Sinusoidal endothelial fenestrae organization regulated by myosin light chain kinase and Rho-kinase in cultured rat sinusoidal endothelial cells

Lanthanum caused endothelial barrier hyperpermeability, loss of VE-cadherin and rearrangement of the actin cytoskeleton, though intracellular Ca2+-mediated RhoA/ROCK and MLCK pathways.

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Mildly Oxidized Low Density Lipoprotein Induces Contraction of Human Endothelial Cells through Activation of Rho/Rho Kinase and Inhibition of Myosin Light Chain Phosphatase

Journal of Biological Chemistry ◽

10.1074/jbc.274.43.30361 ◽

1999 ◽

Vol 274 (43) ◽

pp. 30361-30364 ◽

Cited By ~ 93

Author(s):

Markus Essler ◽

Michaela Retzer ◽

Markus Bauer ◽

Johan W. Heemskerk ◽

Martin Aepfelbacher ◽

...

Keyword(s):

Endothelial Cells ◽

Light Chain ◽

Myosin Light Chain ◽

Low Density Lipoprotein ◽

Rho Kinase ◽

Density Lipoprotein ◽

Low Density ◽

Oxidized Low Density Lipoprotein ◽

Human Endothelial Cells ◽

Myosin Light Chain Phosphatase

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Roles of Inhibitors of Myosin Light Chain Kinase and Tyrosine Kinase on Cation Influx in Agonist-Stimulated Endothelial Cells

Biochemical and Biophysical Research Communications ◽

10.1006/bbrc.1997.6856 ◽

1997 ◽

Vol 235 (3) ◽

pp. 657-662 ◽

Cited By ~ 17

Author(s):

Reiko Takahashi ◽

Hiroshi Watanabe ◽

Xu-Xia Zhang ◽

Hiroyasu Kakizawa ◽

Hideharu Hayashi ◽

...

Keyword(s):

Endothelial Cells ◽

Tyrosine Kinase ◽

Light Chain ◽

Myosin Light Chain Kinase ◽

Myosin Light Chain

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Myosin light chain kinase regulates cell polarization independently of membrane tension or Rho kinase

The Journal of Cell Biology ◽

10.1083/jcb.201409001 ◽

2015 ◽

Vol 209 (2) ◽

pp. 275-288 ◽

Cited By ~ 24

Author(s):

Sunny S. Lou ◽

Alba Diz-Muñoz ◽

Orion D. Weiner ◽

Daniel A. Fletcher ◽

Julie A. Theriot

Keyword(s):

Cell Polarity ◽

Light Chain ◽

Myosin Light Chain Kinase ◽

Myosin Light Chain ◽

Rho Kinase ◽

Model System ◽

Cell Polarization ◽

Membrane Tension ◽

Specific Mechanism

Cells polarize to a single front and rear to achieve rapid actin-based motility, but the mechanisms preventing the formation of multiple fronts are unclear. We developed embryonic zebrafish keratocytes as a model system for investigating establishment of a single axis. We observed that, although keratocytes from 2 d postfertilization (dpf) embryos resembled canonical fan-shaped keratocytes, keratocytes from 4 dpf embryos often formed multiple protrusions despite unchanged membrane tension. Using genomic, genetic, and pharmacological approaches, we determined that the multiple-protrusion phenotype was primarily due to increased myosin light chain kinase (MLCK) expression. MLCK activity influences cell polarity by increasing myosin accumulation in lamellipodia, which locally decreases protrusion lifetime, limiting lamellipodial size and allowing for multiple protrusions to coexist within the context of membrane tension limiting protrusion globally. In contrast, Rho kinase (ROCK) regulates myosin accumulation at the cell rear and does not determine protrusion size. These results suggest a novel MLCK-specific mechanism for controlling cell polarity via regulation of myosin activity in protrusions.

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Rat pulmonary arterial smooth muscle myosin light chain kinase and phosphatase activities decrease with age

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00145.2005 ◽

2006 ◽

Vol 290 (3) ◽

pp. L509-L516 ◽

Cited By ~ 13

Author(s):

J. Belik ◽

Ewa Kerc ◽

Mary D. Pato

Keyword(s):

Smooth Muscle ◽

Light Chain ◽

Myosin Light Chain Kinase ◽

Myosin Light Chain ◽

Rho Kinase ◽

Adult Tissue ◽

Adult Rat ◽

Pulmonary Arterial ◽

Pulmonary Arterial Smooth Muscle ◽

Specific Activities

We and others have shown that the fetal pulmonary arterial smooth muscle potential for contraction and relaxation is significantly reduced compared with the adult. Whether these developmental changes relate to age differences in the expression and/or activity of key enzymes regulating the smooth muscle mechanical properties has not been previously evaluated. Therefore, we studied the catalytic activities and expression of myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP) catalytic (PP1cδ) and regulatory (MYPT) subunits in late fetal, early newborn, and adult rat intrapulmonary arterial tissues. In keeping with the greater force development and relaxation of adult pulmonary artery, Western blot analysis showed that the MLCK, MYPT, and PP1cδ contents increased significantly with age and were highest in the adult rat. In contrast, their specific activities (activity/enzyme content) were significantly higher in the fetal compared with the adult tissue. The fetal and newborn pulmonary arterial muscle relaxant response to the Rho-kinase inhibitor Y-27632 was greater than the adult tissue. In addition to the 130-kDa isoform of MLCK, we documented the presence of minor higher-molecular-weight embryonic isoforms in the fetus and newborn. During fetal life, the lung pulmonary arterial MLCK- and MLCP-specific activities are highest and appear to be related to Rho-kinase activation during lung morphogenesis.

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