CAJ | 학술논문

目的：研究肾脏纤维化过程中转分化的肾小管上皮细胞获得的组织干细胞潜能。方法体外建立局部肾素-血管紧张素（AngⅡ）系统炎性环境下肾小管上皮细胞（NRK-52E）转分化的细胞模型，观察其胚胎肾发育基因 Pax2和组织干细胞表面标志 CD133分子的表达和变化情况。结果局部高浓度 AngⅡ可刺激 NRK-52E 细胞表达 Pax2和 CD133分子，其作用呈剂量和时间依赖关系。结论炎性损伤导致肾小管上皮细胞转分化后可获得组织干细胞潜能。
목적：연구신장섬유화과정중전분화적신소관상피세포획득적조직간세포잠능。방법체외건립국부신소-혈관긴장소（AngⅡ）계통염성배경하신소관상피세포（NRK-52E）전분화적세포모형，관찰기배태신발육기인 Pax2화조직간세포표면표지 CD133분자적표체화변화정황。결과국부고농도 AngⅡ가자격 NRK-52E 세포표체 Pax2화 CD133분자，기작용정제량화시간의뢰관계。결론염성손상도치신소관상피세포전분화후가획득조직간세포잠능。
Objective To study the potency of transdifferentiated renal tubular epithelial cells for acquiring the tissue stem cells during renal fibrosis.Methods The in vitro cellular model of renal tubular epithelial cells(NRK-52E)transdifferentiation under the inflammatory environment of the local renin-angiotensin (AngⅡ)system was established.The expression and change situation of the embryonic kidney developmental gene Pax2 and the tissue stem cell surface marker CD133 were observed.Results Local high concentration of AngⅡcould stimulate the NRK-52E cells to express Pax2 and CD133 molecule,its effect demonstrated the dose-and time-dependent relation.Conclusion The inflammatory damage leads to the transdifferentiated renal tubular epithelial cells po-tency to acquire the tissue stem cell.