Cyclic guanosine monophosphate-dependent protein kinase I promotes adhesion of primary vascular smooth muscle cells

Standard

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, Jahrgang 19, Nr. 10, 01.10.2008, S. 4434-41.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Weinmeister, P, Lukowski, R, Linder, S, Traidl-Hoffmann, C, Hengst, L, Hofmann, F & Feil, R 2008, 'Cyclic guanosine monophosphate-dependent protein kinase I promotes adhesion of primary vascular smooth muscle cells', MOL BIOL CELL, Jg. 19, Nr. 10, S. 4434-41. https://doi.org/10.1091/mbc.E08-04-0370

APA

Vancouver

Bibtex

@article{1966a209d7c34f9d8a3594a26062c07d,
title = "Cyclic guanosine monophosphate-dependent protein kinase I promotes adhesion of primary vascular smooth muscle cells",
abstract = "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.",
keywords = "Animals, Antigens, CD29, Aorta, Cell Adhesion, Cell Membrane, Cells, Cultured, Cyclic GMP, Cyclic GMP-Dependent Protein Kinases, Integrin beta3, Intracellular Signaling Peptides and Proteins, Mice, Models, Biological, Muscle, Smooth, Vascular, Subcellular Fractions",
author = "Pascal Weinmeister and Robert Lukowski and Stefan Linder and Claudia Traidl-Hoffmann and Ludger Hengst and Franz Hofmann and Robert Feil",
year = "2008",
month = oct,
day = "1",
doi = "10.1091/mbc.E08-04-0370",
language = "English",
volume = "19",
pages = "4434--41",
journal = "MOL BIOL CELL",
issn = "1059-1524",
publisher = "American Society for Cell Biology",
number = "10",

}

RIS

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 -