Cyclic guanosine monophosphate-dependent protein kinase I promotes adhesion of primary vascular smooth muscle cells
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Cyclic guanosine monophosphate-dependent protein kinase I promotes adhesion of primary vascular smooth muscle cells. / Weinmeister, Pascal; Lukowski, Robert; Linder, Stefan; Traidl-Hoffmann, Claudia; Hengst, Ludger; Hofmann, Franz; Feil, Robert.
In: MOL BIOL CELL, Vol. 19, No. 10, 01.10.2008, p. 4434-41.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Cyclic guanosine monophosphate-dependent protein kinase I promotes adhesion of primary vascular smooth muscle cells
AU - Weinmeister, Pascal
AU - Lukowski, Robert
AU - Linder, Stefan
AU - Traidl-Hoffmann, Claudia
AU - Hengst, Ludger
AU - Hofmann, Franz
AU - Feil, Robert
PY - 2008/10/1
Y1 - 2008/10/1
N2 - The cyclic guanosine monophosphate (cGMP)/cGMP-dependent protein kinase type I (cGKI) pathway regulates many cellular functions. The current study shows that 8-Br-cGMP stimulates the number of attached primary but not that of subcultured murine vascular smooth muscle cells (VSMCs). These effects of 8-Br-cGMP require the presence of cGKI. In agreement with previous studies, cGKI inhibited the number of cells in repeatedly passaged murine VSMCs. Activation of the cGMP/cGKI pathway in freshly isolated primary VSMCs slightly decreased apoptosis and strongly increased cell adhesion. The stimulation of cell adhesion by cGKI involves an inhibition of the RhoA/Rho kinase pathway and increased exposure of beta(1) and beta(3) integrins on the cell surface. Together, these results identify a novel proadhesive function of cGMP/cGKI signaling in primary VSMCs and suggest that the opposing effects of this pathway on VSMC number depend on the phenotypic context of the cells.
AB - The cyclic guanosine monophosphate (cGMP)/cGMP-dependent protein kinase type I (cGKI) pathway regulates many cellular functions. The current study shows that 8-Br-cGMP stimulates the number of attached primary but not that of subcultured murine vascular smooth muscle cells (VSMCs). These effects of 8-Br-cGMP require the presence of cGKI. In agreement with previous studies, cGKI inhibited the number of cells in repeatedly passaged murine VSMCs. Activation of the cGMP/cGKI pathway in freshly isolated primary VSMCs slightly decreased apoptosis and strongly increased cell adhesion. The stimulation of cell adhesion by cGKI involves an inhibition of the RhoA/Rho kinase pathway and increased exposure of beta(1) and beta(3) integrins on the cell surface. Together, these results identify a novel proadhesive function of cGMP/cGKI signaling in primary VSMCs and suggest that the opposing effects of this pathway on VSMC number depend on the phenotypic context of the cells.
KW - Animals
KW - Antigens, CD29
KW - Aorta
KW - Cell Adhesion
KW - Cell Membrane
KW - Cells, Cultured
KW - Cyclic GMP
KW - Cyclic GMP-Dependent Protein Kinases
KW - Integrin beta3
KW - Intracellular Signaling Peptides and Proteins
KW - Mice
KW - Models, Biological
KW - Muscle, Smooth, Vascular
KW - Subcellular Fractions
U2 - 10.1091/mbc.E08-04-0370
DO - 10.1091/mbc.E08-04-0370
M3 - SCORING: Journal article
C2 - 18685080
VL - 19
SP - 4434
EP - 4441
JO - MOL BIOL CELL
JF - MOL BIOL CELL
SN - 1059-1524
IS - 10
ER -