Circulating levels of adhesion molecules and markers of endothelial activation in acute inflammation induced by prolonged brisk exercise

Bartzeliotou, Αnastasia; Margeli, Alexandra; Tsironi, Maria; Skenderi, Katerina; Bacoula, Chryssa; Chrousos, George P.; Papassotiriou, Ioannis

doi:10.1016/j.clinbiochem.2007.01.013

Cited by 38 publications

(26 citation statements)

References 36 publications

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“…The increase in strain frequency is also analogous to an elevation in normal heart rate (i.e. from 60–120 beats per minute), and in this respect it can be noted that increased levels of circulating TM have been associated with physical exercise [42], [43], which is characterised by elevated shearing and heart rate.…”

Section: Discussionmentioning

confidence: 88%

Regulation of Thrombomodulin Expression and Release in Human Aortic Endothelial Cells by Cyclic Strain

et al. 2014

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Background and ObjectivesThrombomodulin (TM), an integral membrane glycoprotein expressed on the lumenal surface of vascular endothelial cells, promotes anti-coagulant and anti-inflammatory properties. Release of functional TM from the endothelium surface into plasma has also been reported. Much is still unknown however about how endothelial TM is regulated by physiologic hemodynamic forces (and particularly cyclic strain) intrinsic to endothelial-mediated vascular homeostasis.MethodsThis study employed human aortic endothelial cells (HAECs) to investigate the effects of equibiaxial cyclic strain (7.5%, 60 cycles/min, 24 hrs), and to a lesser extent, laminar shear stress (10 dynes/cm2, 24 hrs), on TM expression and release. Time-, dose- and frequency-dependency studies were performed.ResultsOur initial studies demonstrated that cyclic strain strongly downregulated TM expression in a p38- and receptor tyrosine kinase-dependent manner. This was in contrast to the upregulatory effect of shear stress. Moreover, both forces significantly upregulated TM release over a 48 hr period. With continuing focus on the cyclic strain-induced TM release, we noted both dose (0–7.5%) and frequency (0.5–2.0 Hz) dependency, with no attenuation of strain-induced TM release observed following inhibition of MAP kinases (p38, ERK-1/2), receptor tyrosine kinase, or eNOS. The concerted impact of cyclic strain and inflammatory mediators on TM release from HAECs was also investigated. In this respect, both TNFα (100 ng/ml) and ox-LDL (10–50 µg/ml) appeared to potentiate strain-induced TM release. Finally, inhibition of neither MMPs (GM6001) nor rhomboids (3,4-dichloroisocoumarin) had any effect on strain-induced TM release. However, significantly elevated levels (2.1 fold) of TM were observed in isolated microparticle fractions following 7.5% strain for 24 hrs.ConclusionsA preliminary in vitro investigation into the effects of cyclic strain on TM in HAECs is presented. Physiologic cyclic strain was observed to downregulate TM expression, whilst upregulating in a time-, dose- and frequency-dependent manner the release of TM.

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Section: Discussionmentioning

confidence: 88%

Regulation of Thrombomodulin Expression and Release in Human Aortic Endothelial Cells by Cyclic Strain

et al. 2014

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“…Previous studies have shown that the type and the degree of exercises increases oxidative stress, which, in turn causes the generation of reactive oxygen species (ROS), that influences inflammatory markers including C-reactive protein (CRP) (Kasapis and Thompson, 2005;Majka et al, 2009) and genetic factors (Shen and Ordovas, 2009). Athletes have also been reported to have better endothelial function than sedentary controls (Franzoni et al, 2004), although, prolonged, brisk exercise is also reported to transiently raise markers of endothelial activation, such as ICAM-1 and Eselectin (Bartzeliotou et al, 2007). In the light of these studies we have hypothesed that intensive training alters the markers of inflammation, endothelial functions and autoimmunity in adolescent females.…”

