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1.  P19 Cells Overexpressing Lhx1 Differentiate into the Definitive Endoderm by Recapitulating an Embryonic Developmental Pathway 
Yonago Acta Medica  2015;58(1):15-22.
Epiblasts occur at the last pluripotent stage of embryonic development and are important in elucidating how the three germ layers are formed. However, little is known of the molecular mechanisms of their development. We have shown that LIM homeobox 1 (Lhx1) was involved in epiblast development in embryonic stem cells, especially meso- and endodermal differentiation. However, since epiblasts in embryoid bodies spontaneously develop into a further stage, it is difficult to study their development in this system.
Mouse embryonal carcinoma P19 cells which have properties similar to those of epiblasts provided new avenues of investigation into the regulatory mechanism of epiblasts.
Overexpression of Lhx1 in P19 cells induced expression of organizer marker genes (Cer1, Gsc) and endoderm marker genes (Gata6, Foxa2, Sox17) but not extra-embryonic endoderm marker genes (Sox7 or Hnf4alpha).
This study suggested that Lhx1 overexpression caused P19 cells to differentiate into an endodermal lineage. Thus, P19 cells and their derivatives can be a useful model system to study how the three germ layers are formed.
PMCID: PMC4502295  PMID: 26190893
cell differentiation; germ layer; organizer; P19 cells
2.  Bepridil Suppresses Apoptosis in HL-1 Cardiac Atrial Myocytes Expressing Mutant E334K cMyBPC 
Yonago Acta Medica  2013;56(4):93-95.
Besides its antiarrhythmic effect on atrial fibrillation, bepridil protects tissue, yet its effect on apoptosis has never been fully tested. We examine the effect of bepridil on apoptosis of HL-1 cells expressing E334K myosin-binding protein C (MyBPC), a model cell of apoptosis. Bepridil was compared with amiodarone, and its effects on the expression of pro- and anti-apoptotic protein and apoptosis of HL-1 cells expressing mutant E334K MyBPC-green fluorescent protein (GFP) was analyzed using Western blot and a flow cytometer. Bepridil decreased the protein levels of both Bax and cytochrome c of cells expressing E334K MyBPC-GFP with no changes in p53 and Bcl-2, while amiodarone decreased cytochrome c but did not influence Bax except in its highest concentration. It also decreased the number of Annexin-V positive cells of HL-1 cells expressing E334K MyBPC-GFP, and decreased apoptosis of HL-1 cells expressing E334K MyBPC-GFP.
PMCID: PMC3935176  PMID: 24574578
amiodarone; apoptosis; bepridil; HL-1 cell
3.  ZAC, LIT1 (KCNQ1OT1) and p57KIP2 (CDKN1C) are in an imprinted gene network that may play a role in Beckwith–Wiedemann syndrome 
Nucleic Acids Research  2005;33(8):2650-2660.
Loss of genomic imprinting is involved in a number of developmental abnormalities and cancers. ZAC is an imprinted gene expressed from the paternal allele of chromosome 6q24 within a region known to harbor a tumor suppressor gene for several types of neoplasia. p57KIP2 (CDKN1C) is a maternally expressed gene located on chromosome 11p15.5 which encodes a cyclin-dependent kinase inhibitor that may also act as a tumor suppressor gene. Mutations in ZAC and p57KIP2 have been implicated in transient neonatal diabetes mellitus (TNDB) and Beckwith–Wiedemann syndrome, respectively. Patients with these diseases share many characteristics. Here we show that mouse Zac1 and p57Kip2 have a strikingly similar expression pattern. ZAC, a sequence-specific DNA-binding protein, binds within the CpG island of LIT1 (KCNQ1OT1), a paternally expressed, anti-sense RNA thought to negatively regulate p57KIP2 in cis. ZAC induces LIT1 transcription in a methylation-dependent manner. Our data suggest that ZAC may regulate p57KIP2 through LIT1, forming part of a novel signaling pathway regulating cell growth. Mutations in ZAC may, therefore, contribute to Beckwith–Wiedemann syndrome. Furthermore, we find changes in DNA methylation at the LIT1 putative imprinting control region in two patients with TNDB.
PMCID: PMC1097765  PMID: 15888726

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