Abstract:
:Angiotensin II (Ang II), a potent hypertrophic factor for vascular smooth muscle cells (VSMC), induces activation of the ras proto-oncogene product (Ras) and mitogen-activated protein (MAP) kinases, and tyrosine phosphorylation of a focal adhesion-associated protein, paxillin. Forskolin, a direct activator of adenylate cyclase, and dibutyryl cAMP (Bt2 cAMP), a membrane permeable cAMP analogue, potently inhibited Ang II-stimulated protein synthesis. However, they did not inhibit Ang II-induced activation of Ras and MAP kinases. Although both forskolin and Bt2 cAMP potently reduced background tyrosine phosphorylation of paxillin, they allowed Ang II to induce the same reaction. These results indicate that increasing cAMP antagonizes the hypertrophic response to Ang II without affecting Ras and MAP kinase activation in VSMC and suggest that it does not interrupt signaling from the Ang II receptor to focal adhesions.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Takahashi T,Kawahara Y,Okuda M,Yokoyama Mdoi
10.1016/s0014-5793(96)01145-3subject
Has Abstractpub_date
1996-11-11 00:00:00pages
89-92issue
1eissn
0014-5793issn
1873-3468pii
S0014-5793(96)01145-3journal_volume
397pub_type
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