Extracellular matrix remodeling in the vascular wall

Jacob, Marie‐Paule; Badier‐Commander, Cécile; Fontaine, Vincent; Benazzoug, Yasmina; Feldman, Laurent J.; Michel, Jean‐Baptiste

doi:10.1016/s0369-8114(01)00151-1

Cited by 131 publications

(100 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…5,6 Each of the three layers carries out a primary function regulated by its endogenous constituents. 7 The innermost layer, the tunica intima, forms the luminal interface of the aorta and is composed of endothelial cells resting on a basement membrane. This layer regulates diffusion and migration of blood components into the tissues and is largely responsible for primary signal transmission in regulating vascular tone.…”

mentioning

confidence: 99%

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Jones

Beck

Barbour

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

The present study tested the hypothesis that changes in the resident endogenous cellular population accompany alterations in aortic collagen and elastin content during thoracic aortic aneurysm (TAA) development in a murine model. Descending thoracic aortas were analyzed at various time points (2, 4, 8, and 16 weeks) post-TAA induction (0.5 M CaCl 2 , 15 minutes). Aortic tissue sections were subjected to histological staining and morphometric analysis for collagen and elastin, as well as immunostaining for cell-type-specific markers to quantify fibroblasts, myofibroblasts, and smoothmuscle cells. Results were compared with reference control mice processed in the same fashion. Aortic dilatation was accompanied by changes in the elastic architecture that included: a decreased number of elastic lamellae (from 6 to 4); altered area fraction of elastin (elevated at 4 weeks and decreased at 16 weeks); and a decreased area between elastic lamellae (minimum reached at 4 weeks). Total collagen content did not change over time. Increased immunoreactivity for fibroblast and myofibroblast markers was observed at 8-and 16-week post-TAA-induction, whereas immunoreactivity for smooth-muscle cell markers peaked at 4 weeks and returned to baseline by 16 weeks. Therefore, this study demonstrated that changes in aortic elastin content were accompanied by the emergence of a subset of fibroblast-derived myofibroblasts whose altered phenotype may play a significant role in TAA development through the enhancement of extracellular matrix proteolysis.

show abstract

mentioning

confidence: 99%

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Jones

Beck

Barbour

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…Although the ECM is a minor component of most cell types, it has a crucial role in many cellular processes including cell growth, spreading and differentiation (18), and modulating the biological activities of growth factors (22,23). There are also secreted proteins that reside on the ECM, such as sphingomyelinase (24 -27) and matrix metalloproteinases (28,29) that play a role in atherogenesis, with the latter also likely involved in vascular wall remodeling and possibly thrombosis. ECM proteins can also play a role in certain types of cancer/tumor growth (30 -32), multiple sclerosis (33,34), and atherosclerosis (35,36), highlighting the importance of understanding the function of the various components of the ECM.…”

mentioning

confidence: 99%

Trypsin-sensitive and Lipid-containing Sites of the Macrophage Extracellular Matrix Bind Apolipoprotein A-I and Participate in ABCA1-dependent Cholesterol Efflux

Burgess

Kiss

Zachariah

et al. 2002

Journal of Biological Chemistry

View full text Add to dashboard Cite

A unique property of the extracellular matrix of J774 and THP-1 cells has been identified, which contributes to the ability of these cells to promote cholesterol efflux. We demonstrate high level apolipoprotein (apo) A-I binding to macrophage cells (THP-1 and J774) and to their extracellular matrix (ECM). However, high level apoA-I binding is not observed on fibroblasts, HepG2 cells, or U937 cells (a macrophage cell line that does not efflux cholesterol to apoA-I or bind apoA-I on their respective ECM). Binding to the ECM of THP-1 or J774 macrophages depends on the presence of apoA-I C-terminal helices and is markedly reduced with a mutant lacking residues 187-243 (apoA-I⌬(187-243)), suggesting that the hydrophobic C terminus forms a hydrophobic interaction with the ECM. ApoA-I binding is lost upon trypsin treatment or with Triton X-100, a preparation method that de-lipidates the ECM. However, binding is recovered with re-lipidation, and is preserved with ECM prepared using cytochalasin B, which conserves the endogenous phospholipid levels of the ECM. We also demonstrate that specific cholesterol efflux to apoA-I is much reduced in cells released from their native ECM, but fully restored when ECM-depleted cells are added back to ECM in the presence of apoA-I. The apoA-Imediated efflux is deficient in plated or suspension U937 macrophages, but is restored to high levels when the suspension U937 cells are reconstituted with the ECM of J774 cells. The ECM-dependent activity was much reduced in the presence of glyburide, indicating participation of ABCA1 (ATP-binding cassette transporter 1) in the efflux mechanism. These studies establish a novel binding site for apoA-I on the macrophage ECM that may function together with ABCA1 in promoting cholesterol efflux.

show abstract

“…◊ Clefts pontage comme les desmosines, formées à partir de quatre résidus lysine (Figure 1, étape 3). La formation des acides aminés de pontage rend l'élastine insoluble, résistante à l'hydrolyse par la plupart des enzymes et surtout fonctionnelle en lui conférant ses propriétés d'élasticité [1]. Plusieurs maladies connues sont des élastinopathies dues à l'altération ou à la suppression de l'une des protéines constitutives des fibres élastiques.…”

Section: Discussionunclassified

L’invalidation du gène de la fibuline-5 induit une élastinopathie

Jacob

2003

Med Sci (Paris)

View full text Add to dashboard Cite

Extracellular matrix remodeling in the vascular wall

Cited by 131 publications

References 43 publications

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Trypsin-sensitive and Lipid-containing Sites of the Macrophage Extracellular Matrix Bind Apolipoprotein A-I and Participate in ABCA1-dependent Cholesterol Efflux

L’invalidation du gène de la fibuline-5 induit une élastinopathie

Contact Info

Product

Resources

About