Wang Zhe, Li Hongqiu, Zhang Dianbao, Liu Xiaoyu, Zhao Feng, Pang Xining, Wang Qiushi
Department of Blood Transfusion, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004 P. R. China.
Department of Orthopaedics, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004 P. R. China ; Department of Orthopedics, Central Hospital of Shenyang Medical College, No.5 Nanqi Road, Tiexi District, Shenyang, 110024 P.R. China.
Cell Biosci. 2015 Jan 27;5:3. doi: 10.1186/2045-3701-5-3. eCollection 2015.
Both apoptosis and caspase-3 activity in adipose tissue-derived stem cells play an important role in the therapeutic process of diabetes patients. The purpose of this study was to investigate the effect of advanced glycation end products-human serum albumin (AGE-HSA) on apoptosis in human adipose tissue-derived stem cells (ADSCs) and to characterize the signal transduction pathways activated by AGEs that are involved in apoptosis regulation.
AGE-HSA promoted apoptosis and caspase-3 activity in ADSCs. However, the effects of AGE-HSA were significantly attenuated by an inhibitor of p38 MAPK, but not by inhibitors of JNK MAPK or ERK MAPK. AGE-HSA also upregulated the expression of RAGE. Silencing of the RAGE gene inhibited AGE-HSA-induced apoptosis, and activation and expression of phosphorylated p38 MAPK.
These results suggest that AGE-HSA promote the apoptosis of ADSCs in vitro via a RAGE-dependent p38 MAPK pathway.
脂肪组织来源干细胞中的细胞凋亡和半胱天冬酶 -3 活性在糖尿病患者的治疗过程中发挥重要作用。本研究旨在探讨晚期糖基化终产物 - 人血清白蛋白（AGE-HSA）对人脂肪组织来源干细胞（ADSCs）凋亡的影响，并表征参与凋亡调控的 AGEs 激活的信号转导途径。
AGE-HSA 促进了 ADSCs 中的细胞凋亡和半胱天冬酶 -3 活性。然而，p38 MAPK 抑制剂可显著减弱 AGE-HSA 的作用，而 JNK MAPK 或 ERK MAPK 抑制剂则无此作用。AGE-HSA 还上调了 RAGE 的表达。RAGE 基因沉默抑制了 AGE-HSA 诱导的细胞凋亡以及磷酸化 p38 MAPK 的激活和表达。
这些结果表明，AGE-HSA 通过 RAGE 依赖的 p38 MAPK 途径在体外促进 ADSCs 的凋亡。
