(A) iPS cells can form embryoid bodies (EB) and can differentiate in vitro to
endoderm shown by alpha fetoprotein (AFP)(B), mesoderm shown by smooth muscle actin (SMA) and desmin (D, E), and ectoderm shown by GFAP and SMI31 staining (G, H).
Not exact matches
«Through studies like that, we've been able to
show how the main so - called germ layers for the embryo are formed — ectoderm, mesoderm, and
endoderm.
Professor Heiko Lickert, director of the IDR, in collaboration with Professor Gunnar Schotta of LMU München,
showed that the Wnt / β - catenin signaling pathway regulates Sox17, which in turn regulates molecular programs that assign pluripotent cells to the
endoderm, thus inducing an initial differentiation of the stem cells.
But then Stainier and colleagues
showed that the
endoderm was also somehow responsible for the migration of the heart cell buds in the layer of cells above it, known as the mesoderm.
As
shown in Figure 4, all three germ layers developed in our cultures as
shown by alphafetoprotein (AFP) for
endoderm (Figure 4B), smooth muscle actin (SMA) and desmin for mesoderm (Figure 4D, E), glial fibrillary acid protein (GFAP) and SMI31 for ectoderm (Figure 4G, H).
On the other hand, cells of line 4.1 differentiated into
endoderm lineages more easily than cells of line 11.1 (data not
shown).
Black arrowheads
show the presence of LacZ positive cells in the parietal
endoderm.
Black arrows
show the presence of LacZ positive cells in the visceral
endoderm.
(D) Sections of EBs grown under the same conditions as in part (C),
showing that the outer layer consists of visceral
endoderm as marked by Gata6, FoxA2, and Sox17 immunostaining (
shown as red).
J, Hematoxylin and eosin staining of teratoma sections generated from integration - free iPSC lines
showing differentiation in three germ layers: goblet cells in gastro - intestinal (GI) tract (
endoderm); neural rosettes (ectoderm) and blood vessels, muscle and cartilage / bone (mesoderm).
Moreover, as it has recently been
shown that VE can contribute to the embryonic gut [55], the distinction between visceral and definitive
endoderm begins to blur and the inability of ES cells to contribute to the VE becomes more puzzling.
We
show that the fraction of cells present within this state is influenced by factors that both promote and suppress primitive
endoderm differentiation, but conditions that support ES cell self - renewal prevent their progression into differentiation and support an equilibrium between this state and at least one other that resembles the Nanog positive inner cell mass of the mammalian blastocysts.
A more recent study
showed overlapping expression of nanog with GATA - 6 and a Pdgfra reporter, markers of the primitive
endoderm lineage, from the morula to the 64 cell stages [8], suggesting a gradual transition from a pluripotency program to a committed state.
Analysis of Oct4 protein expression in differentiated Ara - C cultures (DACs)
showed a slight increase of Oct4 protein by day four of aggregate formation (Figure 1C), consistent with previous reports examining Oct4 mRNA dynamics [22] and the finding that primitive
endoderm differentiation is accompanied by a transient increase in Oct4 protein levels [23].