scholarly journals Expression profile of mRNAs from human pancreatic islet tumors

2003 ◽  
Vol 31 (3) ◽  
pp. 519-528 ◽  
Author(s):  
L Jin ◽  
H Wang ◽  
T Narita ◽  
R Kikuno ◽  
O Ohara ◽  
...  

In order to understand the tIssue specificity of the endocrine pancreas, it is important to clarify the expression profile of mRNAs in various states of the tIssue. A total of approximately 9000 non-redundant expressed genes from human pancreatic islets and insulinoma have so far been determined as expressed sequence tags (ESTs) and deposited in public databases. In the present study towards the identification of a complete set of genes expressed in human pancreatic islets, we have determined 3'-ESTs of 21267 clones randomly selected from a cDNA library of human pancreatic islet tumors. Clustering analysis generated 6157 non-redundant sequences comprising 2323 groups and 3834 singletons. Nucleotide and peptide database searches show that 3103 of them represent known human sequences or homologs of genes identified in other species and 58 are new members of structurally related families. The sequences were classified on the basis of the putative protein functions encoded, and were assigned to the respective chromosome by database analysis. The sequences were also compared with the EST databases (dbEST and EPConDB) including ESTs from normal pancreatic islet, insulinoma, and fetal pancreas. Since 3384 genes were newly found to be expressed in human pancreatic islets and 587 of them were unique to the islets, this study has considerably expanded the catalog of genes expressed in the endocrine pancreas. The larger collection of pancreatic islet-related ESTs should provide a better genome source for molecular studies of differentiation, tIssue-specific functions, and tumorigenesis of the endocrine pancreas as well as for genetic studies of diabetes mellitus.

Diabetologia ◽  
2012 ◽  
Vol 55 (12) ◽  
pp. 3273-3283 ◽  
Author(s):  
P. Ylipaasto ◽  
T. Smura ◽  
P. Gopalacharyulu ◽  
A. Paananen ◽  
T. Seppänen-Laakso ◽  
...  

Diabetologia ◽  
2004 ◽  
Vol 47 (2) ◽  
pp. 284-299 ◽  
Author(s):  
C. Cras-M�neur ◽  
H. Inoue ◽  
Y. Zhou ◽  
M. Ohsugi ◽  
E. Bernal-Mizrachi ◽  
...  

2009 ◽  
Vol 297 (1) ◽  
pp. G197-G206 ◽  
Author(s):  
Lisa Mee ◽  
Svetlana M. Nabokina ◽  
V. Thillai Sekar ◽  
Veedamali S. Subramanian ◽  
Kathrin Maedler ◽  
...  

Thiamin is essential for the normal function of the endocrine pancreas, but very little is known about uptake mechanism(s) and regulation by beta cells. We addressed these issues using mouse-derived pancreatic beta-TC-6 cells, and freshly isolated primary mouse and human pancreatic islets. Results showed that thiamin uptake by beta-TC-6 cells involves a pH (but not Na+)-dependent carrier-mediated process that is saturable at both the nanomolar (apparent Km = 37.17 ± 9.9 nM) and micromolar (apparent Km = 3.26 ± 0.86 μM) ranges, cis-inhibited by thiamin structural analogs, and trans-stimulated by unlabeled thiamin. Involvement of carrier-mediated process was also confirmed in primary mouse and human pancreatic islets. Both THTR-1 and THTR-2 were found to be expressed in these mouse and human pancreatic preparations. Maintaining beta-TC-6 cells in the presence of a high level of thiamin led to a significant ( P < 0.01) decrease in thiamin uptake, which was associated with a significant downregulation in level of expression of THTR-1 and THTR-2 at the protein and mRNA levels and a decrease in transcriptional (promoter) activity. Modulators of intracellular Ca2+/calmodulin- and protein-tyrosine kinase-mediated pathways also altered thiamin uptake. Finally, confocal imaging of live beta-TC-6 cells showed that clinical mutants of THTR-1 have mixed expression phenotypes and all led to impairment in thiamin uptake. These studies demonstrate for the first time that thiamin uptake by the endocrine pancreas is carrier mediated and is adaptively regulated by the prevailing vitamin level via transcriptional mechanisms. Furthermore, clinical mutants of THTR-1 impair thiamin uptake via different mechanisms.


The Analyst ◽  
2019 ◽  
Vol 144 (8) ◽  
pp. 2541-2549 ◽  
Author(s):  
F. Rafael Castiello ◽  
Maryam Tabrizian

In this work, we demonstrate the potential use of SPRi for secretion-monitoring of pancreatic islets, small micro-organs that regulate glucose homeostasis in the body.


2006 ◽  
Vol 38 (10) ◽  
pp. 3678-3679 ◽  
Author(s):  
O.M. Sabek ◽  
D.R. Marshall ◽  
R. Penmetsa ◽  
O. Scarborough ◽  
A.O. Gaber

2009 ◽  
Vol 39 (1) ◽  
pp. 72-81 ◽  
Author(s):  
B. Kutlu ◽  
A. G. Kayali ◽  
S. Jung ◽  
G. Parnaud ◽  
D. Baxter ◽  
...  

Pancreatic islet transplantation as a potential cure for type 1 diabetes (T1D) cannot be scaled up due to a scarcity of human pancreas donors. In vitro expansion of β-cells from mature human pancreatic islets provides an alternative source of insulin-producing cells. The exact nature of the expanded cells produced by diverse expansion protocols and their potential for differentiation into functional β-cells remain elusive. We performed a large-scale meta-analysis of gene expression in human pancreatic islet cells, which were processed using three different previously described protocols for expansion and for which redifferentiation was attempted. All three expansion protocols induced dramatic changes in the expression profiles of pancreatic islets; many of these changes are shared among the three protocols. Attempts at redifferentiation of expanded cells induce a limited number of gene expression changes. Nevertheless, these fail to restore a pancreatic islet-like gene expression pattern. Comparison with a collection of public microarray datasets confirmed that expanded cells are highly comparable to mesenchymal stem cells. Genes induced in expanded cells are also enriched for targets of transcription factors important for pluripotency induction. The present data increase our understanding of the active pathways in expanded and redifferentiated islets. Knowledge of the mesenchymal stem cell potential may help development of drug therapeutics to restore β-cell mass in T1D patients.


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