Orientation of Nuclei as Indicators of Smooth Muscle Cell Alignment in the Cerebral Artery

1979 ◽  
Vol 16 (1) ◽  
pp. 43-51 ◽  
Author(s):  
James G. Walmsley ◽  
Peter B. Canham
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cerebral Artery ◽  
Cell Alignment

scholarly journals Distinct Effects of Ca2+ Sparks on Cerebral Artery and Airway Smooth Muscle Cell Tone in Mice and Humans

2017 ◽  
Vol 13 (10) ◽  
pp. 1242-1253
Author(s):  
Qing-Yang Zhao ◽  
Yong-Bo Peng ◽  
Xiao-Jing Luo ◽  
Xi Luo ◽  
Hao Xu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Airway Smooth Muscle ◽  
Muscle Cell ◽  
Cerebral Artery ◽  
Airway Smooth Muscle Cell

scholarly journals Interstitial cells from rat middle cerebral artery belong to smooth muscle cell type

2009 ◽  
Vol 13 (11-12) ◽  
pp. 4532-4539 ◽  
Author(s):  
Maksym I. Harhun ◽  
Kinga Szewczyk ◽  
Holger Laux ◽  
Sally A. Prestwich ◽  
Dmitri V. Gordienko ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Middle Cerebral Artery ◽  
Muscle Cell ◽  
Cerebral Artery ◽  
Interstitial Cells ◽  
Cell Type ◽  
Muscle Cell Type

Cyclic stretch induces vascular smooth muscle cell alignment via NO signaling

2002 ◽  
Vol 283 (5) ◽  
pp. H1907-H1914 ◽  
Author(s):  
Paul R. Standley ◽  
Antonino Camaratta ◽  
Brian P. Nolan ◽  
Christian T. Purgason ◽  
Melinda A. Stanley
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cyclic Stretch ◽  
Cell Alignment ◽  
No Donor ◽  
Vsmc Proliferation ◽  
No Signaling

We investigated the effects of cyclic stretch on vascular smooth muscle cell (VSMC) alignment and potential overlap of signaling modalities with stretch-induced proliferation. VSMC were subjected to graded stretch (1 Hz at 100–124% of resting length) for 48 h. Graded stretch resulted in graded VSMC alignment from a minimum of completely random orientation to a maximum of ∼80–85° to the stretch vector. Alignment was reversible within 48 h of stretch cessation and independent of signaling modalities mediating stretch-induced proliferation: modulation of IGF-1, MAPK, phosphatidylinositol 3-kinase, tyrosine kinase, and stretch-activated calcium channels did not affect alignment. Nitric oxide (NO) synthase (NOS) blockade uncoupled alignment. Neither the NO donor, cytokine-induced NOS activity, nor l-citrulline affected alignment, but inhibited VSMC proliferation. Therefore, stretch-induced proliferation and alignment are differentially regulated, with NO a common signaling molecule for both. Targeting NOS in states such as restenosis and hypertension may prove to be beneficial.

Evidence for the involvement of myoendothelial gap junctions in EDHF-mediated relaxation in the rat middle cerebral artery

2006 ◽  
Vol 291 (1) ◽  
pp. H385-H393 ◽  
Author(s):  
Elke M. Sokoya ◽  
Alan R. Burns ◽  
Christopher T. Setiawan ◽  
Harold A. Coleman ◽  
Helena C. Parkington ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Gap Junctions ◽  
Smooth Muscle Cell ◽  
Middle Cerebral Artery ◽  
Muscle Cell ◽  
Cerebral Artery ◽  
Male Rat ◽  
Direct Communication

