详细记录  
题名:Microarray analysis of novel candidate genes responsible for glucose-stimulated insulin secretion in mouse pancreatic beta cell line MIN6.
作者:YAMATO E; TASHIRO F; MIYAZAKI J;
来源:PLoS One. 2013;8(4):e61211. doi: 10.1371/journal.pone.0061211. Epub 2013 Apr 3. [ IF= 4.09 ] ]
URL :10.1371/journal.pone.0061211
日期:20130131
摘要:Elucidating the regulation of glucose-stimulated insulin secretion (GSIS) in
pancreatic islet beta cells is important for understanding and treating diabetes.
MIN6 cells, a transformed beta-cell line derived from a mouse insulinoma, retain
GSIS and are a popular in vitro model for insulin secretion. However, in
long-term culture, MIN6 cells' GSIS capacity is lost. We previously isolated a
subclone, MIN6 clone 4, from the parental MIN6 cells, that shows well-regulated
insulin secretion in response to glucose, glybenclamide, and KCl, even after
prolonged culture. To investigate the molecular mechanisms responsible for
preserving GSIS in this subclone, we compared four groups of MIN6 cells: Pr-LP
(parental MIN6, low passage number), Pr-HP (parental MIN6, high passage number),
C4-LP (MIN6 clone 4, low passage number), and C4-HP (MIN6 clone 4, high passage
number). Based on their capacity for GSIS, we designated the Pr-LP, C4-LP, and
C4-HP cells as "responder cells." In a DNA microarray analysis, we identified a
group of genes with high expression in responder cells ("responder genes"), but
extremely low expression in the Pr-HP cells. Another group of genes
("non-responder genes") was expressed at high levels in the Pr-HP cells, but at
extremely low levels in the responder cells. Some of the responder genes were
involved in secretory machinery or glucose metabolism, including Chrebp, Scgn,
and Syt7. Among the non-responder genes were Car2, Maf, and Gcg, which are not
normally expressed in islet beta cells. Interestingly, we found a
disproportionate number of known imprinted genes among the responder genes. Our
findings suggest that the global expression profiling of GSIS-competent and
GSIS-incompetent MIN6 cells will help delineate the gene regulatory networks for
insulin secretion.

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