scholarly journals Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

2014 ◽  
Vol 34 (5) ◽  
pp. 1497-1506 ◽  
Author(s):  
Maria Alicia Carrillo-Sepulveda ◽  
Takayuki Matsumoto
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Diabetic Rats ◽  
Phenotypic Modulation ◽  
Caveolin 1 ◽  
Type 2 Diabetic

scholarly journals Angiotensin II type 2 receptor activation induces RhoA inhibition through Phosphorylation of its Serine 188 in Vascular Smooth Muscle Cells

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Malvyne Rolli‐Derkinderen ◽  
Christophe Guilluy ◽  
Laurent Loufrani ◽  
Daniel Henrion ◽  
Gervaise Loirand ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Receptor Activation

Urokinase-receptor-mediated phenotypic changes in vascular smooth muscle cells require the involvement of membrane rafts

2009 ◽  
Vol 423 (3) ◽  
pp. 343-351 ◽  
Author(s):  
Julia Kiyan ◽  
Graham Smith ◽  
Hermann Haller ◽  
Inna Dumler
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Lipid Rafts ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Caveolin 1 ◽  
Phenotypic Changes ◽  
Dependent Cell

The cholesterol-enriched membrane microdomains lipid rafts play a key role in cell activation by recruiting and excluding specific signalling components of cell-surface receptors upon receptor engagement. Our previous studies have demonstrated that the GPI (glycosylphosphatidylinositol)-linked uPAR [uPA (urokinase-type plasminogen activator) receptor], which can be found in lipid rafts and in non-raft fractions, can mediate the differentiation of VSMCs (vascular smooth muscle cells) towards a pathophysiological de-differentiated phenotype. However, the mechanism by which uPAR and its ligand uPA regulate VSMC phenotypic changes is not known. In the present study, we provide evidence that the molecular machinery of uPAR-mediated VSMC differentiation employs lipid rafts. We show that the disruption of rafts in VSMCs by membrane cholesterol depletion using MCD (methyl-β-cyclodextrin) or filipin leads to the up-regulation of uPAR and cell de-differentiation. uPAR silencing by means of interfering RNA resulted in an increased expression of contractile proteins. Consequently, disruption of lipid rafts impaired the expression of these proteins and transcriptional activity of related genes. We provide evidence that this effect was mediated by uPAR. Similar effects were observed in VSMCs isolated from Cav1−/− (caveolin-1-deficient) mice. Despite the level of uPAR being significantly higher after the disruption of the rafts, uPA/uPAR-dependent cell migration was impaired. However, caveolin-1 deficiency impaired only uPAR-dependent cell proliferation, whereas cell migration was strongly up-regulated in these cells. Our results provide evidence that rafts are required in the regulation of uPAR-mediated VSMC phenotypic modulations. These findings suggest further that, in the context of uPA/uPAR-dependent processes, caveolae-associated and non-associated rafts represent different signalling membrane domains.

Altered L-type Ca2+ channel currents in vascular smooth muscle cells from experimental diabetic rats

2000 ◽  
Vol 278 (3) ◽  
pp. H714-H722 ◽  
Author(s):  
Rui Wang ◽  
Yuejin Wu ◽  
Guanghua Tang ◽  
Lingyun Wu ◽  
Salma Toma Hanna
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Complications ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
High Concentration ◽  
Voltage Dependent

Vascular complications of diabetes are associated with abnormal Ca2+ handling by vascular smooth muscle cells (SMCs) in which the alteration in L-type voltage-dependent Ca2+ channel (VDCC) currents may play an important role. In the present study, the characteristics of L-type VDCC currents in tail artery SMCs from streptozotocin-induced diabetic rats were examined. The densities, but not the voltage dependence, of L-type VDCC currents were reduced as diabetes progressed from 1 wk to 3 mo. The inhibitory effect of dibutyryl-cAMP on L-type VDCC currents was greater in diabetic SMCs than in age-matched control cells ( P < 0.01). Both the stimulatory effect of BAY K 8644 and the inhibitory effect of nifedipine on L-type VDCC currents were significantly enhanced in diabetic cells. The diabetes-related abnormalities in L-type VDCC currents were mimicked by culturing SMCs with a high concentration of glucose. Our results suggest that the properties of L-type VDCC in diabetic vascular SMCs were significantly altered, partially related to the increased L-type VDCC sensitivity to cAMP and hyperglycemia.

Sign in / Sign up

Export Citation Format

Share Document