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The Role of Protein Kinase C as a Regulator of NG115‐401L Neuronal Cell Calcium Signaling Pathways
Author(s) -
Bose Diptiman D.,
Thomas David W.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1118-a
Subject(s) - protein kinase c , trpc , microbiology and biotechnology , calcium , t type calcium channel , calcium in biology , calcium signaling , signal transduction , chemistry , voltage dependent calcium channel , transient receptor potential channel , biology , receptor , intracellular , biochemistry , organic chemistry
The molecular regulation of non‐voltage gated calcium influx continues to be an important but poorly characterized signaling pathway in cellular physiology. We have previously characterized unique features of calcium influx in the NG115‐401L (401L) neuronal cell line, revealing a phenotype that appears to depend on a conformational coupling mode for the regulation of both calcium influx and release. In this study, we used ratiometric microscope photometry on Fura 2 loaded 401L cells to further probe the apparatus mediating calcium influx when cells are stimulated with pro‐inflammatory hormones such as bradykinin. In particular, we have examined the effects of pharmacological modulation of protein kinase C (PKC) on native 401L cells and on cells overexpressing canonical transient receptor potential (TRPC) ion channels. Our preliminary results reveal that inhibitors of PKC augment calcium influx in 401L cells suggesting that PKC activation serves to suppresses the calcium influx mechanism. In contrast, pharmacological activation of PKC using phorbol ester treatment did not significantly influence calcium influx in both native or TRPC overexpressing 401L cells. Intriguingly, we observed that PKC activation in the presence of extracellular calcium elicited discharge from intracellular calcium stores, suggesting a composite target containing PKC activity regulating both calcium release and influx. This work was supported by a grant from the National Institutes of Neurological Disorders and Stroke (1R15 NS048041‐01A1) to D.W.T.