Expression of developmentally regulated endothelial cell locus 1 was induced by tumor-derived factors including VEGF

Aoki, M.; Koike, Masahiko; Ohmori, Kazuo; Takaishi, Mikiro; Huh, Nam-ho; Nogami, Shigeharu; Kimura, Takeshi

doi:10.1016/j.bbrc.2005.06.009

Cited by 20 publications

(20 citation statements)

References 31 publications

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“…As the present study showed, physical activity up-regulates angiogenic growth factors (VEGF), which are pro-angiogenic and inhibit apoptosis of endothelial cells (EC) on the one hand, but simultaneously induces the expression of developmentally regulated endothelial cell locus 1 (DEL-1) [46], which was shown to mediate phosphatidylserine- and integrin-dependent endothelial uptake of microparticles by endocytosis [25]. In this context, one could speculate that the increase of VEGF and the decrease of circulating EMP after physical exercise might be mediated by an enhanced expression of DEL-1 with a subsequently increased uptake of EMP into the endothelium.…”

Section: Discussionmentioning

confidence: 83%

Effects of High Intensity Training and High Volume Training on Endothelial Microparticles and Angiogenic Growth Factors

et al. 2014

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AimsEndothelial microparticles (EMP) are complex vesicular structures shed from activated or apoptotic endothelial cells. As endurance exercise affects the endothelium, the objective of the study was to examine levels of EMP and angiogenic growth factors following different endurance exercise protocols.Methods12 subjects performed 3 different endurance exercise protocols: 1. High volume training (HVT; 130 min at 55% peak power output (PPO); 2. 4×4 min at 95% PPO; 3. 4×30 sec all-out. EMPs were quantified using flow cytometry after staining platelet-poor-plasma. Events positive for Annexin-V and CD31, and negative for CD42b, were classified as EMPs. Vascular endothelial growth factor (VEGF), migratory inhibiting factor (MIF) and hepatocyte growth factor (HGF) were determined by ELISA technique. For all these measurements venous blood samples were taken pre, 0′, 30′, 60′ and 180′ after each intervention. Furthermore, in vitro experiments were performed to explore the effect of collected sera on target endothelial functions and MP uptake capacities.ResultsVEGF and HGF significantly increased after HIT interventions. All three interventions caused a significant decrease in EMP levels post exercise compared to pre values. The sera taken after exercise increased the uptake of EMP in target endothelial cells compared to sera taken under resting conditions, which was shown to be phosphatidylserin-dependent. Increased EMP uptake was associated with an improved protection of target cells against apoptosis. Sera taken prior and after exercise promoted target endothelial cell migration, which was abrogated after inhibition of VEGF.ConclusionPhysical exercise leads to decreased EMP levels and promotes a phosphatidylserin-dependent uptake of EMP into target endothelial cells, which is associated with a protection of target cells against apoptosis.

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Section: Discussionmentioning

confidence: 83%

Effects of High Intensity Training and High Volume Training on Endothelial Microparticles and Angiogenic Growth Factors

et al. 2014

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“…A heat-induced increase in microparticle clearance in the liver and spleen is unlikely given the known hyperthermia-induced reductions in splanchnic blood flow (Deschamps & Magder, 1994). Meanwhile, microparticle uptake at endothelial cells might be increased via proliferation of the developmentally regulated endothelial cell locus 1 (DEL-1) from upregulated vascular endothelial growth factor signalling (Kanamori et al 1999;Aoki et al 2005). For example, microparticle clearance via macrophages might be increased in heat stress from augmented T-cell activity (Ostberg et al 2001).…”

Section: Baselinementioning

confidence: 99%

Passive heat stress reduces circulating endothelial and platelet microparticles

Bain

Ainslie

Bammert

et al. 2017

Experimental Physiology

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What is the central question of this study? Does passive heat stress of +2°C oesophageal temperature change concentrations of circulating arterial endothelial- and platelet-derived microparticles in healthy adults? What is the main finding and its importance? Concentrations of circulating endothelial- and platelet-derived microparticles were markedly decreased in heat stress. Reductions in circulating microparticles might indicate favourable vascular changes associated with non-pathological hyperthermia. Interest in circulating endothelial- and platelet-derived microparticles (EMPs and PMPs, respectively) has increased because of their potential pathogenic role in vascular disease and as biomarkers for vascular health. Hyperthermia is commonly associated with a pro-inflammatory stress but might also provide vascular protection when the temperature elevation is non-pathological. Circulating microparticles might contribute to the cellular adjustments and resultant vascular impacts of hyperthermia. Here, we determined whether circulating concentrations of arterial EMPs and PMPs are altered by passive heat stress (+2°C oesophageal temperature). Ten healthy young men (age 23 ± 3 years) completed the study. Hyperthermia was achieved by circulating ∼49°C water through a water-perfused suit that covered the entire body except the hands, feet and head. Arterial (radial) blood samples were obtained immediately before heating (normothermia) and in hyperthermia. The mean ± SD oesophageal temperature in normothermia was 37.2 ± 0.1°C and in hyperthermia 39.1 ± 0.1°C. Concentrations of circulating EMPs and PMPs were markedly decreased in hyperthermia. Activation-derived EMPs were reduced by ∼30% (mean ± SD; from 61 ± 8 to 43 ± 7 microparticles μl ; P < 0.05) and apoptosis-derived EMPs by ∼45% (from 46 ± 7 to 23 ± 3 microparticles μl ; P < 0.05). Likewise, circulating PMPs were reduced by ∼75% in response to hyperthermia (from 256 ± 43 to 62 ± 14 microparticles μl ). These beneficial reductions in circulating EMPs and PMPs in response to a 2°C increase in core temperature might partly underlie the reported vascular improvements following therapeutic bouts of physiological hyperthermia.

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“…It is known that the expression of developmentally regulated endothelial cell locus 1 was induced by tumor-derived factors including vascular endothelial growth factor that may lead to shift from normal phospholipid to asymmetry and forming microvesiculation [26,27]. The basic molecular mechanism that is being suggested which may involve in the process of microvesiculation is intracellular calcium overload with subsequent cell activation due to intracellular increases in several regulated proteins (such as gelsolin and calpain) and homeostasic cell membrane enzymes (translocase, floppase, scramblase) [26].…”

Section: Definition Of Endothelial-derived Microparticles and Their Bmentioning

confidence: 99%

Predictive role of circulating endothelial-derived microparticles in cardiovascular diseases

Berezin

Zulli

Kerrigan

et al. 2015

Clinical Biochemistry

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Expression of developmentally regulated endothelial cell locus 1 was induced by tumor-derived factors including VEGF

Cited by 20 publications

References 31 publications

Effects of High Intensity Training and High Volume Training on Endothelial Microparticles and Angiogenic Growth Factors

Effects of High Intensity Training and High Volume Training on Endothelial Microparticles and Angiogenic Growth Factors

Passive heat stress reduces circulating endothelial and platelet microparticles

Predictive role of circulating endothelial-derived microparticles in cardiovascular diseases

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