Maintenance of pancreatic endocrine cells of the neonatal rat: IV. The effect of 3-amino-3-deoxyglucose.

1984 ◽  
Vol 31 (5) ◽  
pp. 657-664
Author(s):  
SHIGERU WAKABAYASHI ◽  
SHOHEI KAGAWA ◽  
KEIKO NAKAO ◽  
KEIKO YOSHIDA ◽  
KOICHI MIMURA ◽  
...  
1984 ◽  
Vol 31 (3) ◽  
pp. 253-261 ◽  
Author(s):  
SHIZUO SHIMIZU ◽  
SHOHEI KAGAWA ◽  
KEIKO NAKAO ◽  
SHIGERU WAKABAYASHI ◽  
KOICHI MIMURA ◽  
...  

Diabetes ◽  
1990 ◽  
Vol 39 (11) ◽  
pp. 1353-1360 ◽  
Author(s):  
J. L. Schwartz ◽  
G. A. Mealing ◽  
J. F. Whitfield ◽  
J. T. Braaten

1983 ◽  
Vol 97 (3) ◽  
pp. 935-939 ◽  
Author(s):  
R Montesano ◽  
P Mouron ◽  
M Amherdt ◽  
L Orci

To evaluate the capacity of pancreatic endocrine cells to reassociate in vitro according to the characteristic topographical pattern observed in the islets of Langerhans in situ, we cultured cells dissociated from neonatal rat pancreas within a three-dimensional collagen matrix. Cell monolayers grown on the surface of collagen gels were covered with a second layer of collagen. This induced the monolayers of endocrine cells to reorganize into smooth-contoured, three-dimensional aggregates, in which non-B cells (identified by electron microscopy and immunofluorescence) had a preferential distribution at the periphery, whereas B cells were concentrated in a central position. These results show that cultured pancreatic endocrine cells have the capacity to reassociate into islet-like organoids in vitro, and that collagen matrices may have a permissive effect on the expression of this potential.


Diabetes ◽  
1990 ◽  
Vol 39 (11) ◽  
pp. 1353-1360 ◽  
Author(s):  
J.-L. Schwartz ◽  
G. A. R. Mealing ◽  
J. F. Whitfield ◽  
J. T. Braaten

Development ◽  
1984 ◽  
Vol 82 (1) ◽  
pp. 131-145
Author(s):  
B. B. Rawdon ◽  
Beverley Kramer ◽  
Ann Andrew

The aim of this experiment was to find out whether or not, at early stages of development, progenitors of the various types of gut endocrine cells are localized to one or more specific regions of the gastrointestinal tract. Transverse strips of blastoderm two to four somites in length were excised between the levels of somites 5 and 27 in chick embryos at 5- to 24-somite stages and were cultured as chorioallantoic grafts. The distribution of endocrine cells in the grafts revealed confined localization of progenitor cells only in the case of insulinimmunoreactive cells. Theprogenitors of cells with somatostatin-, pancreatic polypeptide-, glucagon-, secretin-, gastrin/CCK-, motilin-, neurotensin- and serotonin-like immunoreactivity were distributed along the length of the presumptive gut at the time of explantation; indeed, in many cases they were more widespread than are their differentiated progeny in normal gut of the same age. This finding indicates that conditions in grafts must differ from those that operate in the intact embryo. Also it may explain the occurrence of ectopic gut or pancreatic endocrine cells in tumours of the digestive tract.


2005 ◽  
Vol 12 (4) ◽  
pp. 327-332 ◽  
Author(s):  
Kazuya Edamura ◽  
Koko Nasu ◽  
Yukiko Iwami ◽  
Ryohei Nishimura ◽  
Hiroyuki Ogawa ◽  
...  

2015 ◽  
Vol 22 (16) ◽  
pp. 1483-1495 ◽  
Author(s):  
Prabhu Mathiyalagan ◽  
Samuel T. Keating ◽  
Keith Al-Hasani ◽  
Assam El-Osta

2021 ◽  
Author(s):  
Meritxell Rovira ◽  
Goutham Atla ◽  
Miguel Angel Maestro ◽  
Vane Grau ◽  
Javier García-Hurtado ◽  
...  

SUMMARYUnderstanding genomic regulatory mechanisms of pancreas differentiation is relevant to the pathophysiology of diabetes mellitus, and to the development of replacement therapies. Numerous transcription factors promote β cell differentiation, although less is known about negative regulators. Earlier epigenomic studies suggested that the transcriptional repressor REST could be a suppressor of endocrine gene programs in the embryonic pancreas. However, pancreaticRestknock-out mice failed to show increased numbers of endocrine cells, suggesting that REST is not a major regulator of endocrine differentiation. Using a different conditional allele that enables profound REST inactivation, we now observe a marked increase in the formation of pancreatic endocrine cells. REST inhibition also promoted endocrinogenesis in zebrafish and mouse early postnatal ducts, and induced β-cell specific genes in human adult duct-derived organoids. Finally, we define REST genomic programs that suppress pancreatic endocrine differentiation. These results establish a crucial role of REST as a negative regulator of pancreatic endocrine differentiation.


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