A Structure-Based Biomechanical Model for the Effect of Dissolution of Muscle Cells on Pig Arteries: Elastin Associated With Muscle and Extracellular Matrix

2011 ◽  
Author(s):  
Aristotelis Agianniotis ◽  
Alexander Rachev ◽  
Nikos Stergiopulos
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Biomechanical Model ◽  
Muscle Cells ◽  
In Series ◽  
Minor Part ◽  
The Media ◽  
The One ◽  
A Minor

We developed a structure-based model of the arterial wall to explain the effect of dissolution of smooth muscle cells (SMC) on the mechanical behavior of the artery and to obtain a better understanding of the interaction between the different wall components. Pressure-radius curves and dimensions of zero-stress configuration were measured in 5 control and 5 decellularized porcine common carotid arteries. We found that 13% of elastin is associated with the smooth muscle cells (SMC) whereas the rest 87% is associated with the extracellular matrix (ECM). Further, we found that the elastin related to SMC and the one related to the ECM have circumferential prestretches of 2.04 and 0.89, respectively. We conclude that the majority of elastic in the media is linked to ECM and is under compression at zero load, whereas a minor part is linked to VSM and is under tension (SMC related) at its zero load state. Upon chemical dissolution of the muscle cells elastin in series with SMC do not bear load allowing elastin connected to ECM to release its compressive prestress, leading to the expansion of the artery.

Polarization, migration and homotypical interactions among prostatic smooth muscle cells in a laminin 111‐rich extracellular matrix

2020 ◽  
Author(s):  
Daniel Andrés Osório ◽  
Silvio Roberto Consonni ◽  
Aline Mara dos Santos ◽  
Hernandes F. Carvalho
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells

Abnormal Deposition of Extracellular Matrix Proteins by Cultured Smooth Muscle Cells from Human Varicose Veins

1998 ◽  
Vol 35 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Patricia Sansilvestri-Morel ◽  
Isabelle Nonotte ◽  
Marie-Pierre Fournet-Bourguignon ◽  
Alain Rupin ◽  
Jean-Noël Fabiani ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Varicose Veins ◽  
Extracellular Matrix Proteins ◽  
Muscle Cells ◽  
Matrix Proteins ◽  
Cultured Smooth Muscle Cells

scholarly journals Histochemical and immunohistochemical analysis of ruptured atherosclerotic abdominal aortic aneurysm wall

2010 ◽  
Vol 67 (12) ◽  
pp. 959-964 ◽  
Author(s):  
Irena Tanaskovic ◽  
Aleksandra Mladenovic-Mihailovic ◽  
Slavica Usaj-Knezevic ◽  
Vesna Stankovic ◽  
Aleksandar Aleksic ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Periodic Acid ◽  
Muscle Cells ◽  
Foam Cells ◽  
Abdominal Aortic ◽  
S 100 ◽  
The Media

Background/Aim. The main complication of the atherosclerotic abdominal aortic aneurism (AAA) is her rupture that begins with lesion in intima and rupture. The purpose of this work was to determine immunocytochemical and morphofunctional characteristics of the cells in aortic wall in ruptured atherosclerotic abdominal aortic aneurysm. Method. During the course of this study, 20 samples of atherosclerotic AAA were analyzed, all of them obtained during authopsy. The samples were fixed in 4% formalin and embedded in paraffin. Sections of 5 ?m thickness were stained histochemically (of Heidenhain azan stain and Periodic acid Schiff - PAS stain) and immunocytochemically using a DAKO LSAB+/HRP technique to identify ?-smooth muscle actin (?-SMA), vimentin, myosin heavy chains (MHC), desmin, S-100 protein, CD45 and CD68 (DAKO specification). Results. The results of our study showed that ruptured atherosclerotic AAA is characterized by a complete absence of endothelial cells, the disruption of basal membrane and internal elastic lamina, as well as a presence of the remains of hypocellular complicated atherosclerotic lesion in intima. On the plaque margins, as well as in the media, smooth muscle cells (SMCs) are present, which express a ?-SMA and vimentin (but without MHC or desmin expression), as well as leukocyte infiltration, and a large number of foam cells. Some of the foam cells show a CD68-immunoreactivity, while the others show vimentin- and S-100 protein-immunoreactivity. Media is thinned out with a disorganized elastic lamellas, while adventitia is characterized by inflammatory inflitrate (infection). Conclusion. Rupture of aneurysm occurs from the primary intimal disruption, which spreads into thinned out media and adventitia. Rupture is caused by unstable atherom, hypocellularity, loss of contractile characteristics of smooth muscle cells in intima and media, neovascularization of the media, as well as by the activity of the macrophages in the lesion.

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