scholarly journals Pathophysiological Role of Vascular Smooth Muscle Alkaline Phosphatase in Medial Artery Calcification

2015 ◽  
Vol 30 (5) ◽  
pp. 824-836 ◽  
Author(s):  
Campbell R Sheen ◽  
Pia Kuss ◽  
Sonoko Narisawa ◽  
Manisha C Yadav ◽  
Jessica Nigro ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Pathophysiological Role ◽  
Medial Artery Calcification ◽  
Medial Artery

Pathophysiological Role of the Vascular Smooth Muscle Cell

1990 ◽  
Vol 16 ◽  
pp. S4-S11 ◽  
Author(s):  
Jean-Baptiste Michel ◽  
Nicolas De Roux ◽  
Didier Plissonnier ◽  
Samy Anidjar ◽  
Jean-Loup Salzmann ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Pathophysiological Role

scholarly journals Extracellular pyrophosphate metabolism and calcification in vascular smooth muscle

2011 ◽  
Vol 301 (1) ◽  
pp. H61-H68 ◽  
Author(s):  
Ricardo Villa-Bellosta ◽  
Xiaonan Wang ◽  
José Luis Millán ◽  
George R. Dubyak ◽  
W. Charles O'Neill
Keyword(s):  
Alkaline Phosphatase ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Calcification ◽  
Endogenous Inhibitor ◽  
Inorganic Pyrophosphate ◽  
Inhibitory Role ◽  
Tissue Nonspecific Alkaline Phosphatase ◽  
Hydrolysis Of

Extracellular inorganic pyrophosphate (ePPi) is an important endogenous inhibitor of vascular calcification, but it is not known whether systemic or local vascular PPi metabolism controls calcification. To determine the role of ePPi in vascular smooth muscle, we identified the pathways responsible for ePPi production and hydrolysis in rat and mouse aortas and manipulated them to demonstrate their role in the calcification of isolated aortas in culture. Rat and mouse aortas contained mRNA for ectonucleotide pyrophosphatase/phosphodiesterases (NPP1–3), the putative PPi transporter ANK, and tissue-nonspecific alkaline phosphatase (TNAP). Synthesis of PPi from ATP in aortas was blocked by β,γ-methylene-ATP, an inhibitor of NPPs. Aortas from mice lacking NPP1 ( Enpp1−/−) did not synthesize PPi from ATP and exhibited increased calcification in culture. Although ANK-mediated transport of PPi could not be demonstrated in aortas, aortas from mutant ( ank/ank) mice calcified more in culture than did aortas from normal (ANK/ANK) mice. Hydrolysis of PPi was reduced 25% by β,γ-methylene-ATP and 50% by inhibition of TNAP. Hydrolysis of PPi was increased in cells overexpressing TNAP or NPP3 but not NPP1 and was not reduced in Enpp1−/− aortas. Overexpression of TNAP increased calcification of cultured aortas. The results show that smooth muscle NPP1 and TNAP control vascular calcification through effects on synthesis and hydrolysis of ePPi, indicating an important inhibitory role of locally produced PPi. Smooth muscle ANK also affects calcification, but this may not be mediated through transport of PPi. NPP3 is identified as an additional pyrophosphatase that could influence vascular calcification.

Pathophysiological Role of the Vascular Smooth Muscle Cell

1990 ◽  
Vol 16 ◽  
pp. S4-S11 ◽  
Author(s):  
Jean-Baptiste Michel ◽  
Nicolas De Roux ◽  
Didier Plissonnier ◽  
Samy Anidjar ◽  
Jean-Loup Salzmann ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Pathophysiological Role

scholarly journals The role of mitochondrial bioenergetics and reactive oxygen species in coronary collateral growth

2013 ◽  
Vol 305 (9) ◽  
pp. H1275-H1280 ◽  
Author(s):  
Yuh Fen Pung ◽  
Wai Johnn Sam ◽  
James P. Hardwick ◽  
Liya Yin ◽  
Vahagn Ohanyan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Synthesis ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Energy Production ◽  
Phenotypic Switching ◽  
Oxygen Species ◽  
Coronary Collateral ◽  
Collateral Growth

Coronary collateral growth is a process involving coordination between growth factors expressed in response to ischemia and mechanical forces. Underlying this response is proliferation of vascular smooth muscle and endothelial cells, resulting in an enlargement in the caliber of arterial-arterial anastomoses, i.e., a collateral vessel, sometimes as much as an order of magnitude. An integral element of this cell proliferation is the process known as phenotypic switching in which cells of a particular phenotype, e.g., contractile vascular smooth muscle, must change their phenotype to proliferate. Phenotypic switching requires that protein synthesis occurs and different kinase signaling pathways become activated, necessitating energy to make the switch. Moreover, kinases, using ATP to phosphorylate their targets, have an energy requirement themselves. Mitochondria play a key role in the energy production that enables phenotypic switching, but under conditions where mitochondrial energy production is constrained, e.g., mitochondrial oxidative stress, this switch is impaired. In addition, we discuss the potential importance of uncoupling proteins as modulators of mitochondrial reactive oxygen species production and bioenergetics, as well as the role of AMP kinase as an energy sensor upstream of mammalian target of rapamycin, the master regulator of protein synthesis.

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
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