Role of platelet-derived growth factors in physiology and medicine

Andræ, Johanna; Gallini, R; Betsholtz, Christer

doi:10.1101/gad.1653708

Cited by 2,071 publications

(2,015 citation statements)

References 316 publications

(364 reference statements)

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“…The high proportion of Tomato + GFP + ECs at E15, 5 days after the loss of YS hemogenic activity, therefore suggests active expression of Pdgfrb‐Cre in the ECs. This is unexpected since Pdgfrb expression has not been previously reported in ECs, and it is thought to be exclusively expressed in mural and subsets of mesenchymal cells (Andrae et al, 2008; Gaengel et al, 2009). We cannot exclude the possibility that the endothelial activity of the Pdgfrb‐Cre line reflects recent tracing from an unknown source of Pdgfrb expressing EC progenitors or a transient endothelial expression of Pdgfrb .…”

Section: Resultsmentioning

confidence: 91%

Pdgfrb‐Cre targets lymphatic endothelial cells of both venous and non‐venous origins

Ulvmar

Martínez-Corral

Stanczuk

et al. 2016

Genesis

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The Pdgfrb‐Cre line has been used as a tool to specifically target pericytes and vascular smooth muscle cells. Recent studies showed additional targeting of cardiac and mesenteric lymphatic endothelial cells (LECs) by the Pdgfrb‐Cre transgene. In the heart, this was suggested to provide evidence for a previously unknown nonvenous source of LECs originating from yolk sac (YS) hemogenic endothelium (HemEC). Here we show that Pdgfrb‐Cre does not, however, target YS HemEC or YS‐derived erythro‐myeloid progenitors (EMPs). Instead, a high proportion of ECs in embryonic blood vessels of multiple organs, as well as venous‐derived LECs were targeted. Assessment of temporal Cre activity using the R26‐mTmG double reporter suggested recent occurrence of Pdgfrb‐Cre recombination in both blood and lymphatic ECs. It thus cannot be excluded that Pdgfrb‐Cre mediated targeting of LECs is due to de novo expression of the Pdgfrb‐Cre transgene or their previously established venous endothelial origin. Importantly, Pdgfrb‐Cre targeting of LECs does not provide evidence for YS HemEC origin of the lymphatic vasculature. Our results highlight the need for careful interpretation of lineage tracing using constitutive Cre lines that cannot discriminate active from historical expression. The early vascular targeting by the Pdgfrb‐Cre also warrants consideration for its use in studies of mural cells. genesis 54:350–358, 2016. © 2016 The Authors. Genesis Published by Wiley Periodicals, Inc.

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Section: Resultsmentioning

confidence: 91%

Pdgfrb‐Cre targets lymphatic endothelial cells of both venous and non‐venous origins

Ulvmar

Martínez-Corral

Stanczuk

et al. 2016

Genesis

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“…120 In mice, overexpression of VEGF leads to epididymal hyperplasia associated with increased capillary density, fenestrations and permeability. 107 Isoforms of another pro-angiogenic factor, platelet-derived growth factor (PDGF) and its receptor 121 are present in the epididymis of adult animals, not in the stroma, but in the epithelium, 122 a site inconsistent with a vascular role.…”

Section: Angiogenesis and Its Endogenous Inhibitors In Tumourigenesismentioning

confidence: 99%

Why are epididymal tumours so rare?

Yeung¹,

Wang²,

Cooper³

2012

Asian J Androl

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Epididymal tumour incidence is at most 0.03% of all male cancers. It is an enigma why the human epididymis does not often succumb to cancer, when it expresses markers of stem and cancer cells, and constitutively expresses oncogenes, pro-proliferative and pro-angiogenic factors that allow tumour cells to escape immunosurveillance in cancer-prone tissues. The privileged position of the human epididymis in evading tumourigenicity is reflected in transgenic mouse models in which induction of tumours in other organs is not accompanied by epididymal neoplasia. The epididymis appears to: (i) prevent tumour initiation (it probably lacks stem cells and has strong anti-oxidative mechanisms, active tumour suppressors and inactive oncogene products); (ii) foster tumour monitoring and destruction (by strong immuno-surveillance and -eradication, and cellular senescence); (iii) avert proliferation and angiogenesis (with persistent tight junctions, the presence of anti-angiogenic factors and misplaced pro-angiogenic factors), which together (iv) promote dormancy and restrict dividing cells to hyperplasia. Epididymal cells may be rendered non-responsive to oncogenic stimuli by the constitutive expression of factors generally inducible in tumours, and resistant to the normal epididymal environment, which mimics that of a tumour niche promoting tumour growth. The threshold for tumour initiation may thus be higher in the epididymis than in other organs. Several anti-tumour mechanisms are those that maintain spermatozoa quiescent and immunologically silent, so the low incidence of cancer in the epididymis may be a consequence of its role in sperm maturation and storage. Understanding these mechanisms may throw light on cancer prevention and therapy in general.

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“…PDGFR-β is expressed in mesenchyme, particularly in vascular SMCs and pericytes (Andrae et al, 2008). …”

Section: Vegf Measurementmentioning

confidence: 99%

Ex vivoDetermination of an Estradiol Analogue-Induced Changes on Platelet Morphology and Angiogenic Biomarkers

2015

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Angiogenesis is a closely controlled biological process that takes place during fetal development of blood vessels and wound healing, and includes the development of new blood vessels from preexisting blood vessels. Tumor angiogenesis is a means by which tumors obtain oxygen, nutrition and promote tumor growth. Angiogenesis-regulating proteins are therefore ideal biomarkers in the study of tumor pathophysiology. In our laboratory, a new in silico-designed analogue of 2-methoxyestradiol has been synthesized with angiogenic properties, namely 2-ethyl-3-O-sulfamoyl-estra-1,3,5(10)16-tetraene (ESE-16). The ex vivo influence of ESE-16 on angiogenesis and morphology in platelets of healthy participants was investigated. Scanning electron microscopy revealed no morphological changes in ESE-16-treated platelets. The possible antiangiogenic effect of ESE-16-exposed platelets was determined by means of flow cytometry measurement of angiogenic protein levels, which were significantly increased after platelets were added to tumorigenic breast epithelial cells. This indicates that binding of platelets to cancer cells causes differential release of platelet constituents. Vascular endothelial growth factor levels were decreased in platelets, whereas platelet-derived growth factor and matrix metallopeptidase-9 levels were not significantly affected in platelets. In light of the above-mentioned data, further investigation of ESE-16's influence on morphology and angiogenic markers in platelets of cancer patients is warranted.

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Role of platelet-derived growth factors in physiology and medicine

Cited by 2,071 publications

References 316 publications

Pdgfrb‐Cre targets lymphatic endothelial cells of both venous and non‐venous origins

Pdgfrb‐Cre targets lymphatic endothelial cells of both venous and non‐venous origins

Why are epididymal tumours so rare?

Ex vivoDetermination of an Estradiol Analogue-Induced Changes on Platelet Morphology and Angiogenic Biomarkers

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