Section: Introductionmentioning

confidence: 99%

Altered Antioxidant and Trace-Element Status in Adolescent Female Gymnasts

Al-Shammari¹,

Shafi²,

Nurmi-Lawton³

et al. 2010

International Journal of Sport Nutrition and Exercise Metabolism

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High levels of physical activity have been linked to benefits in cardiovascular and bone health by affecting, in part, changes in proinflammatory profile. Therefore, we have aimed to assess the effects of intensive training on markers of inflammation, endothelial activation and auto-immunity in the absence of the potential confounding effects of incident atherosclerosis. The subjects comprised 25 competitive gymnasts and 19 healthy sedentary adolescent females, aged 8-17 years. Serum soluble intercellular adhesion molecule 1 (sICAM-1), high sensitivity C-reactive protein (hsCRP), heat shock protein 27 (Hsp27) and Hsp27 antibody titres were measured by ELISAs in a sample of adolescent girls who were either physically active (competitive gymnasts) or sedentary. The association between age, body mass index (BMI), dietary intake, serum hsCRP, sICAM-1 and Hsp27 antigen and antibody titres were determined. The mean serum sICAM-1 concentrations were significantly higher in the gymnasts compared to the sedentary females (0.29 ± 0.02 versus 0.23 ± 0.01 mg·L -1 , p < 0.01). In contrast serum hsCRP concentrations were substantially lower in the gymnasts compared to the sedentary adolescent females (0.49 ± 0.03 versus 1.38 ± 0.19 mg·L -1 , p < 0.001). Differences remained significant after adjustment for anthropometric factors. We also found that serum Hsp27 antigen concentrations were determined by dietary saturated fat intake (p < 0.001), and antibody titres to Hsp27 were determined by dietary PUFA (p < 0.001) after adjustment for BMI. Our findings show that young female gymnasts have an altered profile of inflammatory markers and endothelial activation compared to their less physically active peers.

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“…Acute exercise increases interleukins (IL) 6, 8 and 10 as well as the antagonist of the IL-1β receptor (IL-1Ra), with a concomitant increase in the circulating levels of adhesion molecules [14,15,16]. Prolonged physical training with regular exercise reduces C-reactive protein [17] and causes increased secretion of the anti- and proinflammatory cytokine IL-6 combined with reduction in the highly potent inflammatory cytokine tumor necrosis factor alpha (TNF-α) [10].…”

Section: Introductionmentioning

confidence: 99%

Prolonged Physical Training Decreases mRNA Levels of Glucocorticoid Receptor and Inflammatory Genes

Silva

Longui²,

Rocha³

et al. 2010

Horm Res Paediatr

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Background/Aims: Prolonged physical exercise induces adaptive alterations in the hypothalamic-pituitary axis, increasing cortisol metabolism, and reducing cortisol synthesis and glucocorticoid sensitivity. The mechanisms responsible for this relative glucocorticoid resistance remain unknown but may involve expression of genes encoding glucocorticoid receptor (GR) and/or inflammatory molecules of nuclear factor kappa B1 (NFkB1) signaling pathway and cytokines. This study aimed to determine the impact of prolonged physical training on the expression of genes involved in glucocorticoid action and inflammatory response. Methods: Normal sedentary male cadets of the Brazilian Air Force Academy were submitted to 6 weeks of standardized physical training. Eighteen of 29 initially selected cadets were able to fully complete the training program. Fasting glucose, insulin and cortisol levels, cytokine concentration and the expression of genes encoding GR, NFkB1, inhibitor of NFkB1 and IkB kinase A were determined before and after the training period. Results: Prolonged physical exercise reduced the basal cortisol levels and the percent cortisol reduction after dexamethasone. These findings were associated with a significant reduction in the mRNA levels of GR (6.3%), NFkB1 (63%), inhibitor of NFkB1 (25%) and IkB kinase A (46%) with concomitant reduction in cytokine concentrations (ELISA). Conclusions: Prolonged physical training decreases the glucocorticoid sensitivity and the mRNA levels of the GR gene combined with decreased mRNA of genes related to the NFkB pathway.

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Circulating levels of adhesion molecules and markers of endothelial activation in acute inflammation induced by prolonged brisk exercise

Cited by 38 publications

References 36 publications

Regulation of Thrombomodulin Expression and Release in Human Aortic Endothelial Cells by Cyclic Strain

Regulation of Thrombomodulin Expression and Release in Human Aortic Endothelial Cells by Cyclic Strain

Altered Antioxidant and Trace-Element Status in Adolescent Female Gymnasts

Prolonged Physical Training Decreases mRNA Levels of Glucocorticoid Receptor and Inflammatory Genes

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