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Vol. 59, Issue 5, 1012-1021, May 2001
in Signaling from the Histamine
H1 Receptor to the Nucleus
Institute of Cell Signalling and School of Biomedical Sciences,
Medical School, Queen's Medical Centre, Nottingham, United Kingdom
Stimulation of histamine H1 receptors produced a marked
activation of inositol phospholipid hydrolysis, intracellular calcium mobilization, and stimulation of the c-fos promoter in CHO-H1 cells
expressing the H1 receptor at a level of 3 pmol/mg protein. The latter response was determined using a luciferase-based reporter gene (pGL3). This response to histamine was not sensitive to inhibition by pertussis toxin but could be completely attenuated by the protein kinase C (PKC) inhibitor Ro-31-8220, or by 24-h pretreatment with the
phorbol esters phorbol 12,13-dibutyrate or
phorbol-12-myristate-13-acetate. Several isoforms of PKC can be
detected in CHO-H1 cells (
, 
, 
, µ, 
, 
) but only PKC
and PKC were down-regulated by prolonged treatment with phorbol
esters. Of the two isoforms that were down-regulated, only protein
kinase C was translocated to CHO-H1 cell membranes after stimulation
with either histamine or phorbol esters. The PKC inhibitor Gö
6976, which inhibits PKC but not PKC, was also able to
significantly attenuate the c-fos-luciferase response to histamine. The
mitogen-activated protein kinase kinase inhibitor PD 98059 markedly
inhibited the response to histamine, suggesting that the likely major
target for PKC was the mitogen-activated protein kinase pathway.
These data suggest that the histamine H1 receptor can
signal to the nucleus via PKC after activation of phospholipase
C
.
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