P21(cip)-Overexpression in the Mouse beta Cells Leads to the Improved Recovery from Streptozotocin-Induced Diabetes | |
Yang, Jie ; Zhang, Weiqi ; Jiang, Wei ; Sun, Xiaoning ; Han, Yuhua ; Ding, Mingxiao ; Shi, Yan ; Deng, Hongkui | |
刊名 | plos one
![]() |
2009 | |
关键词 | HEPATOCYTE GROWTH-FACTOR PARTIAL-PANCREATECTOMY ISLET TRANSPLANTATION TRANSGENIC MICE INSULIN GENE CYCLE ARREST IN-VIVO REGENERATION PANCREAS MODEL |
DOI | 10.1371/journal.pone.0008344 |
英文摘要 | Under normal conditions, the regeneration of mouse beta cells is mainly dependent on their own duplication. Although there is evidence that pancreatic progenitor cells exist around duct, whether non-beta cells in the islet could also potentially contribute to beta cell regeneration in vivo is still controversial. Here, we developed a novel transgenic mouse model to study the pancreatic beta cell regeneration, which could specifically inhibit beta cell proliferation by overexpressing p21(cip) in beta cells via regulation of the Tet-on system. We discovered that p21 overexpression could inhibit beta-cell duplication in the transgenic mice and these mice would gradually suffer from hyperglycemia. Importantly, the recovery efficiency of the p21-overexpressing mice from streptozotocin-induced diabetes was significantly higher than control mice, which is embodied by better physiological quality and earlier emergence of insulin expressing cells. Furthermore, in the islets of these streptozotocin-treated transgenic mice, we found a large population of proliferating cells which expressed pancreatic duodenal homeobox 1 (PDX1) but not markers of terminally differentiated cells. Transcription factors characteristic of early pancreatic development, such as Nkx2.2 and NeuroD1, and pancreatic progenitor markers, such as Ngn3 and c-Met, could also be detected in these islets. Thus, our work showed for the first time that when b cell self-duplication is repressed by p21 overexpression, the markers for embryonic pancreatic progenitor cells could be detected in islets, which might contribute to the recovery of these transgenic mice from streptozotocin-induced diabetes. These discoveries could be important for exploring new diabetes therapies that directly promote the regeneration of pancreatic progenitors to differentiate into islet beta cells in vivo.; http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000272834200011&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701 ; Multidisciplinary Sciences; SCI(E); PubMed; 12; ARTICLE; 12; e8344; 4 |
语种 | 英语 |
内容类型 | 期刊论文 |
源URL | [http://ir.pku.edu.cn/handle/20.500.11897/197502] ![]() |
专题 | 生命科学学院 |
推荐引用方式 GB/T 7714 | Yang, Jie,Zhang, Weiqi,Jiang, Wei,et al. P21(cip)-Overexpression in the Mouse beta Cells Leads to the Improved Recovery from Streptozotocin-Induced Diabetes[J]. plos one,2009. |
APA | Yang, Jie.,Zhang, Weiqi.,Jiang, Wei.,Sun, Xiaoning.,Han, Yuhua.,...&Deng, Hongkui.(2009).P21(cip)-Overexpression in the Mouse beta Cells Leads to the Improved Recovery from Streptozotocin-Induced Diabetes.plos one. |
MLA | Yang, Jie,et al."P21(cip)-Overexpression in the Mouse beta Cells Leads to the Improved Recovery from Streptozotocin-Induced Diabetes".plos one (2009). |
个性服务 |
查看访问统计 |
相关权益政策 |
暂无数据 |
收藏/分享 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论