scholarly journals A conserved MADS-box phosphorylation motif regulates differentiation and mitochondrial function in skeletal, cardiac, and smooth muscle cells

2015 ◽  
Vol 6 (10) ◽  
pp. e1944-e1944 ◽  
Author(s):  
W Mughal ◽  
L Nguyen ◽  
S Pustylnik ◽  
S C da Silva Rosa ◽  
S Piotrowski ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mitochondrial Function ◽  
Muscle Cells ◽  
Mads Box ◽  
Phosphorylation Motif

A kinase anchor protein 121 regulates mitochondrial function and survival in cardiac and smooth muscle cells

2007 ◽  
Vol 42 (6) ◽  
pp. S81-S82
Author(s):  
Cinzia Perrino ◽  
Giuseppe Gargiulo ◽  
Giuseppe Ambrosio ◽  
Rosalia Guerriero ◽  
Massimo Chiariello
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mitochondrial Function ◽  
Muscle Cells ◽  
Anchor Protein

Altered mitochondrial function in proliferating airway smooth muscle cells

2019 ◽  
Author(s):  
Charalambos Michaeloudes ◽  
Julia Frankenberg Garcia ◽  
Bingling Xu ◽  
Xia Li ◽  
Christopher Hui ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Mitochondrial Function ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells

scholarly journals Differential Mitochondrial Adaptation in Primary Vascular Smooth Muscle Cells from a Diabetic Rat Model

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Amy C. Keller ◽  
Leslie A. Knaub ◽  
P. Mason McClatchey ◽  
Chelsea A. Connon ◽  
Ron Bouchard ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mitochondrial Function ◽  
High Glucose ◽  
Vascular Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Muscle Cells ◽  
Nutrient Stress

Diabetes affects more than 330 million people worldwide and causes elevated cardiovascular disease risk. Mitochondria are critical for vascular function, generate cellular reactive oxygen species (ROS), and are perturbed by diabetes, representing a novel target for therapeutics. We hypothesized that adaptive mitochondrial plasticity in response to nutrient stress would be impaired in diabetes cellular physiology via a nitric oxide synthase- (NOS-) mediated decrease in mitochondrial function. Primary smooth muscle cells (SMCs) from aorta of the nonobese, insulin resistant rat diabetes model Goto-Kakizaki (GK) and the Wistar control rat were exposed to high glucose (25 mM). At baseline, significantly greater nitric oxide evolution, ROS production, and respiratory control ratio (RCR) were observed in GK SMCs. Upon exposure to high glucose, expression of phosphorylated eNOS, uncoupled respiration, and expression of mitochondrial complexes I, II, III, and V were significantly decreased in GK SMCs (p<0.05). Mitochondrial superoxide increased with high glucose in Wistar SMCs (p<0.05) with no change in the GK beyond elevated baseline concentrations. Baseline comparisons show persistent metabolic perturbations in a diabetes phenotype. Overall, nutrient stress in GK SMCs caused a persistent decline in eNOS and mitochondrial function and disrupted mitochondrial plasticity, illustrating eNOS and mitochondria as potential therapeutic targets.

4-Hydroxy tempol-induced impairment of mitochondrial function and augmentation of glucose transport in vascular endothelial and smooth muscle cells

2004 ◽  
Vol 67 (10) ◽  
pp. 1985-1995 ◽  
Author(s):  
Evgenia Alpert ◽  
Hamutal Altman ◽  
Hanan Totary ◽  
Arie Gruzman ◽  
Dana Barnea ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Glucose Transport ◽  
Mitochondrial Function ◽  
Muscle Cells ◽  
Vascular Endothelial

Experimental studies of mitochondrial function in CADASIL vascular smooth muscle cells

2013 ◽  
Vol 319 (3) ◽  
pp. 134-143 ◽  
Author(s):  
Matti Viitanen ◽  
Erik Sundström ◽  
Marc Baumann ◽  
Minna Poyhonen ◽  
Saara Tikka ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mitochondrial Function ◽  
Experimental Studies ◽  
Muscle Cells

scholarly journals Telmisartan modulates mitochondrial function in vascular smooth muscle cells

2012 ◽  
Vol 36 (5) ◽  
pp. 433-439 ◽  
Author(s):  
Kiyo Takeuchi ◽  
Koichi Yamamoto ◽  
Mitsuru Ohishi ◽  
Hikari Takeshita ◽  
Kazuhiro Hongyo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mitochondrial Function ◽  
Muscle Cells

Requirement of the MADS-box transcription factor MEF2C for vascular development

Development ◽  
1998 ◽  
Vol 125 (22) ◽  
pp. 4565-4574 ◽  
Author(s):  
Q. Lin ◽  
J. Lu ◽  
H. Yanagisawa ◽  
R. Webb ◽  
G.E. Lyons ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Transcription Factor ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cells ◽  
Target Genes ◽  
Vascular Development ◽  
Muscle Cells ◽  
Mads Box ◽  
Vascular Plexus

The embryonic vasculature develops from endothelial cells that form a primitive vascular plexus which recruits smooth muscle cells to form the arterial and venous systems. The MADS-box transcription factor MEF2C is expressed in developing endothelial cells and smooth muscle cells (SMCs), as well as in surrounding mesenchyme, during embryogenesis. Targeted deletion of the mouse MEF2C gene resulted in severe vascular abnormalities and lethality in homozygous mutants by embryonic day 9.5. Endothelial cells were present and were able to differentiate, but failed to organize normally into a vascular plexus, and smooth muscle cells did not differentiate in MEF2C mutant embryos. These vascular defects resemble those in mice lacking the vascular-specific endothelial cell growth factor VEGF or its receptor Flt-1, both of which are expressed in MEF2C mutant embryos. These results reveal multiple roles for MEF2C in vascular development and suggest that MEF2-dependent target genes mediate endothelial cell organization and SMC differentiation.

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