RGD Reference Report - Glucose modulates Pax6 expression through the JNK/p38 MAP kinase pathway in pancreatic beta-cells. - Rat Genome Database

RGD Reference Report - Glucose modulates Pax6 expression through the JNK/p38 MAP kinase pathway in pancreatic beta-cells. - Rat Genome Database

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General

Glucose modulates Pax6 expression through the JNK/p38 MAP kinase pathway in pancreatic beta-cells.
Authors:	Balakrishnan, Sivasangari Sadasivam, Mohanraj Kannan, Arun Panneerselvam, Antojenifer Prahalathan, Chidambaram
Citation:	Balakrishnan S, etal., Life Sci. 2014 Jul 25;109(1):1-7. doi: 10.1016/j.lfs.2014.06.009. Epub 2014 Jun 20.
RGD ID:	12790973
Pubmed:	PMID:24953606 (View Abstract at PubMed)
DOI:	DOI:10.1016/j.lfs.2014.06.009 (Journal Full-text)
AIM: The paired and homeodomain-containing transcription factor, paired box 6 (Pax6), has shown to play pivotal roles in beta-cell function, including cell survival, insulin biosynthesis and secretion. The present study investigates the signaling events that regulate the modulation of Pax6 expression by glucose and the role of this modulation in cell survival in rat insulinoma-1E (INS-1E) cells. MAIN METHODS: INS-1E cells were incubated on 1mM (low) or 25 mM (high) glucose overnight. To elucidate the signaling pathways that regulate Pax6 expression, we utilized specific inhibitors. The siRNA transfection of Pax6 into INS-1E cells was performed by electroporation. The mRNA and protein levels were determined by real-time PCR and Western blotting, respectively. KEY FINDINGS: We found that the mRNA and protein levels of Pax6 were reduced by approximately 4-fold in high, compared to low, glucose-treated cells. Staurosporine, the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the p38 mitogen-activated protein kinase (p38 MAPK) inhibitor SB203580 significantly increased Pax6 levels in high glucose-treated INS-1E cells compared to their respective controls. However, neither calcium ionophore nor the extracellular signal-regulated kinase (ERK) inhibitor U0126 resulted in any alteration in Pax6 protein expression. Further, a siRNA-mediated knockdown of Pax6 significantly decreased the expression of tumor-suppressor phosphatase with tensin homology (PTEN) while increasing cell viability in low glucose-treated INS-1E cells. SIGNIFICANCE: This study addresses the signaling events that regulate the glucose-dependent expression of Pax6 and the role of these events in cell survival in pancreatic beta cells.

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Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
cellular response to glucose stimulus		IEP		12790973		RGD
positive regulation of response to biotic stimulus		IMP		12790973	glucose-induced insulinoma cell death	RGD

Objects Annotated

Genes (Rattus norvegicus)

Pax6 (paired box 6)

Additional Information