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Involvement of the cGMP Signalling Pathway in the Regulation of Viability in Insulin-Secreting BRIN-BD11 Cells

Involvement of the cGMP Signalling Pathway in the Regulation of Viability in Insulin-Secreting BRIN-BD11 Cells

Anna Kaminski, Hongwei Gao, Noel G Morgan

FEBS Lett. 2004 Feb 13;559(1-3):118-24.

PMID: 14960318

Abstract:

We have evaluated the hypothesis that cGMP may serve as an intracellular messenger regulating the viability of pancreatic beta-cells. A direct activator of soluble guanylyl cyclase, YC-1, caused a time- and dose-dependent loss of viability in clonal BRIN-BD11 beta-cells. This was accompanied by a rise in cGMP and was antagonised by Rp-8-pCPT-cGMPS, a selective inhibitor of protein kinase G (PKG). Reverse transcription polymerase chain reaction analysis confirmed that BRIN-BD11 cells (and human islets) express all three known isoforms of PKG (PKG-Ialpha, -Ibeta and II). Cell death induced by YC-1 was not sensitive to cell-permeable caspase inhibitors and was not accompanied by oligonucleosomal DNA fragmentation. The response was, however, inhibited by actinomycin D, suggesting that a transcription-dependent pathway of programmed cell death is involved in the actions of cGMP.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42415610	PKG Iα Inhibitor, Cell-Permeable			Price

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