scholarly journals SUN1/2 Are Essential for RhoA/ROCK-Regulated Actomyosin Activity in Isolated Vascular Smooth Muscle Cells

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 132
Author(s):  
Lauren Porter ◽  
Rose-Marie Minaisah ◽  
Sultan Ahmed ◽  
Seema Ali ◽  
Rosemary Norton ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Coiled Coil ◽  
Muscle Cells ◽  
Linc Complex ◽  
Cell Type ◽  
Rhoa Activity ◽  
Predominant Cell Type

Vascular smooth muscle cells (VSMCs) are the predominant cell type in the blood vessel wall. Changes in VSMC actomyosin activity and morphology are prevalent in cardiovascular disease. The actin cytoskeleton actively defines cellular shape and the LInker of Nucleoskeleton and Cytoskeleton (LINC) complex, comprised of nesprin and the Sad1p, UNC-84 (SUN)-domain family members SUN1/2, has emerged as a key regulator of actin cytoskeletal organisation. Although SUN1 and SUN2 function is partially redundant, they possess specific functions and LINC complex composition is tailored for cell-type-specific functions. We investigated the importance of SUN1 and SUN2 in regulating actomyosin activity and cell morphology in VSMCs. We demonstrate that siRNA-mediated depletion of either SUN1 or SUN2 altered VSMC spreading and impaired actomyosin activity and RhoA activity. Importantly, these findings were recapitulated using aortic VSMCs isolated from wild-type and SUN2 knockout (SUN2 KO) mice. Inhibition of actomyosin activity, using the rho-associated, coiled-coil-containing protein kinase1/2 (ROCK1/2) inhibitor Y27632 or blebbistatin, reduced SUN2 mobility in the nuclear envelope and decreased the association between SUN2 and lamin A, confirming that SUN2 dynamics and interactions are influenced by actomyosin activity. We propose that the LINC complex exists in a mechanical feedback circuit with RhoA to regulate VSMC actomyosin activity and morphology.

IL-1α-dependent sterile inflammation in atherosclerosis is cell type-dependent and driven by necrotic vascular smooth muscle cells

2012 ◽  
Vol 56 (5-6) ◽  
pp. 372
Author(s):  
Yue Zheng ◽  
Melanie Humphry ◽  
Martin R. Bennett ◽  
Murray C.H. Clarke
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Sterile Inflammation ◽  
Cell Type

scholarly journals Extracellular Vesicles Mediate Communication between Endothelial and Vascular Smooth Muscle Cells

2021 ◽  
Vol 23 (1) ◽  
pp. 331
Author(s):  
Marie Fontaine ◽  
Stéphanie Herkenne ◽  
Olivier Ek ◽  
Alicia Paquot ◽  
Amandine Boeckx ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Extracellular Vesicles ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Communication Tool ◽  
Cell Type ◽  
Cell Functions

The recruitment of pericytes and vascular smooth muscle cells (SMCs) that enwrap endothelial cells (ECs) is a crucial process for vascular maturation and stabilization. Communication between these two cell types is crucial during vascular development and in maintaining vessel homeostasis. Extracellular vesicles (EVs) have emerged as a new communication tool involving the exchange of microRNAs between cells. In the present study, we searched for microRNAs that could be transferred via EVs from ECs to SMCs and vice versa. Thanks to a microRNA profiling experiment, we found that two microRNAs are more exported in each cell type in coculture experiments: while miR-539 is more secreted by ECs, miR-582 is more present in EVs from SMCs. Functional assays revealed that both microRNAs can modulate both cell-type phenotypes. We further identified miR-539 and miR-582 targets, in agreement with their respective cell functions. The results obtained in vivo in the neovascularization model suggest that miR-539 and miR-582 might cooperate to trigger the process of blood vessel coverage by smooth muscle cells in a mature plexus. Taken together, these results are the first to highlight the role of miR-539 and miR-582 in angiogenesis and communication between ECs and SMCs.

scholarly journals Rho/ROCK Signal Cascade Mediates Asymmetric Dimethylarginine-Induced Vascular Smooth Muscle Cells Migration and Phenotype Change

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yi-ming Zhou ◽  
Xi Lan ◽  
Han-bin Guo ◽  
Yan Zhang ◽  
Li Ma ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Asymmetric Dimethylarginine ◽  
Rho Kinase ◽  
Muscle Cells ◽  
Signal Pathway ◽  
Rock Inhibitor ◽  
Rhoa Activity

Asymmetric dimethylarginine (ADMA) induces vascular smooth muscle cells (VSMCs) migration. VSMC phenotype change is a prerequisite of migration. RhoA and Rho-kinase (ROCK) mediate migration of VSMCs. We hypothesize that ADMA induces VSMC migration via the activation of Rho/ROCK signal pathway and due to VSMCs phenotype change. ADMA activates Rho/ROCK signal pathway that interpreted by the elevation of RhoA activity and phosphorylation level of a ROCK substrate. Pretreatment with ROCK inhibitor, Y27632 completely reverses the induction of ADMA on ROCK and in turn inhibits ADMA-induced VSMCs migration. When the Rho/ROCK signal pathway has been blocked by pretreatment with Y27632, the induction of ERK signal pathway by ADMA is completely abrogated. Elimination of ADMA via overexpression of dimethylarginine dimethylaminohydrolase 2 (DDAH2) and L-arginine both blocks the effects of ADMA on the activation of Rho/ROCK and extra cellular signal-regulated kinase (ERK) in VSMCs. The expression of differentiated phenotype relative proteins was reduced and the actin cytoskeleton was disassembled by ADMA, which were blocked by Y27632, further interpreting that ADMA inducing VSMCs migration via Rho/ROCK signal pathway is due to its effect on the VSMCs phenotype change. Our present study may help to provide novel insights into the therapy and prevention of atherosclerosis.

Abstract 009: Ribosomal Profiling of Vascular Smooth Muscle Cells in Vivo Identifies Cell-type Specific Transcripts and Enrichment of Blood Pressure Associated Genes

2018 ◽  
Vol 38 (Suppl_1) ◽  
Author(s):  
Audrey C Cleuren ◽  
Martijn A van der Ent ◽  
Kristina L Hunker ◽  
Min-Lee Yang ◽  
Hui Jiang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Type ◽  
Cell Type Specific

Hypertension‐evoked RhoA activity in vascular smooth muscle cells requires RGS5

2018 ◽  
Vol 32 (4) ◽  
pp. 2021-2035 ◽  
Author(s):  
Caroline Arnold ◽  
Eda Demirel ◽  
Anja Feldner ◽  
Guillem Genové ◽  
Hangjun Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Rhoa Activity

1450: Diabetes-Related Alterations in Connexin43-Derived GAP Junction Permeability in Short Term Cultures of RAT Corporal Vascular Smooth Muscle Cells

2004 ◽  
Vol 171 (4S) ◽  
pp. 382-382
Author(s):  
George Christ ◽  
Hong-Zhan Wang ◽  
Vergas Valiunas ◽  
Peter Brink ◽  
Stony Brook
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junction ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Short Term

GROWTH-RELATED SIGNALING IN VASCULAR SMOOTH MUSCLE CELLS IS DEREGULATED BY TCDD DURING THE G /G TRANSITION 0 1

1997 ◽  
Vol 51 (4) ◽  
pp. 369-386 ◽  
Author(s):  
Thomas J. Weber ◽  
Yang-Yi Fan ◽  
Robert S. Chapkin ◽  
Kenneth S. Ramos
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells
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