scholarly journals The Role of Mechanotransduction on Vascular Smooth Muscle Myocytes Cytoskeleton and Contractile Function

2014 ◽  
Vol 297 (9) ◽  
pp. 1758-1769 ◽  
Author(s):  
George J.C. Ye ◽  
Alexander P. Nesmith ◽  
Kevin Kit Parker
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Contractile Function

Role of Sarcoplasmic Reticulum in the Contractile Function of Vascular Smooth Muscle as Studied by 2,5-Di-(Tert-Butyl)-1,4-Benzohydroquinone

Neurosignals ◽  
1992 ◽  
Vol 1 (4) ◽  
pp. 182-193 ◽  
Author(s):  
Hiroyuki Shimamoto ◽  
Ingrid L.A. Majarais ◽  
Yoriko Shimamoto ◽  
Chiu-Yin Kwan ◽  
Edwin E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Vascular Smooth Muscle ◽  
Contractile Function ◽  
Tert Butyl

Defective autophagy in vascular smooth muscle cells alters contractility and Ca2+ homeostasis in mice

2015 ◽  
Vol 308 (6) ◽  
pp. H557-H567 ◽  
Author(s):  
Cédéric F. Michiels ◽  
Paul Fransen ◽  
Dorien G. De Munck ◽  
Guido R. Y. De Meyer ◽  
Wim Martinet
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Vascular Smooth Muscle ◽  
Vascular Reactivity ◽  
Contractile Function ◽  
Cell Types ◽  
Resting Membrane Potential ◽  
Plasmic Reticulum ◽  
Old Mice

Autophagy is an evolutionary preserved process that prevents the accumulation of unwanted cytosolic material through the formation of autophagosomes. Although autophagy has been extensively studied to understand its function in normal physiology, the role of vascular smooth muscle (SM) cell (VSMC) autophagy in Ca2+ mobilization and contraction remains poorly understood. Recent evidence shows that autophagy is involved in controlling contractile function and Ca2+ homeostasis in certain cell types. Therefore, autophagy might also regulate contractile capacity and Ca2+-mobilizing pathways in VSMCs. Contractility (organ chambers) and Ca2+ homeostasis (myograph) were investigated in aortic segments of 3.5-mo-old mice containing a SM cell-specific deletion of autophagy-related 7 ( Atg7; Atg7 fl/ fl SM22α -Cre+ mice) and in segments of corresponding control mice ( Atg7+/+ SM22α -Cre+). Our results indicate that voltage-gated Ca2+ channels (VGCCs) of Atg7 fl/ fl SM22α -Cre+ VSMCs were more sensitive to depolarization, independent of changes in resting membrane potential. Contractions elicited with K+ (50 mM) or the VGCC agonist BAY K8644 (100 nM) were significantly higher due to increased VGCC expression and activity. Interestingly, the sarcoplasmic reticulum of Atg7 fl/ fl SM22α -Cre+ VSMCs was enlarged, which, combined with increased sarco(endo)plasmic reticulum Ca2+-ATPase 2 expression and higher store-operated Ca2+ entry, promoted inositol 1,4,5-trisphosphate-mediated contractions of Atg7 fl/ fl SM22α -Cre+ segments and maximized the Ca2+ storing capacity of the sarcoplasmic reticulum. Moreover, decreased plasma membrane Ca2+-ATPase expression in Atg7 fl/ fl SM22α -Cre+ VSMCs hampered Ca2+ extrusion to the extracellular environment. Overall, our study indicates that defective autophagy in VSMCs leads to an imbalance between Ca2+ release/influx and Ca2+ reuptake/extrusion, resulting in higher basal Ca2+ concentrations and significant effects on vascular reactivity.

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.

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