Biology and flow cytometry of proangiogenic hematopoietic progenitors cells

Rose, Jonathan A.; Erzurum, Serpil C.; Asosingh, Kewal

doi:10.1002/cyto.a.22596

Cited by 36 publications

(39 citation statements)

References 129 publications

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“…A variety of bone marrow-derived cells, including mature hematopoietic cells and hematopoietic progenitor cells, can induce angiogenic activity (29). Among these cells, proangiogenic progenitor cells are the major contributors to angiogenesis (29).…”

Section: Resultsmentioning

confidence: 99%

“…Healthy donor lungs not used for transplantation were used as controls. Serum NO was determined by measure of total NO i.e., nitrite and nitrate as published previously (29, 32). …”

Section: Methodsmentioning

confidence: 99%

“…Proangiogenic progenitor cells include a subset of hematopoietic stem cells and lineage progenitors with the capacity to promote neovascularization (reviewed in(29)). We recently reported that proangiogenic progenitor cells from asthmatic patients and ovalbumin (OVA) mouse model express high levels of eotaxin-1(30).…”

Section: Introductionmentioning

confidence: 99%

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Eotaxin-Rich Proangiogenic Hematopoietic Progenitor Cells and CCR3+ Endothelium in the Atopic Asthmatic Response

Asosingh

Vasanji²,

Tipton

et al. 2016

The Journal of Immunology

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Angiogenesis is closely linked to and precedes eosinophilic infiltration in asthma. Eosinophils are recruited into the airway by chemoattractant eotaxins, which are expressed by endothelial cells, smooth muscles cells, epithelial cells, and hematopoietic cells. We hypothesized that bone marrow-derived proangiogenic progenitor cells that contain eotaxins contribute to the initiation of angiogenesis and inflammation in asthma. Whole lung allergen challenge of atopic asthma patients revealed vascular activation occurs within hours of challenge, and prior to airway inflammation. The eotaxin receptor CCR3 was expressed at high levels on submucosal endothelial cells in patients and murine model of asthma. Exvivo exposure of murine endothelial cells to eotaxins induced migration and angiogenesis. In mechanistic studies, wildtype mice transplanted with eotaxin-1/2 deficient bone marrow had markedly less angiogenesis and inflammation in an atopic asthma model, while adoptive transfer of proangiogenic progenitor cells from wildtype mice in an atopic asthma model into the eotaxin-1/2 deficient mice led to angiogenesis and airway inflammation. The findings indicate that TH2-promoting hematopoietic progenitor cells are rapidly recruited to the lung upon allergen exposure and release eotaxins that coordinately activate endothelial cells, angiogenesis, and airway inflammation.

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Section: Resultsmentioning

confidence: 99%

“…Healthy donor lungs not used for transplantation were used as controls. Serum NO was determined by measure of total NO i.e., nitrite and nitrate as published previously (29, 32). …”

Section: Methodsmentioning

confidence: 99%

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Eotaxin-Rich Proangiogenic Hematopoietic Progenitor Cells and CCR3+ Endothelium in the Atopic Asthmatic Response

Asosingh

Vasanji²,

Tipton

et al. 2016

The Journal of Immunology

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“…In a state of hypoperfusion, the hypoxia-inducible factors initiate angiogenesis (the formation of blood vessels) through the up-regulation of pro-angiogenic factors [25]. The main player in this blood vessel formation is VEGF, which induces differentiation and proliferation of endothelial cells from its progenitors, the hemangioblast and the angioblast [46]. This forms an inefficiently differentiated primitive vascular plexus (vasculogenesis) [47].…”

Section: Involvement Of Angiogenesis and Not Apoptosismentioning

confidence: 99%

Pathogenic Angiogenic Mechanisms in Alzheimer's Disease

Singh¹,

Pfeifer²,

Jefferies³

2017

Physiologic and Pathologic Angiogenesis - Signaling Mechanisms and Targeted Therapy

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Vascular dysfunction is a crucial pathological hallmark of Alzheimer's disease (AD). Studies have reported that beta amyloid (Aβ) causes increased blood vessel growth in the brains of AD mouse models, a phenomenon that is also seen in AD patients. This has given way to an alternative angiogenesis hypothesis according to which, increased leakiness in the blood vessels disrupts the blood-brain barrier (BBB) and allows unwanted blood products to enter the brain causing progression of disease pathology, promoting amyloid clumping and aggregation along with impaired cerebral blood flow. Furthermore, the expression of melanotransferrin in AD model and patients may contribute to angiogenesis. The objective of this chapter is to attempt to establish a link between the vascular damage and AD pathology. Curbing the vascular changes and resulting damage seen in the brains of AD model mice and improving their cognition by treating with FDA-approved anti-angiogenic drugs may expedite the translational potential of this research into clinical trials in human patients. This direction into targeting angiogenesis will facilitate new preventive and therapeutic interventions for AD and related vascular diseases.

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“…Basically, two types of proangiogenic hematopoietic cells have been identified, one with a more mature phenotype and corresponding to mature Tie2 + monocytic cells and an immature progenitor cell population, corresponding to proangiogenic hematopoietic progenitor cells or CFU-Hill (17). The studies carried out in these last years on proangiogenic hematopoietic cells have led to the conclusion that these cells derive from the differentiation of a subset of hematopoietic progenitor cells, characterized by positivity for CD34, CD133 and VEGF-R2, mobilized from bone marrow by angiogenic growth factors and contributing in vivo to an angiogenetic response only through an indirect effect based on paracrine mechanisms (18)(19)(20)(21).…”

mentioning

confidence: 99%