Loss and apoptosis of smooth muscle cells in intracranial aneurysms studies with in situ DNA end labeling and antibody against single-stranded DNA

1997 ◽  
Vol 139 (5) ◽  
pp. 469-475 ◽  
Author(s):  
T. Sakaki ◽  
E. Kohmura ◽  
T. Kishiguchi ◽  
T. Yuguchi ◽  
T. Yamashita ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intracranial Aneurysms ◽  
Muscle Cells ◽  
Single Stranded Dna

Histological maturation of vascular smooth muscle cells in in situ tissue-engineered vasculature

Biomaterials ◽  
2014 ◽  
Vol 35 (11) ◽  
pp. 3589-3595 ◽  
Author(s):  
Noriko Isayama ◽  
Goki Matsumura ◽  
Hideki Sato ◽  
Shojiro Matsuda ◽  
Kenji Yamazaki
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

Atheromatosis of arterial intima

2016 ◽  
Vol 94 (8) ◽  
pp. 582-590
Author(s):  
Vladimir N. Titov ◽  
T. A. Rozhkova ◽  
V. A. Amelyushkina
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Proteolytic Enzymes ◽  
Muscle Cells ◽  
Acid Hydrolases ◽  
The Matrix ◽  
Arterial Intima ◽  
Hydrolysis Of

Phylogenetically late arterial intima of the elastic type contains no proteins for the transfer of ligandless oxidized low density lipoproteins (LDLP) for sedentary macrophages adsorbed on the matrix. Phylogenetically early cells realize the extracellular digestive reaction by releasing proteolytic enzymes (metalloproteinases) into intimal matrix that hydrolize matrix proteoglycans, adsorbed ligandless LDLP, detritus, and complete lysosomal hydrolysis of the most hydrophobic polyenic cholesterol esters (poly-ECS). Smooth muscle cells migrate from the middle muscular layer of the arterial wall, change their contractile phenotype to secretory one, and synthesize in situ de novomatrix proteoglycans. The arterial wall has three layers (monolayer endothelium, intimal media (smooth muscle cells), and adventitia) only in elastic type arteries. It is desirable to elucidate functional differences between phylogenetically early sedentarymacrophages and monocytes-macrophages of later origin and understand whether theydepends on specific features of activity of scavenger eceptors, CD36 translocases, expression of acid hydrolases synthesis for poly-ECS or realization of the extracellular digestion reaction. We believe that formation of atheromatous masses takes place in the matrix of arterial intima rather than in lysosomes taking into account limited possibilities for monocytes-macrophages to realize endocytosis of ligandless LDLP from the matrix. Given that atheromatosis is a syndrome of deficit of essential polyenic fatty acids (PFA) in the cells, intimal atheromatosisshould be regarded only as partial utilization of excess PFA in the matrix of elastic type arteries. At later stages of phylogenesis, intima was formed from media smooth muscle cells.

Subendothelial smooth muscle cells of human aorta express macrophage antigen in situ and in vitro

1997 ◽  
Vol 135 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Elena R Andreeva ◽  
Inna M Pugach ◽  
Alexander N Orekhov
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Human Aorta

scholarly journals Microvascular pericytes contain muscle and nonmuscle actins.

1985 ◽  
Vol 101 (1) ◽  
pp. 43-52 ◽  
Author(s):  
I M Herman ◽  
P A D'Amore
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Plasma Membrane ◽  
Fluorescence Microscopy ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Stress Fibers ◽  
Fiber Bundles

We have affinity-fractionated rabbit antiactin immunoglobulins (IgG) into classes that bind preferentially to either muscle or nonmuscle actins. The pools of muscle- and nonmuscle-specific actin antibodies were used in conjunction with fluorescence microscopy to characterize the actin in vascular pericytes, endothelial cells (EC), and smooth muscle cells (SMC) in vitro and in situ. Nonmuscle-specific antiactin IgG stained the stress fibers of cultured EC and pericytes but did not stain the stress fibers of cultured SMC, although the cortical cytoplasm associated with the plasma membrane of SMC did react with nonmuscle-specific antiactin. Whereas the muscle-specific antiactin IgG failed to stain EC stress fibers and only faintly stained their cortical cytoplasm, these antibodies reacted strongly with the fiber bundles of cultured SMC and pericytes. Similar results were obtained in situ. The muscle-specific antiactin reacted strongly with the vascular SMC of arteries and arterioles as well as with the perivascular cells (pericytes) associated with capillaries and post-capillary venules. The non-muscle-specific antiactin stained the endothelium and the pericytes but did not react with SMC. These findings indicate that pericytes in culture and in situ possess both muscle and nonmuscle isoactins and support the hypothesis that the pericyte may represent the capillary and venular correlate of the SMC.

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