Effect of Age and Acute Exercise on Circulating Angioregulatory Factors

Author(s):  
Meredith J. Luttrell ◽  
Benjamin R. Mardis ◽  
Joshua M. Bock ◽  
Erika Iwamoto ◽  
Satoshi Hanada ◽  
...  

The balance of angiogenic factors, including vascular endothelial growth factor (VEGF), and angiostatic factors, like thrombospondin-1 (TSP-1) and endostatin, controls striated muscle angiogenic responses to exercise training. The effect of age on circulating levels of these factors following a bout of exercise is unclear. The authors hypothesized that older adults would have lower circulating VEGF but higher TSP-1 and endostatin after exercise compared with young adults. Ten young and nine older participants cycled for 45 min at 60% estimated HRmax. Serum [VEGF], [TSP-1], and [endostatin] obtained before (PREX), immediately after (POSTX0), and 3 hr after (POSTX3) exercise were analyzed. [VEGF] increased in older adults only from PREX to POSTX0 (p < .05). [TSP-1] increased in both age groups (p < .05). There was no effect of age or exercise on [endostatin]. In conclusion, immediately after exercise, both groups had a similar increase in [TSP-1], but [VEGF] increased in older adults only.

2005 ◽  
Vol 2005 (5) ◽  
pp. 293-297 ◽  
Author(s):  
Ariadne Malamitsi-Puchner ◽  
Theodora Boutsikou ◽  
Emmanuel Economou ◽  
Angeliki Sarandakou ◽  
Evangelos Makrakis ◽  
...  

The angiogenic factors vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) are respectively up- and downregulated by hypoxia. We aimed to study circulating levels of the above factors in intrauterine growth restriction (IUGR) and to correlate their levels with the customized centiles of the infants. The study included 25 IUGR and 25 appropriate for gestational age (AGA) full-term, singleton infants and their mothers. Maternal (MS), fetal (UC), and neonatal day 1 (N1) and 4 (N4) blood was examined. MS and N1 PlGF, as well as UC VEGF levels correlated with the customized centiles of the infants (r=0.39,P=.007,r=0.34,P=.01, andr=−0.41,P=.004, resp). Furthermore, UC, N1, and N4 VEGF levels were higher in girls (r=0.36,P=.01,r=0.33,P=.02, andr=0.41,P=.005resp). In conclusion, positive and negative correlations of examined factors with the customized centiles of the infant could rely on placental function and intrauterine oxygen concentrations—both being usually lower in IUGR cases—while higher VEGF levels in girls should possibly be attributed to the stimulating action of estrogens.


2006 ◽  
Vol 203 (6) ◽  
pp. 1447-1458 ◽  
Author(s):  
Kiichiro Yano ◽  
Patricia C. Liaw ◽  
Janet M. Mullington ◽  
Shu-Ching Shih ◽  
Hitomi Okada ◽  
...  

Sepsis, the systemic inflammatory response to infection, is a leading cause of morbidity and mortality. The mechanisms of sepsis pathophysiology remain obscure but are likely to involve a complex interplay between mediators of the inflammatory and coagulation pathways. An improved understanding of these mechanisms should provide an important foundation for developing novel therapies. In this study, we show that sepsis is associated with a time-dependent increase in circulating levels of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) in animal and human models of sepsis. Adenovirus-mediated overexpression of soluble Flt-1 (sFlt-1) in a mouse model of endotoxemia attenuated the rise in VEGF and PlGF levels and blocked the effect of endotoxemia on cardiac function, vascular permeability, and mortality. Similarly, in a cecal ligation puncture (CLP) model, adenovirus–sFlt-1 protected against cardiac dysfunction and mortality. When administered in a therapeutic regimen beginning 1 h after the onset of endotoxemia or CLP, sFlt peptide resulted in marked improvement in cardiac physiology and survival. Systemic administration of antibodies against the transmembrane receptor Flk-1 but not Flt-1 protected against sepsis mortality. Adenovirus-mediated overexpression of VEGF but not PlGF exacerbated the lipopolysaccharide-mediated toxic effects. Together, these data support a pathophysiological role for VEGF in mediating the sepsis phenotype.


2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 19569-19569
Author(s):  
A. Ocana ◽  
A. Rodríguez-Barbero ◽  
M. Pericacho ◽  
L. Bellido ◽  
E. Fonseca ◽  
...  

19569 Background: The expression of Erythropoietin (EPO) receptors on cancer cells and the correlation of EPO receptor levels with angiogenesis and progression in some cancers have suggested that EPO could acts directly as an angiogenic factor. The purpose of this study was to assess the effect of treatment with human recombinant erythropoietic agents (rHuEPO) in cancer patients with chemotherapy-induced anaemia on Endoglin and Vascular Endothelial Growth Factor (VEGF) circulating levels as a possible marker of angiogenesis. Methods: Endoglin and VEGF were measured in serum samples from 25 cancer patients with chemotherapy-induced anaemia before and after 3 to 4 weeks of treatment with rHuEPO (Epoetin alfa 150 UI/Kg three times per week; darbepoetin alfa 150 mcg/weekly). A group of 28 healthy voluntaries were used as control. Endoglin and VEGF were analyzed using an ELISA commercial Kit (R&D Systems; Ciudad-Pais). T- student test was used to study the association between variables. Paired comparisons before and after treatment were performed using the Wilcoxon rank-sum test. Results: VEGF serum levels were significantly higher in cancer patients than in controls (476,66±72,56 pg/ml versus 227,34±24,58 pg/ml, p<0.001, respectively). Endoglin levels were significantly higher in patients than controls, although this difference did not reach statistical significance (4.75±0.30ng/ml versus 4.18±0.12 ng/ml, p=0.075). Similar results were found in the different subgroups of patients (Breast cancer, endoglin p=0.019; VEGF p=0.009; Colon cancer, endoglin p=0.084; VEGF p<0.001). Using the Wilcoxon rank-sum test no statistically significant differences in endoglin (p=0.510) and VEGF (p=0.313) serum levels were found between samples obtained before and after treatment with rHuEPO agents. When considering the type of rHuEPO, no differences were observed. In a similar manner, no difference was observed depending on chemotherapy regimen or cancer type. Conclusions: Although the follow up is short and the number of patients is small, our exploratory results do not support that rHuEpo treatment in anaemic cancer patients induce angiogenic serum markers. No significant financial relationships to disclose.


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