Bovine distal pulmonary arterial media is composed of a uniform population of well-differentiated smooth muscle cells with low proliferative capabilities

2003 ◽  
Vol 285 (4) ◽  
pp. L819-L828 ◽  
Author(s):  
Leopold Stiebellehner ◽  
Maria G. Frid ◽  
John T. Reeves ◽  
Robert B. Low ◽  
Meena Gnanasekharan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Pulmonary Circulation ◽  
Main Pulmonary Artery ◽  
Muscle Cells ◽  
Hypoxic Exposure ◽  
Growth Responses ◽  
The Media ◽  
Well Differentiated ◽  
Uniform Population

The media of the normal bovine main pulmonary artery (MPA) is composed of phenotypically heterogeneous smooth muscle cells (SMC) with markedly different proliferative capabilities in response to serum, mitogens, and hypoxia. Little, however, is known of the SMC phenotype in distal pulmonary arteries (PA), particularly in arterioles, which regulate the pulmonary circulation. With a panel of muscle-specific antibodies against α-smooth muscle (SM)-actin, SM-myosin heavy chains (SM-MHC), SM-MHC-B isoform, desmin, and meta-vinculin, we demonstrate a progressive increase in phenotypic uniformity and level of differentiation of SMC along the proximal-to-distal axis of normal adult bovine pulmonary circulation so that the media of distal PA (1,500- to 100-μm diameter) is composed of a phenotypically uniform population of “well-differentiated” SMC. Similarly, when isolated and assessed in vitro, distal PA-SMC is composed of a single, uniform population of differentiated SMC that exhibited minimal growth responses to a variety of mitogens while their cell size increased substantially in response to serum. Their growth was inhibited by hypoxic exposure under all conditions tested. Distal PA-SMC also differed from MPA-SMC by exhibiting a distinct pattern of DNA synthesis in response to serum and mitogens. Thus, in contrast to the MPA, distal PA media is composed of an apparently uniform population of well-differentiated SMC that are proliferation resistant and have a substantial capacity to hypertrophy in response to growth-promoting stimuli. We thus speculate that distinct SMC phenotypes present in distal vs. proximal PA may confer different response mechanisms during remodeling in conditions such as hypertension.

Potentiation of PDGF-Induced Growth Responses in Coronary Artery Smooth Muscle Cells by Thromboxane

1995 ◽  
pp. 53-58 ◽  
Author(s):  
T.-Ph. Zucker ◽  
T. Morinelli ◽  
P. V. Halushka ◽  
A. Sachinidis ◽  
H. Vetter ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Growth Responses

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.

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.

The Studies on Biocompatibility of Self-Expanding NiTi Stent and Apoptosis of Smooth Muscle Cells after Stenting

2005 ◽  
Vol 288-289 ◽  
pp. 587-590 ◽  
Author(s):  
Chun Jiang Li ◽  
Yu Feng Zheng ◽  
Chao Li ◽  
Lian Cheng Zhao
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Niti Alloy ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Vessel Remodeling ◽  
Proliferation And Apoptosis ◽  
The Media ◽  
Atherosclerotic Process ◽  
Stent Surface

The biocompatibility of the NiTi alloy self-expanding stent, its dilating effect on the vascular wall, and the apoptosis of smooth muscle cells (SMCs) were studied by implantation of stent into the rabbit’s abdominal aorta for different period. All the animals lived throughout the study. There was no detectable migration or dissection of the stent, and there were no acute closures or sub-acute thromboses in the vessels. The rates of patency were 100% both at the beginning when the stent was implanted and at the end when the animal was sacrificed. It may be concluded that the vascular intima covers the whole stent at the 8-week point. The atherosclerotic process existed in the vascular intima in contact with the stent surface, while the proliferation and apoptosis of SMCs occured simultaneously. After stent implantation, the apoptosis happened in both intima and media, which indicated that the stent might not only stimulate the intima but also compress the media, leading to proliferation and apoptosis. This might contribute to vessel remodeling after stenting.

Expression and function of periostin-like factor in vascular smooth muscle cells

2007 ◽  
Vol 292 (5) ◽  
pp. C1672-C1680 ◽  
Author(s):  
Judith Litvin ◽  
Xing Chen ◽  
Sheri Keleman ◽  
Shimei Zhu ◽  
Michael Autieri
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Clinical Manifestations ◽  
Muscle Cells ◽  
Antibody Treatment ◽  
The Media ◽  
Vascular Proliferative Diseases ◽  
And Function

In injured blood vessels activated vascular smooth muscle cells (VSMCs) migrate from the media to the intima, proliferate and synthesize matrix proteins. This results in occlusion of the lumen and detrimental clinical manifestations. We have identified a novel isoform of the periostin family of proteins referred to as periostin-like factor (PLF). PLF expression in VSMCs was increased following treatment with mitogenic compounds, suggesting that PLF plays a role in VSMC activation. Correspondingly, proliferation of the cells was significantly reduced with anti-PLF antibody treatment. PLF expression increased VSMC migration, an essential cellular process leading to vascular restenosis after injury. PLF protein was localized to neointimal VSMC of rat and swine balloon angioplasty injured arteries, as well as in human arteries with transplant restenosis, supporting the hypothesis that PLF is involved in VSMC activation and vascular proliferative diseases. Taken together, these data suggest a role for PLF in the regulation of vascular proliferative disease.

Hypoxia, leukocytes, and the pulmonary circulation

2005 ◽  
Vol 98 (2) ◽  
pp. 715-721 ◽  
Author(s):  
Kurt R. Stenmark ◽  
Neil J. Davie ◽  
John T. Reeves ◽  
Maria G. Frid
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Pulmonary Circulation ◽  
Vessel Wall ◽  
Critical Role ◽  
Muscle Cells ◽  
Lung Epithelial Cells ◽  
Vasa Vasorum ◽  
Pulmonary Vessel

Data are rapidly accumulating in support of the idea that circulating monocytes and/or mononuclear fibrocytes are recruited to the pulmonary circulation of chronically hypoxic animals and that these cells play an important role in the pulmonary hypertensive process. Hypoxic induction of monocyte chemoattractant protein-1, stromal cell-derived factor-1, vascular endothelial growth factor-A, endothelin-1, and tumor growth factor-β1in pulmonary vessel wall cells, either directly or indirectly via signals from hypoxic lung epithelial cells, may be a critical first step in the recruitment of circulating leukocytes to the pulmonary circulation. In addition, hypoxic stress appears to induce release of increased numbers of monocytic progenitor cells from the bone marrow, and these cells may have upregulated expression of receptors for the chemokines produced by the lung circulation, which thus facilitates their specific recruitment to the pulmonary site. Once present, macrophages/fibrocytes may exert paracrine effects on resident pulmonary vessel wall cells stimulating proliferation, phenotypic modulation, and migration of resident fibroblasts and smooth muscle cells. They may also contribute directly to the remodeling process through increased production of collagen and/or differentiation into myofibroblasts. In addition, they could play a critical role in initiating and/or supporting neovascularization of the pulmonary artery vasa vasorum. The expanded vasa network may then act as a conduit for further delivery of circulating mononuclear cells to the pulmonary arterial wall, creating a feedforward loop of pathological remodeling. Future studies will need to determine the mechanisms that selectively induce leukocyte/fibrocyte recruitment to the lung circulation under hypoxic conditions, their direct role in the remodeling process via production of extracellular matrix and/or differentiation into myofibroblasts, their impact on the phenotype of resident smooth muscle cells and adventitial fibroblasts, and their role in the neovascularization observed in hypoxic pulmonary hypertension.

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