scholarly journals Differential Effect of Hypoxia in Human and Mouse Vascular Smooth Muscle Cell Migration through LRP1-pPyk2-MMP-9 Axis

2015 ◽  
Vol 2015 ◽  
pp. 1-9
Author(s):  
E. Revuelta-López ◽  
J. Castellano ◽  
D. de Gonzalo-Calvo ◽  
L. Nasarre ◽  
L. Badimon ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Animal Models ◽  
Vascular Smooth Muscle ◽  
Differential Effect ◽  
Translational Study ◽  
Hypoxic Conditions ◽  
Inverse Effect ◽  
Smooth Muscle Cell Migration ◽  
Human And Mouse

LRP1-pPyk2 axis is essential for the upregulatory effect of hypoxia on MMP-9 activation and human VSMC (hVSMC) migration. Currently, there are not efficient models for the translational study of atherosclerosis. The morphological and physiological features of atherosclerosis are different between human and animal models, particularly in mouse models. Therefore, the aim of current investigation was to compare the effect of hypoxia on LRP1-Pyk2-MMP-9 axis in human and mouse vascular smooth muscle cells (mVSMC) and its consequences on VSMC migration. We demonstrated that hypoxic modulation of LRP1-pPyk2-MMP-9 axis is opposite between hVSMC and mVSMC. The modulation of LRP1/pPyk2 levels by hypoxia is positive in hVSMC but negative in mVSMC. We showed that the inverse effect of LRP1/pPyk2 axis is associated with a differential effect of hypoxia on MMP-9 expression and activation. Hypoxia-induced MMP-9 activation was concomitant with an increased hVSMC migratory capacity. Surprisingly, mVSMC migrate under hypoxic conditions despite the downregulatory effect of hypoxia on MMP-9 expression or activation. Our results highlight the crucial role of LRP1-pPyk2-MMP-9 axis in vascular cell migration. In addition, we propose that the extrapolation of results from animal models to humans is not suitable for this specific mechanism in hypoxia-related vascular conditions.

scholarly journals Unexpected Role of the Copper Transporter ATP7A in PDGF-Induced Vascular Smooth Muscle Cell Migration

2010 ◽  
Vol 107 (6) ◽  
pp. 787-799 ◽  
Author(s):  
Takashi Ashino ◽  
Varadarajan Sudhahar ◽  
Norifumi Urao ◽  
Jin Oshikawa ◽  
Gin-Fu Chen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Copper Transporter ◽  
Smooth Muscle Cell Migration

Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation

2014 ◽  
Vol 63 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Junxia Zhang ◽  
Haiwei Wang ◽  
Lijun Zhang ◽  
Tengteng Zhang ◽  
Beibei Wang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Botulinum Toxin ◽  
Vascular Smooth Muscle ◽  
Chlamydia Pneumoniae ◽  
Leading Edge ◽  
Primary Role ◽  
Phosphatidylinositol 3 Kinase ◽  
Smooth Muscle Cell Migration

Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum toxin substrate 1 (Rac1) is to generate a protrusive force at the leading edge that contributes to cell migration. Whether Rac1 activation plays a role in C. pneumoniae infection-induced VSMC migration is not well defined. In the present study, we therefore examined Rac1 activation in C. pneumoniae-infected rat primary VSMCs and the role of Rac1 activation in C. pneumoniae infection-induced VSMC migration. Glutathione S-transferase pull-down assay results showed that Rac1 was activated in C. pneumoniae-infected rat primary VSMCs. A Rac1 inhibitor, NSC23766 (50 µM,) suppressed Rac1 activation stimulated by C. pneumoniae infection, and thereby inhibited C. pneumoniae infection-induced VSMC migration. In addition, C. pneumoniae infection-induced Rac1 activation in the VSMCs was blocked by LY294002 (25 µM), an inhibitor of phosphatidylinositol 3-kinase (PI3K). Taken together, these data suggest that C. pneumoniae infection promotes VSMC migration, possibly through activating Rac1 via PI3K.

scholarly journals Testosterone Induces Vascular Smooth Muscle Cell Migration by NADPH Oxidase and c-Src–Dependent Pathways

Hypertension ◽  
2012 ◽  
Vol 59 (6) ◽  
pp. 1263-1271 ◽  
Author(s):  
Andreia Z. Chignalia ◽  
Elke Z. Schuldt ◽  
Lívia L. Camargo ◽  
Augusto C. Montezano ◽  
Gláucia E. Callera ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Vascular Smooth Muscle ◽  
Nadph Oxidase ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Smooth Muscle Cell Migration
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