详细记录  
题名:TGF-beta superfamily member nodal stimulates human beta-cell proliferation while maintaining cellular viability.
作者:BOERNER BP; GEORGE NM; TARGY NM; SARVETNICK NE;
来源:Endocrinology. 2013 Nov;154(11):4099-112. doi: 10.1210/en.2013-1197. Epub 2013 [ IF= 4.72 ] ]
URL :10.1210/en.2013-1197
日期:20131203
摘要:In an effort to expand human islets and enhance allogeneic islet transplant for
the treatment of type 1 diabetes, identifying signaling pathways that stimulate
human beta-cell proliferation is paramount. TGF-beta superfamily members, in
particular activin-A, are likely involved in islet development and may contribute
to beta-cell proliferation. Nodal, another TGF-beta member, is present in both
embryonic and adult rodent islets. Nodal, along with its coreceptor, Cripto, are
pro-proliferative factors in certain cell types. Although Nodal stimulates
apoptosis of rat insulinoma cells (INS-1), Nodal and Cripto signaling have not
been studied in the context of human islets. The current study investigated the
effects of Nodal and Cripto on human beta-cell proliferation, differentiation,
and viability. In the human pancreas and isolated human islets, we observed Nodal
mRNA and protein expression, with protein expression observed in beta and
alpha-cells. Cripto expression was absent from human islets. Furthermore, in
cultured human islets, exogenous Nodal stimulated modest beta-cell proliferation
and inhibited alpha-cell proliferation with no effect on cellular viability,
apoptosis, or differentiation. Nodal stimulated the phosphorylation of mothers
against decapentaplegic (SMAD)-2, with no effect on AKT or MAPK signaling,
suggesting phosphorylated SMAD signaling was involved in beta-cell proliferation.
Cripto had no effect on human islet cell proliferation, differentiation, or
viability. In conclusion, Nodal stimulates human beta-cell proliferation while
maintaining cellular viability. Nodal signaling warrants further exploration to
better understand and enhance human beta-cell proliferative capacity.

================  评  论  部  分=================

重要性:
分类:(参照 Faculty of 1000 的分类体系)


评语:

评论密码:   返回前页  [全部]