TGF-β signalling prevents pancreatic beta cell death after proliferation

被引:9
|
作者
Lei, Chen [1 ,2 ,3 ]
Zhou, Xiaoling [3 ]
Pang, Yi [4 ]
Mao, Yuanyuan [4 ]
Lu, Xixuan [4 ]
Li, Meijuan [4 ]
Zhang, Jie [4 ]
机构
[1] Xi An Jiao Tong Univ, Sch Med, Dept Physiol, Xian 710061, Peoples R China
[2] Ningxia Med Univ, Gen Hosp, Dept Endocrinol, Yinchuan 750004, Peoples R China
[3] Ningxia Med Univ, Gen Hosp, Dept Nephrol, Yinchuan 750004, Peoples R China
[4] Ningxia Med Univ, Yinchuan 750004, Peoples R China
关键词
EXTRACELLULAR-MATRIX; INSULIN-SECRETION; PRIMARY MECHANISM; IN-VITRO; PREGNANCY; MICE; MASS; REPLICATION; EXPRESSION; GROWTH;
D O I
10.1111/cpr.12183
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
ObjectivesMaintenance of functional beta cell mass is critical for prevention of diabetes. The transforminggrowth factor-beta (TGF-) receptor signalling pathway plays an essential role in pancreatic development. However, its involvement in control of post-natal beta cell growth has only been recently reported. Materials and methodsHere, we studied the role of TGF- receptor signalling in beta cell proliferation after 50% partial pancreatectomy (PPx), using beta cell-specific TGF- receptor II (TBR2)-mutated mice. ResultsConsistent with previous reports, we found that inhibition of TGF- receptor signalling in beta cells resulted in slightly higher beta cell mass 1week after PPx, due to greater beta cell proliferation. However, beta cell mass in these beta cell-specific TBR2-mutated mice significantly decreased by 12weeks after PPx, resulting from increase in beta cell apoptosis. ConclusionsOur data thus suggest that TGF- receptor signalling may be required for prevention of beta cell death after proliferation, and highlight this pathway as an essential regulator during post-natal beta cell homoeostasis.
引用
收藏
页码:356 / 362
页数:7
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