The Adventitia: A Progenitor Cell Niche for the Vessel Wall

Majesky, Mark W.; Dong, Xiaoxin; Hoglund, Virginia; Daum, Günter; Mahoney, William M.

doi:10.1159/000331413

Cited by 105 publications

(101 citation statements)

References 168 publications

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“…121 Extrapolating from stem/ progenitor cell niches in other tissues, it is anticipated that the Wnt, Notch, and BMP signaling pathways may also play roles in the adventitial niche. 122 In addition to their interactions with each other, it is probable that different VW-PCs are also under the regulatory control of other vascular wall cell populations that help to maintain the stem cell niche, namely adventitial fibroblasts, adventitial and perivascular adipocytes, resident and migratory inflammatory cells (macrophages, mast cells, neutrophils, and lymphocytes), and adventitial neurons (Figure 3). Considerable preclinical and clinical research has identified an association between epicardial adipose tissue and cardiovascular disease, which seems at least, in part, to be mediated via the paracrine effects of adipokines on coronary atherosclerosis.…”

Section: Vascular Wall Stem Cell Nichementioning

confidence: 99%

“…Recent reviews have aptly described the adventitia as a dynamic and complex biological processing center for the retrieval, integration, storage, and release of key regulators of vessel wall function. 122,125 It provides an interface connecting the rest of the vessel wall to the highly cellular and cytokinerich perivascular adipose and connective tissue, as well as the peripheral circulation by virtue of its content of thin-walled microvessels. Thus, it is well situated to serve as an injury sensor for the rest of the vessel wall, and this is reflected by its early activation in different vascular disease models, such as atherosclerosis, 11 ligation and balloon injury, 126 aneurysm formation, 127 and pulmonary hypertension.…”

Section: Vascular Wall Stem Cell Nichementioning

confidence: 99%

“…62 Other adventitial stimuli that may also be relevant to progenitor cell biology include the augmentation of reactive oxygen species and extracellular purines and pyrimidines in response to hypoxia and inflammation, 125 and the effect of biomechanical forces caused by vascular pulsations and adventitial stretch. 122 Research efforts must also focus on the developmental origins of postnatal VW-PCs, addressing unanswered questions relating to the embryonic formation of the adventitia and its interface with the media, and the selective and architectural seeding of this territory with progenitor cells. Interest also centers on the heterogeneous prevalence of VW-PCs in different vascular beds.…”

Section: Vascular Wall Stem Cell Nichementioning

confidence: 99%

See 2 more Smart Citations

Vascular Wall Progenitor Cells in Health and Disease

Psaltis

Simari

2015

Circulation Research

173

155

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The vasculature plays an indispensible role in organ development and maintenance of tissue homeostasis, such that disturbances to it impact greatly on developmental and postnatal health. Although cell turnover in healthy blood vessels is low, it increases considerably under pathological conditions. The principle sources for this phenomenon have long been considered to be the recruitment of cells from the peripheral circulation and the re-entry of mature cells in the vessel wall back into cell cycle. However, recent discoveries have also uncovered the presence of a range of multipotent and lineage-restricted progenitor cells in the mural layers of postnatal blood vessels, possessing high proliferative capacity and potential to generate endothelial, smooth muscle, hematopoietic or mesenchymal cell progeny. In particular, the tunica adventitia has emerged as a progenitor-rich compartment with niche-like characteristics that support and regulate vascular wall progenitor cells. Preliminary data indicate the involvement of some of these vascular wall progenitor cells in vascular disease states, adding weight to the notion that the adventitia is integral to vascular wall pathogenesis, and raising potential implications for clinical therapies. This review discusses the current body of evidence for the existence of vascular wall progenitor cell subpopulations from development to adulthood and addresses the gains made and significant challenges that lie ahead in trying to accurately delineate their identities, origins, regulatory pathways, and relevance to normal vascular structure and function, as well as disease.

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Section: Vascular Wall Stem Cell Nichementioning

confidence: 99%

Section: Vascular Wall Stem Cell Nichementioning

confidence: 99%

Section: Vascular Wall Stem Cell Nichementioning

confidence: 99%

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Vascular Wall Progenitor Cells in Health and Disease

Psaltis

Simari

2015

Circulation Research

173

155

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“…The possibility of adventitial migration of fibroblasts to the media and ongoing phenotypic switching within the media and intima were shown in patients with advanced CKD and ESRD with severe neointimal hyperplasia (12) as well as in patients with a new AVF (13,14). In fact, recent studies have shown that the adventitia may have an important role in neointimal hyperplasia lesion formation, as a hub for recruitment of inflammatory cells that may directly stimulate medial SMC migration and proliferation and as a source of neointimal precursor cells that contribute to the cellular mass of developing neointimal hyperplasia lesions (15). In such "outside-in" mechanisms of cell migration, a subpopulation of fibroblasts from adventitia undergoes a phenotypic switch into migratory myofibroblasts.…”

Section: Mechanisms Of Intimal Hyperplasiamentioning

confidence: 99%

Novel Paradigms for Dialysis Vascular Access

Remuzzi

Ene-Iordache

2013

Clinical Journal of the American Society of Nephrology

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SummaryFailure of hemodialysis access is caused mostly by venous intimal hyperplasia, a fibro-muscular thickening of the vessel wall. The pathogenesis of venous neointimal hyperplasia in primary arteriovenous fistulae consists of processes that have been identified as upstream and downstream events. Upstream events are the initial events producing injury of the endothelial layer (surgical trauma, hemodynamic shear stress, vessel wall injury due to needle punctures, etc.). Downstream events are the responses of the vascular wall at the endothelial injury that consist of a cascade of processes including leukocyte adhesion, migration of smooth muscle cells from the media to the intimal layer, and proliferation. In arteriovenous fistulae, the stenoses occur in specific sites, consistently related to the local hemodynamics determined by the vessel geometry and blood flow pattern. Recent findings that the localization of these sites matches areas of disturbed flow may add new insights into the pathogenesis of neointimal hyperplasia in the venous side of vascular access after the creation of the anastomosis. The detailed study of fluid flow motion acting on the vascular wall in anastomosed vessels and in the arm vasculature at the patient-specific level may help to elucidate the role of hemodynamics in vascular remodeling and neointimal hyperplasia formation. These computational approaches may also help in surgical planning for the amelioration of clinical outcome. This review aims to discuss the role of the disturbed flow condition in acting as upstream event in the pathogenesis of venous intimal hyperplasia and in producing subsequent local vascular remodeling in autogenous arteriovenous fistulae used for hemodialysis access. The potential use of blood flow analysis in the management of vascular access is also discussed.

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“…7,8 Indeed, it has been suggested that the adventitia may be a contributing source of long-lasting neointimal VSMCs after injury. 9 Several potential stem and progenitor cell populations have been identified as residing in the tunica media and/or adventitia, [1][2][3][4]6,[8][9][10] including stem cell antigen-1 + (Sca1 + ) CD45 + adventitial macrophage progenitor cells 7,8 and Sca1…”

mentioning

confidence: 99%