The mechanisms underlying endothelium-dependent hyperpolarizing factor (EDHF) in the middle cerebral artery (MCA) remain largely unresolved. In particular, very little is known regarding the way in which the signal is transmitted from endothelium to smooth muscle. The present study tested the hypothesis that direct communication via myoendothelial gap junctions contributes to the EDHF response in the male rat MCA. EDHF-mediated dilations were elicited in rat MCAs by luminal application of ATP or UTP in the presence of Nω-nitro-l-arginine methyl ester and indomethacin. Maximum dilation to luminal ATP (10−4 M) was reduced significantly after incubation with a gap peptide cocktail (9 ± 4%, n = 6) compared with a scrambled gap peptide cocktail (99 ± 1%, n = 6, P < 0.05). A gap peptide cocktail had no effect on amplitude of endothelial cell hyperpolarization in response to 3 × 10−5 M UTP (22 ± 3 vs. 22 ± 1 mV, n = 4), whereas smooth muscle cell hyperpolarization was significantly attenuated (17 ± 1 vs. 6 ± 1 mV, n = 4, P = 0.004). Connexin (Cx) 37 was localized to smooth muscle and Cx43 to endothelium, whereas Cx40 was found in endothelium and smooth muscle. Electron microscopy revealed the existence of frequent myoendothelial junctions. The total number of myoendothelial junctions per 5 μm of MCA sectioned was 2.5 ± 0.5. Our results suggest that myoendothelial communication contributes to smooth muscle cell hyperpolarization and EDHF dilation in male rat MCA.

scholarly journals Cyclic stretch stimulates vascular smooth muscle cell alignment by redox-dependent activation of Notch3

2011 ◽  
Vol 300 (5) ◽  
pp. H1770-H1780 ◽  
Author(s):  
Jian-Hong Zhu ◽  
Chun-Lin Chen ◽  
Sheila Flavahan ◽  
Jennifer Harr ◽  
Baogen Su ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Butyl Ester ◽  
Physiological Role ◽  
Cyclic Stretch ◽  
Cell Alignment ◽  
Proteolytic Activation

Mice deficient in Notch3 have defects in arterial vascular smooth muscle cell (VSMC) mechanosensitivity, including impaired myogenic responses and autoregulation, and inappropriate VMSC orientation. Experiments were performed to determine if Notch3 is activated by mechanical stimulation and contributes to mechanosensitive responses of VSMCs, including cell realignment. Cyclic, uniaxial stretch (10%, 1 Hz) of human VSMCs caused Notch3 activation, demonstrated by a stretch-induced increase in hairy and enhancer of split 1/hairy-related transcription factor-1 expression, translocation of Notch3 to the nucleus, and a decrease in the Notch3 extracellular domain. These effects were prevented by inhibiting the expression [small interfering (si)RNA] or proteolytic activation of Notch3 { N-( R)-[2-(hydroxyaminocarbonyl)methyl]−4-methylpentanoyl-l-naphthylalanyl-l-alanine-2-aminoethyl amide (TAPI-1; 50 μmol/l) to inhibit TNF-α-converting enzyme (TACE) or N-[ N-(3,5-difluorophenacetyl-l-alanyl)]- S-phenylglycine t-butyl ester (DAPT; 20 μmol/l) to inhibit γ-secretase}. Stretch increased the activity of ROS within VSMCs, determined using dichlorodihydrofluorescein fluorescence. Catalase (1,200 U/ml), which degrades H2O2, inhibited the stretch-induced activation of Notch3, whereas in nonstretched cells, increasing H2O2 activity [H2O2 or manganese(III) tetrakis(1-methyl-4-pyridyl)porphyrin] caused activation of Notch3. Stretch increased the activity of TACE, which was prevented by catalase. Stretch-induced activation of p38 MAPK in VSMCs was inhibited either by catalase or by inhibiting Notch3 expression (siRNA). Stretch caused VSMCs to realign perpendicular to the direction of the mechanical stimulus, which was significantly inhibited by catalase or by inhibiting the expression (siRNA) or activation of Notch3 (TAPI-1 or DAPT). Therefore, cyclic uniaxial stretch activates Notch3 signaling through a ROS-mediated mechanism, and the presence of Notch3 is necessary for proper stretch-induced cell alignment in VSMCs. This mechanism may contribute to the physiological role of Notch3 in mediating developmental maturation of VSMCs.

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