Increased levels of circulating endothelial cells in chronic periaortitis as a marker of active disease

Moroni, Gabriella; Papa, Nicoletta Del; Moronetti, Lorenza Mazzeo; Vitali, Claudio; Maglione, Wanda; Comina, D.P.; Urgnani, Francesca; Sandri, S; Ponticelli, Claudio; Cortelezzi, Agostino

doi:10.1111/j.1523-1755.2005.00434.x

Cited by 27 publications

(14 citation statements)

References 32 publications

(37 reference statements)

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“…EPC are believed to be a distinct population from that of mature circulating endothelial cells (CEC), which are EC that may have detached from the endothelial vasculature after injury [23,24]. Although there are suggestions of a common ancestry for these two populations (reviewed in reference [25]), increased CEC number is viewed as a reflection of severe vascular damage [26] whereas increased EPC number is interpreted as an important index of vascular repair [27][28][29][30]. Unfortunately the ability to clearly distinguish various endothelial phenotypes in peripheral blood is limited and therefore ascribing a specific functional role to EPC in vivo may be premature.…”

Section: Endothelial Progenitor Cellsmentioning

confidence: 99%

Vascular Disease: A New Progenitor Biology

Metharom¹,

Caplice

2007

CVP

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Vascular disease is primarily the result of atherosclerosis which affects all layers of the adult vessel wall. Our understanding of atherosclerosis has evolved over the past three decades; from initial hypotheses based on lipid deposition and fibrocellular proliferation within the intima of the vessel wall to a more complex interplay between conventional risk factors, inflammation and the immune system implicating pan-vascular biologic processes. More recently circulating progenitor cells have been shown to possess diverse differentiation capacity within the remodelling vessel wall. Current investigation of atherosclerosis therefore encompasses an expanding field of biological science; from molecular genetics, classical vascular biology, and immunology to stem cell biology and vasculogenesis. However, a decade after their initial description, scientists still know little about the proximate relationship between vascular progenitor cells and atherosclerosis progression or stability. In recent years, the discovery of progenitor cells of myeloid origin has offered the exciting prospect of merging classical concepts of myeloid cell biology in atherosclerosis with evolving concepts of myeloid cell plasticity and endothelial / smooth muscle cells differentiation within the injured vessel wall. In this context, early stage atherosclerosis associated with vascular injury may involve neovascularisation and re-endothelialisation in which a significant contribution comes from bone marrow-derived vascular progenitor cells. For this review, emphasis will be on endothelial progenitor cells (EPC), smooth muscle progenitor cells (SPC) and putative myeloid precursors.

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Section: Endothelial Progenitor Cellsmentioning

confidence: 99%

Vascular Disease: A New Progenitor Biology

Metharom¹,

Caplice

2007

CVP

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“…CEC exhibit no long-term proliferation potential and circulate in the peripheral blood. An increase in CEC number is viewed as a reflection of severe vascular damage [13]. Duda et al reported that CEC can be defined as a discrete population of cells expressing CD31 bright CD45 − CD34 dim CD1 33 − [14].…”

Section: Mature Circulating Endothelial Cells and Vascular Repairmentioning

confidence: 99%

Regeneration of the vascular compartment

Becher

Nickenig

Werner

2010

Herz

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Throughout life, damage to the vascular endothelium is pivotal in the development of cardiovascular disease. Therefore, a detailed understanding of the underlying mechanisms involved in endothelial cell restoration is of fundamental importance for preventive and therapeutic concepts in cardiovascular disease. The goal of regenerative medicine is the use of tissue-specific progenitor cells for a more effective repair process with reduction of fibrocellular remodelling, fibrosis and loss of functional properties.According to the hitherto assumed primary model of endothelial regeneration only adjacent and intact mature endothelial cells replace damaged endothelium. Since Asahara and colleagues first described that a peripheral blood mononuclear cell population was able to differentiate into endothelial cells in vitro and incorporate into ischemic tissue at sites of angiogenesis in vivo, the model of endothelial regeneration has been extended. The majority of clinical trials on human cell therapy for ischemic vascular disease are based on cell surface antigen expression of CD34 or VEGFR2 to identify endothelial progenitor cells.A precise characterization of the angiogenic properties of different subsets of endothelial regenerating cells and their course of action to gain sufficient long-term regeneration of the injured vessel is a necessary precondition before clinical trials of human cell therapy become a routine reality.

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“…In a recent study, Moroni et al [18] found that patients with CP had a significantly increased number of circulating endothelial cells (CECs) in comparison to healthy subjects, patients with diffuse ATS, and patients with renal insufficiency of variable degree and etiology. These data indicate that endothelial injury, as part of immune-mediated inflammatory vascular damage, may play a role in the pathogenesis of CP.…”

Section: Potential Role Of Atherosclerosis In Chronic Periaortitismentioning

confidence: 99%

Rethinking the Triggering Inflammatory Processes of Chronic Periaortitis

Meier

Vogt²,

Blanc³

2006

Nephron Exp Nephrol

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Chronic periaortitis (CP) is an uncommon inflammatory disease which primarily involves the infrarenal portion of the abdominal aorta. However, CP should be regarded as a generalized disease with three different pathophysiological entities, namely idiopathic retroperitoneal fibrosis (RPF), inflammatory abdominal aortic aneurysm and perianeurysmal RPF. These entities share similar histopathological characteristics and finally will lead to fibrosis of the retroperitoneal space. Beside fibrosis, an infiltrate with variable chronic inflammatory cell is present. The majority of these cells are lymphocytes and macrophages as well as vascular endothelial cells, most of which are HLA-DR-positive. B and T cells are present with a majority of T cells of the T-helper phenotype. Cytokine gene expression analysis shows the presence of interleukin (IL)-1α, IL-2, IL-4, interferon-γ and IL-2 receptors. Adhesion molecules such as E-selectin, intercellular adhesion molecule-1 and the vascular cell adhesion molecule-1 were also found in aortic tissue, and may play a significant role in CP pathophysiology. Although CP pathogenesis remains unknown, an exaggeratedinflammatory response to advanced atherosclerosis (ATS) has been postulatedto be the main process. Autoimmunity has also beenproposed as a contributing factor based on immunohistochemical studies. The suspected allergen may be a component of ceroid, which is elaborated within the atheroma. We review the pathogenesis and the pathophysiology of CP, and its potential links with ATS. Clinically relevant issues are summarized in each section with regard to the current working hypothesis of this complex inflammatory disease.

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Increased levels of circulating endothelial cells in chronic periaortitis as a marker of active disease

Abstract: The presence of a high number of CECs in the active phase of chronic periaortitis and their normalization during inactive disease suggest that endothelial damage may play a role in the pathogenesis of the disease.

Cited by 27 publications

References 32 publications

Vascular Disease: A New Progenitor Biology

Vascular Disease: A New Progenitor Biology

Regeneration of the vascular compartment

Rethinking the Triggering Inflammatory Processes of Chronic Periaortitis

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