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J Biol Chem, Vol. 274, Issue 34, 23761-23769, August 20, 1999
,
From the Unité INSERM 99 and the During chronic liver diseases, hepatic stellate
cells (HSC) acquire a myofibroblastic phenotype, proliferate, and
synthetize fibrosis components. Myofibroblastic HSC (mHSC) also
participate to the regulation of intrahepatic blood flow, because of
their contractile properties. Here, we examined whether human mHSC
express natriuretic peptide receptors (NPR). Only NPR-B mRNA was
identified, which was functional as demonstrated in binding studies and
by increased cGMP levels in response to C-type natriuretic peptide (CNP). CNP inhibited mHSC proliferation, an effect blocked by the
protein kinase G inhibitor 8-(4 chlorophenylthio)-cGMP and by the NPR
antagonist HS-142-1 and reproduced by analogs of cGMP. Growth
inhibition was associated with a reduction of extracellular signal-regulated kinase and c-Jun N-terminal kinase and with a blockade
of AP-1 DNA binding. CNP and cGMP analogs also blunted mHSC contraction
elicited by thrombin, by suppressing calcium influx. The relaxing
properties of CNP were mediated by a blockade of store-operated calcium
channels, as demonstrated using a calcium-free/calcium readdition
protocol. These results constitute the first evidence for a hepatic
effect of CNP and identify mHSC as a target cell. Activation of NPR-B
by CNP in human mHSC leads to inhibition of both growth and
contraction. These data suggest that during chronic liver diseases, CNP
may counteract both liver fibrogenesis and associated portal hypertension.
Departement
de Pathologie, Hôpital Henri Mondor, AP-HP,
94010 Créteil, France and the § Unité
INSERM 446, Faculté de Pharmacie,
92296 Chatenay-Malabry, France
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