A new adhesive protein mediating the interaction between mesenchymal cells and elastin fibers: Elastonectin

1988 ◽  
Vol 53 (1) ◽  
pp. 209-211
Author(s):  
Ladislas Robert ◽  
William Hornebeck
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Muscle Cells ◽  
Mesenchymal Cells ◽  
Elastic Fibers ◽  
Elastic Tissue ◽  
Adhesive Protein

An inducible adhesive protein was demonstrated in smooth muscle cells and fibroblasts which mediate the adhesion of mesenchymal cells to elastic fibers. It is proposed to designate it elastonectin. This protein plays probably an important role in the morphogenesis of elastic tissue and its degradation is probably involved in the formation of the atherosclerotic plaque.

Processing of Chimeric Antisense Oligonucleotides by Human Vascular Smooth Muscle Cells and Human Atherosclerotic Plaque

Circulation ◽  
1996 ◽  
Vol 93 (4) ◽  
pp. 772-780 ◽  
Author(s):  
J. Geoffrey Pickering ◽  
Jeffrey M. Isner ◽  
Carol M. Ford ◽  
Lawrence Weir ◽  
Andrew Lazarovits ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Antisense Oligonucleotides ◽  
Muscle Cells ◽  
Human Atherosclerotic Plaque

scholarly journals Stromal cells from human long-term marrow cultures are mesenchymal cells that differentiate following a vascular smooth muscle differentiation pathway

Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 66-76 ◽  
Author(s):  
MC Galmiche ◽  
VE Koteliansky ◽  
J Briere ◽  
P Herve ◽  
P Charbord
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Stromal Cells ◽  
Muscle Cells ◽  
Mesenchymal Cells ◽  
Myoid Cells ◽  
Marrow Cultures

In human long-term marrow cultures connective tissue-forming stromal cells are an essential cellular component of the adherent layer where granulomonocytic progenitors are generated from week 2 onward. We have previously found that most stromal cells in confluent cultures were stained by monoclonal antibodies directed against smooth muscle- specific actin isoforms. The present study was carried out to evaluate the time course of alpha-SM-positive stromal cells and to search for other cytoskeletal proteins specific for smooth muscle cells. It was found that the expression of alpha-SM in stromal cells was time dependent. Most of the adherent spindle-shaped, vimentin-positive stromal cells observed during the first 2 weeks of culture were alpha- SM negative. On the contrary, from week 3 to week 7, most interdigitated stromal cells contained stress fibers whose backbone was made of alpha-SM-positive microfilaments. In addition, in confluent cultures, other proteins specific for smooth muscle were detected: metavinculin, h-caldesmon, smooth muscle myosin heavy chains, and calponin. This study confirms the similarity between stromal cells and smooth muscle cells. Moreover, our results reveal that cells in vivo with the phenotype closest to that of stromal cells are immature fetal smooth muscle cells and subendothelial intimal smooth muscle cells; a cell subset with limited development following birth but extensively recruited in atherosclerotic lesions. Stromal cells very probably derive from mesenchymal cells that differentiate along this distinctive vascular smooth muscle cell pathway. In humans, this differentiation seems crucial for the maintenance of granulomonopoiesis. These in vitro studies were completed by examination of trephine bone marrow biopsies from adults without hematologic abnormalities. These studies revealed the presence of alpha-SM-positive cells at diverse locations: vascular smooth muscle cells in the media of arteries and arterioles, pericytes lining capillaries, myoid cells lining sinuses at the abluminal side of endothelial cells or found within the hematopoietic logettes, and endosteal cells lining bone trabeculae. More or less mature cells of the granulocytic series were in intimate contact with the thin cytoplasmic extensions of myoid cells. Myoid cells may be the in vivo counterpart of stromal cells with the above-described vascular smooth muscle phenotype.

Abstract 381: IL-19 Inhibits Atherosclerosis in LDLR-/- Mice by Modulating Cholesterol Uptake in Macrophages and Vascular Smooth Muscle Cells

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Khatuna Gabunia ◽  
Stephen P Ellison ◽  
James M Richards ◽  
Sheri E Kelemen ◽  
Michael V Autieri
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Scavenger Receptor ◽  
Muscle Cells ◽  
Wild Type ◽  
Anti Inflammatory ◽  
M2 Phenotype

