和细胞因子分泌。细胞中的RHCG抑制恢复了角蛋白1和菊甲的表达。此外,RHCG过表达促进核因子-κB磷酸化和细胞外信号调节蛋白激酶信号通路。重要的是,当这些信号通路被抑制时，RHCG对角质形成细胞的作用减弱。
结论：这些发现支持RHCG在银屑病炎症发展中的重要作用，并提示RHCG可作为银屑病治疗的潜在靶点。
目的：我们在此探讨RHCG对银屑病炎症下角质形成细胞的影响。
方法：进行细胞计数试剂盒-8测定以评估增殖。通过蛋白质印迹和酶联免疫吸附测定评估RHCG蛋白表达。通过定量逆转录聚合酶链反应分析促炎细胞因子和分化标志物的表达。
结果：银屑病皮肤中RHCGmRNA和蛋白水平均升高。值得注意的是,用M5鸡尾酒处理的培养的角质形成细胞，模仿银屑病炎症，表现出较高的RHCG表达。此外，RHCG过表达促进角质形成细胞增殖，伴随着白细胞介素（IL）-1β的产生增加，IL-6、IL-8和肿瘤坏死因子-α。RHCG过表达还导致分化标志物角蛋白17的更高表达。相反，RHCG基因敲低减少角质形成细胞增殖和细胞因子分泌。细胞中的RHCG抑制恢复了角蛋白1和菊甲的表达。此外,RHCG过表达促进核因子-κB磷酸化和细胞外信号调节蛋白激酶信号通路。重要的是,当这些信号通路被抑制时，RHCG对角质形成细胞的作用减弱。
结论：这些发现支持RHCG在银屑病炎症发展中的重要作用，并提示RHCG可作为银屑病治疗的潜在靶点。
