Effect of acute exercise on circulating angiogenic cell and microparticle populations

Lansford, Kasey A.; Shill, Daniel D.; Dicks, Andrew B; Marshburn, Meagan P.; Southern, William M.; Jenkins, Nathan T.

doi:10.1113/ep085505

Cited by 57 publications

(103 citation statements)

References 43 publications

(114 reference statements)

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“…; Lansford et al. ), and our findings, therefore, suggest that the eventual increase in plasma [EMV] does not necessarily represent endothelial activation and EMV shedding, but may result from hemoconcentration.…”

Section: Discussionsupporting

confidence: 45%

Whole‐body heat stress and exercise stimulate the appearance of platelet microvesicles in plasma with limited influence of vascular shear stress

Wilhelm

González‐Alonso

Chiesa

et al. 2017

Physiological Reports

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Intense, large muscle mass exercise increases circulating microvesicles, but our understanding of microvesicle dynamics and mechanisms inducing their release remains limited. However, increased vascular shear stress is generally thought to be involved. Here, we manipulated exercise‐independent and exercise‐dependent shear stress using systemic heat stress with localized single‐leg cooling (low shear) followed by single‐leg knee extensor exercise with the cooled or heated leg (Study 1, n = 8) and whole‐body passive heat stress followed by cycling (Study 2, n = 8). We quantified femoral artery shear rates (SRs) and arterial and venous platelet microvesicles (PMV–CD41+) and endothelial microvesicles (EMV–CD62E+). In Study 1, mild passive heat stress while one leg remained cooled did not affect [microvesicle] (P ≥ 0.05). Single‐leg knee extensor exercise increased active leg SRs by ~12‐fold and increased arterial and venous [PMVs] by two‐ to threefold, even in the nonexercising contralateral leg (P < 0.05). In Study 2, moderate whole‐body passive heat stress increased arterial [PMV] compared with baseline (mean±SE, from 19.9 ± 1.5 to 35.5 ± 5.4 PMV . μL−1.103, P < 0.05), and cycling with heat stress increased [PMV] further in the venous circulation (from 27.5 ± 2.2 at baseline to 57.5 ± 7.2 PMV . μL−1.103 during cycling with heat stress, P < 0.05), with a tendency for increased appearance of PMV across exercising limbs. Taken together, these findings demonstrate that whole‐body heat stress may increase arterial [PMV], and intense exercise engaging either large or small muscle mass promote PMV formation locally and systemically, with no influence upon [EMV]. Local shear stress, however, does not appear to be the major stimulus modulating PMV formation in healthy humans.

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Section: Discussionsupporting

confidence: 45%

Whole‐body heat stress and exercise stimulate the appearance of platelet microvesicles in plasma with limited influence of vascular shear stress

Wilhelm

González‐Alonso

Chiesa

et al. 2017

Physiological Reports

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“…Some recent studies have begun to examine these issues, although the sex differences remain unclear with some studies reporting lower and others higher resting levels of CD62E+ MPs in sedentary younger women compared with men (Durrer et al , 2015; Gustafson et al , 2015). In addition, some studies are beginning to explore MP responses to an acute bout of aerobic exercise and find differential responses between men and women in CD62E+ (Durrer et al , 2015; Lansford et al , 2016; Shill et al , 2018) and CD34+ MPs (Lansford et al , 2016), suggesting sex differences in responses to vascular stressors with exercise. Thus, future studies specifically designed to examine mechanisms related to sex differences in various populations and in response to an exercise or nutritional intervention might provide better indication as to the use of MPs as sex-specific biomarkers of CVD risk.…”

Section: Discussionmentioning

confidence: 99%

“…Differences among groups were compared using ANOVAs. For our main analyses, power calculations using previous cross-sectional comparisons of MPs in populations with various levels of CVD risk factors (Preston et al , 2003; Lansford et al , 2016) estimated a sample size of n=11/group to yield detectable differences and 80% power. As forty-one percent of chronic stroke subjects were also diagnosed with diabetes mellitus, a sub-analysis was performed to distinguish effects of chronic stroke and T2DM by dividing the chronic stroke group into stroke(diabetes+) and stroke(diabetes-).…”

Section: Methodsmentioning

confidence: 99%

Type 2 diabetes and older age contribute to elevated plasma microparticle concentrations independent of chronic stroke