IL-19 is a recently described, putative anti-inflammatory cytokine which had previously been ascribed to be leukocyte specific. IL-19 is not detected in normal artery, but we detected IL-19 in multiple cell types in human atherosclerotic plaque suggesting a role for this interleukin in atherosclerosis. The purpose of this study was to determine whether administration of exogenous IL-19 could attenuate development of pre-formed atherosclerotic plaque, and to identify potential molecular mechanisms. LDLR-/- mice were fed high-fat diet for 12 weeks and then administered with 10ng/g/day IL-19 or PBS for an additional 8 weeks. En face analysis demonstrated that IL-19 could halt, but not reverse existing plaque (26.7+/-1.7%, 41.03+/-3.1%, 23.70+/-2.6% for baseline, PBS control, and IL-19-treated mice). Foam cell formation by macrophages and vascular smooth muscle cells (VSMC) is a hallmark event during atherosclerosis. Nothing has been reported regarding IL-19 effects on macrophage or VSMC lipid uptake; we therefore investigated whether IL-19 affects macrophage and VSMC cholesterol handling. Addition of IL-19 to wild-type bone marrow derived macrophages (BMDM) significantly promoted oxLDL uptake, conversely, BMDM from IL-19-/- mice had significantly less oxLDL uptake compared to wild-type BMDM. Addition of IL-19 to wild type BMDM significantly increased expression of scavenger receptor B1 (SR-B1), and decreased expression of inflammatory cytokines TNFα, IL-12b, MCP1. Interestingly, converse results were obtained with VSMC, as addition of IL-19 to wild-type VSMC decreased uptake of oxLDL ( p<0.05 ) and decreased expression of scavenger receptor CD36. VSMC isolated from IL-19-/- mice had increased uptake of oxLDL (p<0.0001). It is reported that M2 macrophages participate in plaque regression. IL-19 decreased IL-12b and significantly promoted the polarization of anti-inflammatory M2 phenotype in BMDM as evidenced by the increased expression of YM1 and IL-10 mRNA. These data demonstrate that IL-19 can inhibit progression of existing atherosclerotic plaque by modulating lipid metabolism in VSMC and macrophages and by promoting macrophage differentiation into an alternative, anti-inflammatory M2 phenotype.

Lymphangioma of the Pancreas With “Ovarian-like” Mesenchymal Stroma: A Case Report With Emphasis on Histogenesis

2003 ◽  
Vol 127 (11) ◽  
pp. 1513-1516 ◽  
Author(s):  
Lizhen Gui ◽  
Steven A. Bigler ◽  
Charu Subramony
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Case Report ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mesenchymal Cells ◽  
Developmental Anomaly ◽  
Mesenchymal Stroma ◽  
Multiple Cysts ◽  
Lymphoid Aggregates

Abstract Pancreatic lymphangiomas, which occur predominantly in women, are rare and account for only 1% of all lymphangiomas. The characteristic histologic features include multiple cysts lined by endothelial cells, irregularly distributed smooth muscle cells, and lymphoid aggregates in the wall of the cyst. We describe a 36-year-old woman with lymphangioma of the pancreas with “ovarian-like” mesenchymal stroma in the wall. This stroma, composed of uncommitted mesenchymal cells, has not been described previously in the wall of pancreatic lymphangiomas. Multiple small lymphatic channels that are found in this stroma recapitulate the development of lymphatic channels in the embryo. Lymphangioma of the pancreas may arise from distension of these lymphatic channels. Pancreatic lymphangioma may, therefore, be a developmental anomaly rather than a true neoplasm.

The induction of atherosclerotic plaque-like mounds in cultures of aortic smooth muscle cells

1975 ◽  
Vol 18 (1) ◽  
Author(s):  
James F. May ◽  
Wendelin J. Paule ◽  
Donald E. Rounds ◽  
David H. Blankenhorn ◽  
Tibor Zemplenyi
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

The Effects of Extracellular Matrix Protein Insufficiency and Treatment on the Stiffness of Arterial Smooth Muscle Cells

2013 ◽  
Author(s):  
Gabriela Espinosa ◽  
Lisa Bennett ◽  
William Gardner ◽  
Jessica Wagenseil
Keyword(s):  
Mechanical Properties ◽  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Elastic Tissue ◽  
Newborn Mice ◽  
Ecm Proteins ◽  
Wall Stiffness ◽  
Deficient Mice

Increased arterial stiffness is directly correlated with hypertension and cardiovascular disease. Stiffness of the conducting arteries is largely determined by the extracellular matrix (ECM) proteins in the wall, such as collagen and elastin, produced by the smooth muscle cells (SMCs) found in the medial layer. Elastin is deposited as soluble tropoelastin and is later crosslinked into elastin fibers. Newborn mice lacking the elastin protein ( Eln−/−) have increased arterial wall stiffness and SMCs with altered proliferation, migration and morphology [1]. Vessel elasticity is also mediated by other ECM proteins, such as fibulin-4. Elastic tissue, such as lung, skin, and arteries, from fibulin-4 deficient ( Fbln4−/−) mice show no decrease in elastin content, but have reduced elasticity due to disrupted elastin fibers [2]. Arteries from both elastin and fibulin-4 deficient mice have been previously studied, but the mechanical properties of their SMCs have not been investigated. Recent experiments comparing arterial SMCs from old and young animals suggest that mechanical properties of the SMCs themselves may contribute to changes in wall stiffness [3]. Hence, we investigated the stiffness of isolated arterial SMCs from elastin and fibulin-4 deficient mice using atomic force microscopy (AFM). In addition, we studied the effects of two elastin treatments on the mechanical properties of SMCs from Eln+/+ and Eln−/− mice. Differences between the treatments may elucidate the importance of soluble versus crosslinked elastin on single cell stiffness.

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