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Department of Physiology and Biophysics, University of Tennessee, Memphis, Tennessee 38163
Our laboratory has previously reported that
the antimitogenic effect of nitric oxide (NO) in primary cultures of
rat aortic smooth muscle cells may be attributed to activation of
protein tyrosine phosphatase and dephosphorylation of protein
phosphotyrosine [G. S. Dhaunsi, C. Matthews, K. Kaur, and A. Hassid. Am. J. Physiol. 272 (Heart Circ. Physiol. 41):
H1342-H1349, 1997]. The goal of the current study was to
investigate the role of cytoplasmic Ca in this process and to identify
protein substrates that are dephosphorylated by treatment with NO.
Treatment of primary rat aortic smooth muscle cell cultures with the NO
donor
S-nitroso-N-acetylpenicillamine (SNAP) decreased cytoplasmic Ca levels and elicited phosphotyrosine dephosphorylation. Both effects were mimicked by the extracellular and
intracellular Ca chelators ethylene glycol-bis(
-aminoethyl ether)-N,N,N',N'-tetraacetic
acid (EGTA) and
1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), respectively, and by the Ca channel blocker nifedipine. Conversely, elevation of cytoplasmic Ca via the use of the Ca ionophore
A-23187 or high extracellular K+
prevented or attenuated SNAP-induced dephosphorylation. Both BAPTA and
nifedipine also decreased DNA synthesis, providing further evidence to
link dephosphorylation to antimitogenesis. Two of the proteins
dephosphorylated by treatment of cells with NO or EGTA were identified
as the focal adhesion proteins, cortactin and paxillin. These results
indicate that NO-induced dephosphorylation of protein phosphotyrosine
is mediated by reduction of cytoplasmic Ca and suggest that
dephosphorylation of focal adhesion proteins may be of relevance to the
antimitogenic effect of NO.
calcium; focal adhesion proteins; vascular smooth muscle; cell proliferation; nitric oxide donor; nitric oxide
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