Neointima formation on vascular elastic laminae and collagen matrices scaffolds implanted in the rat aortae

Liu, Shu Q.; Tieché, Christopher; Alkema, Paul K.

doi:10.1016/j.biomaterials.2003.08.044

Cited by 34 publications

(38 citation statements)

References 58 publications

(84 reference statements)

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“…Upon adhesion to ECM molecules, such as collagen and fibronectin, ␤1 integrin facilitates leukocyte infiltration into the site of injury (43)(44)(45). In contrast, some ECM structures are poor substrates for leukocyte accumulation and activation, such as elastin (46,47). Elastic laminae extracted from rat aorta are resistant to leukocyte adhesion and transmigration in vivo and in vitro compared with the collagen-enriched adventitia extracted from the same aorta (46,47).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, some ECM structures are poor substrates for leukocyte accumulation and activation, such as elastin (46,47). Elastic laminae extracted from rat aorta are resistant to leukocyte adhesion and transmigration in vivo and in vitro compared with the collagen-enriched adventitia extracted from the same aorta (46,47). Deficiency in fibulin 2 and fibulin 5 in animals results in disrupted elastic laminae accompanied by an increase in vascular adhesion molecules and tissue factor expression as well as thrombus formation after carotid artery ligation injury (23), suggesting that the elastin-enriched ECM present in healthy aortas protects against vascular injury.…”

Section: Discussionmentioning

confidence: 99%

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Expression of Versican V3 by Arterial Smooth Muscle Cells Alters Tumor Growth Factor β (TGFβ)-, Epidermal Growth Factor (EGF)-, and Nuclear Factor κB (NFκB)-dependent Signaling Pathways, Creating a Microenvironment That Resists Monocyte Adhesion

Kang

Yoon

Braun

et al. 2014

Journal of Biological Chemistry

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Background: Monocyte accumulation contributes to inflammatory disease progression. Results: ASMCs overexpressing V3 resist monocyte adhesion by promoting elastogenesis, depleting hyaluronan, and reducing VCAM1, via differentially regulating TGF␤-, EGF-, and NFB-signaling pathways. Conclusion: V3 expression by ASMCs generates a microenvironment resistant to monocyte adhesion. Significance: Modifying ECM components via V3 expression alters monocyte adhesion, which suggests therapeutic possibilities to treat inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Expression of Versican V3 by Arterial Smooth Muscle Cells Alters Tumor Growth Factor β (TGFβ)-, Epidermal Growth Factor (EGF)-, and Nuclear Factor κB (NFκB)-dependent Signaling Pathways, Creating a Microenvironment That Resists Monocyte Adhesion

Kang

Yoon

Braun

et al. 2014

Journal of Biological Chemistry

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“…Such a treatment removes the cellular components, basal lamina, and medial collagen matrix, leaving an aortic matrix scaffold with medial elastic laminae and collagen-dominant adventitia, as detected by immunohistochemistry (10).…”

Section: Methodsmentioning

confidence: 99%

“…Recent studies, however, have demonstrated that arterial elastic laminae also participate in the regulation of arterial morphogenesis and pathogenesis (7)(8)(9)(10)(11)(12). An important contribution of elastic laminae is to confine smooth muscle cells (SMCs) 2 to the arterial media by inhibiting SMC proliferation (8,9) and migration (10), thus preventing intimal hyperplasia under physiological conditions. Arterial elastic laminae also exhibit thrombosis-resistant properties.…”

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confidence: 99%

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Negative Regulation of Monocyte Adhesion to Arterial Elastic Laminae by Signal Regulatory Protein α and Src Homology 2 Domain-containing Protein-Tyrosine Phosphatase-1