Landers‐Ramos

Serra

Blumenthal

et al. 2018

Experimental Physiology

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The elevated circulating concentration of endothelial microparticles (MPs) may provide an index of the extent and nature of cellular damage in chronic stroke. The purpose of this study was to determine the circulating concentrations of CD31 /CD42b , CD62E and CD34 MPs in chronic stroke subjects, focusing on the effects of chronic stroke by comparison with both older adults without a history of stroke but with type 2 diabetes mellitus (T2DM) and older and young healthy controls. Plasma from three groups of sedentary older (50-75 years) men and women (chronic stroke, T2DM or older healthy) as well as a group of younger (18-39 years) healthy controls was isolated from fasting blood, and CD31 /CD42b , CD62E and CD34 MPs were quantified using flow cytometry (n = 17/group). Concentrations of CD31 /CD42b and CD62E MPs were higher in the T2DM group (P < 0.05), but not chronic stroke, compared to older and younger healthy adults. CD62E MP and CD34 MP concentrations were elevated in the older compared to younger adults (P < 0.05 for both). Sub-analyses excluding chronic stroke subjects who were also diagnosed with diabetes [stroke (diabetes )] revealed lower CD31 /CD42b (P < 0.05) and CD62E (P = 0.08) MPs in the stroke (diabetes ) group compared to the T2DM group. CD31 /CD42b MP and CD62E MP concentrations were each associated with fasting glucose levels and CD31 /CD42b MPs also were associated with triglyceride levels. As MPs have been proposed as potential targets for diagnosing, treating and identifying the clinical progression of T2DM, our study provides further support for the use of CD31 /CD42b and CD62E MPs in the clinical progression of T2DM and associated vascular complications.

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“…Indeed, a number of different subtypes of PBMCs with pro-angiogenic potential have been identified including CD34−/CD31+ (Landers-Ramos et al 2015), CD62E+ (Lansford et al 2016), angiogenic T-cells (Hur et al 2007; Kushner et al 2010), and angiogenic monocytes (Favre et al 2013), among others. Future studies investigating both the number and function of a variety of different pro-angiogenic PBMCs would provide a more comprehensive assessment of the heterogeneous response of CACs to aerobic exercise training.…”

Section: Discussionmentioning

confidence: 99%

Short-term exercise training improves flow-mediated dilation and circulating angiogenic cell number in older sedentary adults

Landers‐Ramos

Corrigan

Guth

et al. 2016

Appl. Physiol. Nutr. Metab.

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Cardiovascular disease risk increases with age due, in part, to impaired endothelial function and decreased circulating angiogenic cell (CAC) number and function. We sought to determine if 10 days of aerobic exercise training improves endothelial function, CAC number, and intracellular redox balance in older sedentary adults. Eleven healthy subjects (4 men, 7 women), 61 ± 2 years of age participated in 60 min of aerobic exercise at 70% maximal oxygen consumption for 10 consecutive days while maintaining body weight. Before and after training, endothelial function was measured as flow-mediated dilation of the brachial artery and fasting blood was drawn to enumerate 3 CAC subtypes. Intracellular reactive oxygen species (ROS) and nitric oxide (NO) in CD34+ CACs were measured using fluorescent probes and reinforced via real-time quantitative polymerase chain reaction. Flow-mediated dilation improved significantly following training (10% ± 1.3% before vs. 16% ± 1.4% after training; P < 0.05). Likewise, CD34+/KDR+ number increased 104% and KDR+ number increased 151% (P < 0.05 for both), although CD34+ number was not significantly altered (P > 0.05). Intracellular NO and ROS levels in CD34+ CACs were not different after training (P > 0.05 for both). Messenger RNA expression of SOD1, endothelial nitric oxide synthase, and NADPH oxidase 2 and neutrophil cytosolic factor 1 in CD34+ CACs was not significantly altered with training (P > 0.05). In conclusion, 10 consecutive days of aerobic exercise increased flow-mediated dilation and CAC number in older, previously sedentary adults, but did not affect intracellular redox balance in CD34+ CACs. Overall, these data indicate that even short-term aerobic exercise training can have a significant impact on cardiovascular disease risk factors.

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Effect of acute exercise on circulating angiogenic cell and microparticle populations

Abstract: New Findings r What is the central question of this study?What is the effect of acute endurance exercise on circulating angiogenic cell (CAC) and microparticle (MP)

Cited by 57 publications

References 43 publications

Whole‐body heat stress and exercise stimulate the appearance of platelet microvesicles in plasma with limited influence of vascular shear stress

Whole‐body heat stress and exercise stimulate the appearance of platelet microvesicles in plasma with limited influence of vascular shear stress

Type 2 diabetes and older age contribute to elevated plasma microparticle concentrations independent of chronic stroke

Short-term exercise training improves flow-mediated dilation and circulating angiogenic cell number in older sedentary adults

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