High Glucose Aggravates the Detrimental Effects of Pancreatic Stellate Cells on Beta-Cell Function

被引:18
作者
Zha, Min [1 ]
Xu, Wei [1 ]
Zhai, Qing [2 ]
Li, Fengfei [1 ]
Chen, Bijun [1 ]
Sun, Zilin [1 ]
机构
[1] Southeast Univ, Sch Med, Inst Diabet, Zhongda Hosp,Dept Endocrinol, Nanjing 210009, Jiangsu, Peoples R China
[2] Yijishan Hosp, Wannan Med Coll, Dept Endocrinol & Genet Metab, Wuhu 241001, Anhui, Peoples R China
关键词
ISLET FIBROSIS; INSULIN-SECRETION; MATRIX SYNTHESIS; INFLAMMATION; MODEL; PROLIFERATION; HYPERGLYCEMIA; IDENTIFICATION; ACTIVATION; EXPRESSION;
D O I
10.1155/2014/165612
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background and Aims. We here assess the effects of PSCs on beta-cell function and apoptosis in vivo and in vitro. Materials and Methods. PSCs were transplanted into Wistar and Goto-Kakizaki (GK) rats. Sixteen weeks after transplantation, beta-cell function, apoptosis, and islet fibrosis were assessed. In vitro the effects of PSCs conditioned medium(PSCs-CM) and/or high concentration of glucose on INS-1 cell function was assessed by measuring insulin secretion, INS-1 cell survival, apoptosis, and endoplasmic reticulum stress (ER stress) associated CHOP expression. Results. PSCs transplantation exacerbated the impaired beta-cell function in GK rats, but had no significant effects in Wistar rats. In vitro, PSCs-CM caused impaired INS-1 cell viability and insulin secretion and increased apoptosis, which were more pronounced in the presence of high glucose. Conclusion. Our study demonstrates that PSCs induce beta-cell failure in vitro and in vivo.
引用
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页数:8
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