Effects of low dose endotoxemia on endothelial progenitor cells in humans

Mayr, Florian; Spiel, Alexander; Leitner, Judith; Firbas, Christa; Jilma, Bernd

doi:10.1016/j.atherosclerosis.2007.04.003

Cited by 37 publications

(30 citation statements)

References 29 publications

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“…For instance, studies by Mao et al (20) demonstrated intravenous delivery of EPC attenuated LPS-induced lung injury including reduced pulmonary edema, hemorrhage, and inflammation. However, reports demonstrated that endotoxin can decrease EPC numbers by as much as 62% (21). Despite some discrepancies regarding the direct effect of sepsis on EPCs, clinical data show a remarkable correlation between patients' survival rates and circulating EPCs during septic shock (4,5,27).…”

Section: Discussionmentioning

confidence: 99%

Hydrogel-embedded endothelial progenitor cells evade LPS and mitigate endotoxemia

Ghaly

Rabadi

Weber

et al. 2011

American Journal of Physiology-Renal Physiology

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Section: Discussionmentioning

confidence: 99%

Hydrogel-embedded endothelial progenitor cells evade LPS and mitigate endotoxemia

Ghaly

Rabadi

Weber

et al. 2011

American Journal of Physiology-Renal Physiology

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“…LPS, a well-known component of gram-negative bacteria, is a major contributor to the activation of the innate immune system [34] . Increased serum levels of LPS have been reported to promote the progression of CVD in humans [7,35] . In this study, we observed that subcutaneous injections of LPS alone resulted in enhanced atherosclerotic lesion size in ApoE -/-mice.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein A-I inhibits LPS-induced atherosclerosis in ApoE−/− mice possibly via activated STAT3-mediated upregulation of tristetraprolin

Yin

Tang

Tu³

et al. 2013

Acta Pharmacol Sin

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Aim: To investigate the effects of the major component of high-density lipoprotein apolipoprotein A-I (apoA-I) on the development of atherosclerosis in LPS-challenged ApoE -/-mice and the underlying mechanisms. Methods: Male ApoE-KO mice were daily injected with LPS (25 μg, sc) or PBS for 4 weeks. The LPS-challenged mice were intravenously injected with rAAV-apoA-I-GFP or rAAV-GFP. After the animals were killed, blood, livers and aortas were collected for biochemical and histological analyses. For ex vivo experiments, the abdominal cavity macrophages were harvested from each treatment group of mice, and cultured with autologous serum, then treated with LPS. Results: Chronic administration of LPS in ApoE -/-mice significantly increased the expression of inflammatory cytokines (TNF-α, IL-1β, IL-6, and MCP-1), increased infiltration of inflammatory cells, and enhanced the development of atherosclerosis. In LPS-challenged mice injected with rAAV-apoA-I-GFP, viral particles and human apoA-I were detected in the livers, total plasma human apoA-I levels were grammatically increased; HDL-cholesterol level was significantly increased, TG and TC were slightly increased. Furthermore, overexpression of apoA-I significantly suppressed the expression of proinflammatory cytokines, reduced the infiltration of inflammatory cells, and decreased the extent of atherosclerotic lesions. Moreover, overexpression of apoA-I significantly increased the expression of the cytokine mRNA-destabilizing protein tristetraprolin (TTP), and phosphorylation of JAK2 and STAT3 in aortas. In ex vivo mouse macrophages, the serum from mice overexpressing apoA-I significantly increased the expression of TTP, accompanied by accelerated decay of mRNAs of the inflammatory cytokines. Conclusion: ApoA-I potently suppresses LPS-induced atherosclerosis by inhibiting the inflammatory response possibly via activation of STAT3 and upregulation of TTP.

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“…An experimental in vitro study (41) has suggested that CRP can downregulate the production of angiogenic chemokines by EC-CFUs and impair EC-CFU migration toward VEGF. Mayr et al (27) recently reported a two-thirds reduction in the proportion of circulating EPCs (CD34…”

Section: Cd34mentioning

confidence: 99%

Circulating endothelial progenitor cells are not affected by acute systemic inflammation

Padfield¹,

Tura²,

Haeck³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Vascular injury causes acute systemic inflammation and mobilizes endothelial progenitor cells (EPCs) and endothelial cell (EC) colony-forming units (EC-CFUs). Whether such mobilization occurs as part of a nonspecific acute phase response or is a phenomenon specific to vascular injury remains unclear. We aimed to determine the effect of acute systemic inflammation on EPCs and EC-CFU mobilization in the absence of vascular injury. Salmonella typhus vaccination was used as a model of acute systemic inflammation. In a double-blind randomized crossover study, 12 healthy volunteers received S. typhus vaccination or placebo. Phenotypic EPC populations enumerated by flow cytometry [CD34+VEGF receptor (VEGF)R-2+CD133+, CD14+VEGFR-2+Tie2+, CD45−CD34+, as a surrogate for late outgrowth EPCs, and CD34+CXCR-4+], EC-CFUs, and serum cytokine concentrations (high sensitivity C-reactive protein, IL-6, and stromal-derived factor-1) were quantified during the first 7 days. Vaccination increased circulating leukocyte (9.8 ± 0.6 vs. 5.1 ± 0.2 × 109cells/l, P < 0.0001), serum IL-6 [0.95 (0–1.7) vs. 0 (0–0) ng/l, P = 0.016], and VEGF-A [60 (45–94) vs. 43 (21–64) pg/l, P = 0.006] concentrations at 6 h and serum high sensitivity C-reactive protein at 24 h [2.7 (1.4–3.6) vs. 0.4 (0.2–0.8) mg/l, P = 0.037]. Vaccination caused a 56.7 ± 7.6% increase in CD14+cells at 6 h ( P < 0.001) and a 22.4 ± 6.9% increase in CD34+cells at 7 days ( P = 0.04). EC-CFUs, putative vascular progenitors, and the serum stromal-derived factor-1 concentration were unaffected throughout the study period ( P > 0.05 for all). In conclusion, acute systemic inflammation causes nonspecific mobilization of hematopoietic progenitor cells, although it does not selectively mobilize putative vascular progenitors. We suggest that systemic inflammation is not the primary stimulus for EPC mobilization after acute vascular injury.

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Effects of low dose endotoxemia on endothelial progenitor cells in humans

Cited by 37 publications

References 29 publications

Hydrogel-embedded endothelial progenitor cells evade LPS and mitigate endotoxemia

Hydrogel-embedded endothelial progenitor cells evade LPS and mitigate endotoxemia

Apolipoprotein A-I inhibits LPS-induced atherosclerosis in ApoE−/− mice possibly via activated STAT3-mediated upregulation of tristetraprolin

Circulating endothelial progenitor cells are not affected by acute systemic inflammation

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