Fibrin and Activated Platelets Cooperatively Guide Stem Cells to a Vascular Injury and Promote Differentiation Towards an Endothelial Cell Phenotype

Boer, Hetty C. de; Verseyden, C.; Ulfman, Laurien H.; Zwaginga, Jaap‐Jan; Bot, Ilze; Biessen, Erik A.L.; Rabelink, Ton J.; Zonneveld, Anton Jan van

doi:10.1161/01.atv.0000222982.55731.f1

Cited by 138 publications

(140 citation statements)

References 35 publications

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“…Of note, all patients included in the study were given ASA at 2 All patients received ASA plus heparin. 3 All patients received ASA. 4 All patients received ASA plus low-molecular-weight heparin.…”

Section: Platelets Inflammation and Antiinflammatory Drugs In Acs Anmentioning

confidence: 99%

“…Platelets recruit circulating endothelial progenitor cells to sites of vascular injury and may induce a prothrombotic state by platelet-endothelium-and platelet-leucocyte-endothelium interactions (3). During adhesion, platelets are activated and release potent inflammatory and mitogenic substances into the local microenvironment, thereby altering function of endothelial cells (4).…”

mentioning

confidence: 99%

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Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

Müller¹,

Chatterjee²,

Rath³

et al. 2015

Thromb Haemost

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SummaryPlatelets play a pivotal role in chronic inflammation leading to progression of atherosclerosis and acute coronary events. Recent discoveries on novel mechanisms and platelet-dependent inflammatory targets underpin the role of platelets to maintain a chronic inflammatory condition in cardiovascular disease. There is strong and clinically relevant crosslink between chronic inflammation and platelet activation. Antiplatelet therapy is a cornerstone in the prevention and treatment of acute cardiovascular events. The benefit of antiplatelet agents has mainly been attributed to their direct anti-aggregatory impact. Some anti-inflammatory off-target effects have also been described. However, it is unclear whether these effects are secondary due to inhibition of platelet activation or are caused by direct distinct mechanisms interfering with inflammatory pathways. This article will highlight novel platelet associated targets that contribute to inflammation in cardiovascular disease and elucidate mechanisms by which currently available antiplatelet agents evolve anti-inflammatory capacities, in particular by carving out the differential mechanisms directly or indirectly affecting platelet mediated inflammation. It will further illustrate the prognostic impact of antiplatelet therapies by reducing inflammatory marker release in recent cardiovascular trials.

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Section: Platelets Inflammation and Antiinflammatory Drugs In Acs Anmentioning

confidence: 99%

mentioning

confidence: 99%

Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

Müller¹,

Chatterjee²,

Rath³

et al. 2015

Thromb Haemost

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show abstract

“…Under normal circumstances, EPC contribute to vascular homeostasis by replacing apoptotic or lost endothelial cells (4,5). In addition, EPC can be home to sites of denudation (6), ischemia, or elevated shear stress to stimulate neovascularization or arteriogenesis (7,8). In patients with type 1 (9) and type 2 diabetes (10) and in diabetic animals (11)(12)(13), the number of circulating EPC is decreased, and functional parameters such as adhesion, migration, and the paracrine secretion of proangiogenic factors are impaired, likely as a consequence of hyperglycemia.…”

Section: Introductionmentioning

confidence: 99%

Differentiation of Bone Marrow-Derived Endothelial Progenitor Cells Is Shifted into a Proinflammatory Phenotype by Hyperglycemia

Loomans

Haperen

Duijs

et al. 2009

Mol Med

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Bone marrow (BM)-derived endothelial progenitor cells (EPC) contribute to vascular maintenance by participating in angiogenesis, re-endothelialization, and remodeling. Myeloid progenitor cells in the BM are functionally and quantitatively an important precursor pool for cells that contribute to these processes. However, these precursor pools in the BM also give rise to important effector cells of the innate immune system, such as macrophages and dendritic cells. We hypothesized that the disturbed repair responses that are being observed in diabetes mellitus are also related to an effect on functional and differentiation characteristics at the level of this bone marrow precursor pool. Indeed, we observed that bone marrow differentiation cultures for EPC, macrophages (Mph), or dendritic cells (DC) from hyperglycemic BM yielded 40% fewer EPC and 50% more Mph compared with control BM. These changes were directly related to the hemoglobin A 1C levels of the donor mice. BM-derived DC numbers were not affected by hyperglycemia. The composition of the BM was not altered; in particular, the numbers of CD31 + /Ly6C + cells, which serve as common progenitors for EPC, Mph, and DC, were unaffected. In addition, BM-derived EPC from hyperglycemic mice were less angiogenic and more proinflammatory in regards to endocytosis, T-cell activation, and interleukin 12 production. HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibition by statin supplementation of the culture medium counteracted these hyperglycemia-induced changes. Our study results show that hyperglycemia alters the differentiation fate of BM precursor cells, reducing the potential to generate vascular regenerative cells and favoring the development of proinflammatory cells.

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“…Furthermore, adhesion molecules, such as selectins and -integrins, as well as activated platelets promote adhesion and differentiation of EPCs [65,66]. Vascular smooth muscle cells may also sequester circulating EPCs through chemokine secretion [67].…”

Section: Vasculogenesismentioning

confidence: 99%

Inflammatory and Angiogenic Abnormalities in Diabetic Wound Healing: Role of Neuropeptides and Therapeutic Perspectives

Tellechea¹

2012

TOCVJ

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Diabetic foot ulceration (DFU) is one of the most costly and debilitating complications of diabetes and is the leading cause of non-traumatic amputations, affecting 15% of the diabetic population. Impaired wound healing in diabetic patients without large-vessel disease has been attributed to microvascular dysfunction, neuropathy, and abnormal cellular and inflammatory responses. These abnormalities have been examined mainly in animal models although a few studies have been undertaken in diabetic patients. This review provides an overview of the inflammatory and vascular abnormalities in DFU and emphasises the role of angiogenic growth factors, endothelial progenitor cells (EPCs), and neuropeptides as mediators of wound healing and potential therapeutic agents for these chronic, non-healing ulcers.

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Fibrin and Activated Platelets Cooperatively Guide Stem Cells to a Vascular Injury and Promote Differentiation Towards an Endothelial Cell Phenotype

Abstract: We provide evidence that hemostatic factors, associated with vascular injury, provide a regulatory microenvironment for re-endothelialization mediated by circulating progenitor cells.

Cited by 138 publications

References 35 publications

Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

Differentiation of Bone Marrow-Derived Endothelial Progenitor Cells Is Shifted into a Proinflammatory Phenotype by Hyperglycemia

Inflammatory and Angiogenic Abnormalities in Diabetic Wound Healing: Role of Neuropeptides and Therapeutic Perspectives

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