Necroptosis is a novel manner of programmed cell death and important for tissue development, homeostasis, damage, and repair. Activation of receptor-interacting protein kinase 3 (RIPK3), a key member of receptor-interacting protein family in contributing significantly to necroptosis, in tissues is a hallmark of cells dying by necroptosis. However, there are few studies that examine the expression of RIPK3 in the glandular cells of stomachs under physiological condition. We have therefore conducted this study to immunohistochemically characterize the key element of necroptosis, RIPK3, in the mouse and human stomach. Results showed that RIPK3 positive cells could be observed in the surface mucosal cells, granular cells, and lamina propria cells in both mouse and human stomach tissues. Ratios of PCNA/RIPK3 positive cells in the glandular cells were ~ 2.1 in mouse and ~ 4.15 in human sections respectively. Morphological and double immunofluorescence analysis confirmed that these RIPK3 positive cells were mucous, parietal and lamina propria cells. Our results indicate that the expression of RIPK3 in different cell types might contribute to cell turnover of gastric mucosa in the mouse and human stomach under physiological condition.

坏死性凋亡是一种新的程序性细胞死亡方式，对组织发育、体内平衡、损伤和修复很重要。受体相互作用蛋白激酶 3 (RIPK3) 是受体相互作用蛋白家族的关键成员，对坏死性凋亡有显着贡献，在组织中激活是细胞因坏死性凋亡而死亡的标志。然而，很少有研究在生理条件下检查胃腺细胞中RIPK3的表达。因此，我们进行了这项研究，以免疫组织化学表征小鼠和人胃中坏死性凋亡的关键因素 RIPK3。结果表明，在小鼠和人胃组织的表面黏膜细胞、颗粒细胞和固有层细胞中均可以观察到RIPK3阳性细胞。腺细胞中 PCNA/RIPK3 阳性细胞的比率在小鼠和人体切片中分别为 ~ 2.1 和 ~ 4.15。形态学和双重免疫荧光分析证实这些RIPK3阳性细胞为粘液细胞、壁细胞和固有层细胞。我们的研究结果表明，RIPK3 在不同细胞类型中的表达可能有助于生理条件下小鼠和人胃中胃粘膜的细胞更新。