Liu

Alkema

Tieché

et al. 2005

Journal of Biological Chemistry

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Elastic laminae are extracellular matrix constituents that not only contribute to the stability and elasticity of arteries but also play a role in regulating arterial morphogenesis and pathogenesis. We demonstrate here that an important function of arterial elastic laminae is to prevent monocyte adhesion, which is mediated by the inhibitory receptor signal regulatory protein (SIRP) ␣ and Src homology 2 domain-containing protein-tyrosine phosphatase (SHP)-1. In a matrix-based arterial reconstruction model in vivo, elastic laminae were resistant to leukocyte adhesion and transmigration compared with the collagen-dominant arterial adventitia. The density of leukocytes within the elastic lamina-dominant media was about 58 -70-fold lower than that within the adventitia from 1 to 30 days. An in vitro assay confirmed the inhibitory effect of elastic laminae on monocyte adhesion. The exposure of monocytes to elastic laminae induced activation of SIRP ␣, which in turn activated SHP-1. Elastic lamina degradation peptides extracted from arterial specimens could also activate SIRP ␣ and SHP-1. The knockdown of SIRP ␣ and SHP-1 by specific small interfering RNA diminished the inhibitory effect of elastic laminae, resulting in a significant increase in monocyte adhesion. These observations suggest that SIRP ␣ and SHP-1 potentially mediate the inhibitory effect of elastic laminae on monocyte adhesion.Arterial elastic laminae have long been considered a structure that determines the strength and elasticity of blood vessels (1-6). Recent studies, however, have demonstrated that arterial elastic laminae also participate in the regulation of arterial morphogenesis and pathogenesis (7-12). An important contribution of elastic laminae is to confine smooth muscle cells (SMCs) 2 to the arterial media by inhibiting SMC proliferation (8, 9) and migration (10), thus preventing intimal hyperplasia under physiological conditions. Arterial elastic laminae also exhibit thrombosis-resistant properties. When implanted in an artery, elastic lamina scaffolds are associated with significantly lower leukocyte adhesion and thrombosis compared with collagen matrix scaffolds (10).These observations suggest an inhibitory role for elastic laminae relative to collagen matrix. Although such a role is well documented, the mechanisms remain poorly understood.Leukocytes are known to express the inhibitory receptor SIRP ␣ (also known as Src homology 2 domain-containing tyrosine phosphatase substrate-1), a transmembrane glycoprotein receptor that exerts an inhibitory effect on cell mitogenic (13-18) and inflammatory (19,20) activities. Upon ligand binding, SIRP ␣ transmits inhibitory signals through tyrosine phosphorylation of its intracellular immunoreceptor tyrosine-based inhibitory motif (15-18, 21, 22). The phosphorylation of the immunoreceptor tyrosine-based inhibitory motif initiates the recruitment of Src homology 2 domain-containing protein-tyrosine phosphatase (SHP)-1 to SIRP ␣, which is known as a substrate of SHP-1 (21, 22). The recruitment of SH...

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Tissue Engineering at the Blood‐Contacting Surface: A Review of Challenges and Strategies in Vascular Graft Development

Radke

Jia

Sharma

et al. 2018

Adv Healthcare Materials

205

166

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Tissue engineered vascular grafts (TEVGs) are beginning to achieve clinical success and hold promise as a source of grafting material when donor grafts are unsuitable or unavailable. Significant technological advances have generated small-diameter TEVGs that are mechanically stable and promote functional remodeling by regenerating host cells. However, developing a biocompatible blood-contacting surface remains a major challenge. The TEVG luminal surface must avoid negative inflammatory responses and thrombogenesis immediately upon implantation and promote endothelialization. The surface has therefore become a primary focus for research and development efforts. The current state of TEVGs is herein reviewed with an emphasis on the blood-contacting surface. General vascular physiology and developmental challenges and strategies are briefly described, followed by an overview of the materials currently employed in TEVGs. The use of biodegradable materials and stem cells requires careful control of graft composition, degradation behavior, and cell recruitment ability to ensure that a physiologically relevant vessel structure is ultimately achieved. The establishment of a stable monolayer of endothelial cells and the quiescence of smooth muscle cells are critical to the maintenance of patency. Several strategies to modify blood-contacting surfaces to resist thrombosis and control cellular recruitment are reviewed, including coatings of biomimetic peptides and heparin.

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Neointima formation on vascular elastic laminae and collagen matrices scaffolds implanted in the rat aortae

Cited by 34 publications

References 58 publications

Expression of Versican V3 by Arterial Smooth Muscle Cells Alters Tumor Growth Factor β (TGFβ)-, Epidermal Growth Factor (EGF)-, and Nuclear Factor κB (NFκB)-dependent Signaling Pathways, Creating a Microenvironment That Resists Monocyte Adhesion

Expression of Versican V3 by Arterial Smooth Muscle Cells Alters Tumor Growth Factor β (TGFβ)-, Epidermal Growth Factor (EGF)-, and Nuclear Factor κB (NFκB)-dependent Signaling Pathways, Creating a Microenvironment That Resists Monocyte Adhesion

Negative Regulation of Monocyte Adhesion to Arterial Elastic Laminae by Signal Regulatory Protein α and Src Homology 2 Domain-containing Protein-Tyrosine Phosphatase-1

Tissue Engineering at the Blood‐Contacting Surface: A Review of Challenges and Strategies in Vascular Graft Development

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