NT-proBNP and the anti-inflammatory cytokines are correlated with endothelial progenitor cells’ response to cardiac surgery

2008 ◽  
Vol 199 (1) ◽  
pp. 138-146 ◽  
Author(s):  
Francesca Cesari ◽  
Roberto Caporale ◽  
Rossella Marcucci ◽  
Sabina Caciolli ◽  
Pier Luigi Stefano ◽  
...  
2007 ◽  
Vol 83 (2) ◽  
pp. 598-605 ◽  
Author(s):  
Neil Roberts ◽  
Qingzhong Xiao ◽  
Graeme Weir ◽  
Qingbo Xu ◽  
Marjan Jahangiri

2010 ◽  
Vol 55 (1) ◽  
pp. 30-38 ◽  
Author(s):  
Cristiano Spadaccio ◽  
Francesco Pollari ◽  
Adele Casacalenda ◽  
Gennaro Alfano ◽  
Jorge Genovese ◽  
...  

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
David J. Coulson ◽  
Sherin Bakhashab ◽  
Jevi Septyani Latief ◽  
Jolanta U. Weaver

Abstract Background Type 1 diabetes (T1DM) is associated with premature cardiovascular disease (CVD) and a pro-inflammatory state whilst the proangiogenic miR-126-3p/-5p may play a role in CVD. Animal studies established miR-126 to be pro-angiogenic. We hypothesised miR-126-3p/-5p are reduced in T1DM whilst pro-inflammatory cytokines are increased. Methods 29 well controlled, T1DM patients without CVD and 20 healthy controls (HCs) were studied. MiR-126-3p/-5p were assayed in plasma and peripheral blood mononuclear cells (PBMCs) whilst Chemokine C-X-C Receptor 1/2 (CXCR1/2) mRNA in PBMCs by real-time quantitative PCR. Cytokines were assayed by the Mesoscale Discovery. Ingenuity Pathway Analysis (IPA) was used to predict target genes, cellular functions and pathological states regulated by miR-126-3p/-5p. IPA generated both direct and indirect causations between different targets and analysed whether these effects would be inhibitory or stimulatory based on the published evidence. Results T1DM patients had a relatively good diabetic control (HbA1c = 7.4 ± 0.7% or 57.3 ± 7.6 mmol/mol). Homeostatic cytokine IL-7, pro-inflammatory cytokines IL-8 and TNF-α, and vascular endothelial growth factor-C (VEGF-C) were increased in T1DM, versus HCs; p = 0.008, p = 0.003, p = 0.041 and p = 0.013 respectively. MiR-126-5p was significantly upregulated in PBMCs in T1DM versus HCs; p = 0.01, but not in plasma. MiR-126-3p was unchanged. CXCR1/2 were elevated in T1DM versus HCs; p = 0.009 and p < 0.001 respectively. MiR-126-5p was positively correlated with CXCR1/2, and with HbA1c whilst negatively correlated with circulating endothelial progenitor cells (CD34+CD133+CD45dim) and fibronectin adhesion assay in a combined group of T1DM patients and HCs; p = 0.028 p = 0.049 p = 0.035 p = 0.047 and p = 0.004 respectively. IPA predicted miR-126-5p to be anti-inflammatory through the inhibition of chemokine C–C motif ligand 27, chymotrypsin-like elastase 2A and IL-7, whilst miR-126-3p had no direct anti-inflammatory effect. Simultaneously IPA predicted IL-7 as the most upstream cytokine target. Conclusions T1DM without apparent CVD or diabetic complications is an inflammatory state characterised not only by raised pro-inflammatory cytokines but also by increased receptor CXCR1/2 and miR-126-5p. MiR-126-5p upregulation may represent a compensatory response. Pro-miR-126-5p therapies or anti-IL-7 therapies may be a new option to reduce both inflammation and CVD risk in T1DM. Further research is required in a large prospective study in patients with T1DM.


2020 ◽  
pp. 455-460
Author(s):  
A.R. SARAEV ◽  
◽  
SH.K. NAZAROV ◽  
S.G. ALI-ZADE ◽  
◽  
...  

Objective: To study the sepsis markers informativeness to assess the role of monocytes in the pathogenesis of generalized peritonitis (GP). Methods: The study included 160 patients with GP, who were divided into 3 groups, according to the stages of the disease. To establish the activity of monocytes was made a determination of the level of cytokine TNF-α and presepsin in the blood. Results: Studies showed that the level of TNF-α in patient with septic shock was reliably lower (24.5±13.3 pg/ml) than in patients with endogenous intoxication and abdominal sepsis. The value of TNF-α in deceased patients also was low – 4.8±0.9 pg/ml. This indicates a decrease in the ability of monocytes in GP at the stage of septic shock to exude a sufficient amount of pro-inflammatory cytokines in response to endotoxin aggression. The level of presepsin increased by stages and amounted to 355.6±8.6, 783.4±24.0 and 1587.7±70.5 pg/ml, respectively. This indicates the circulation in the blood of the CD14 receptor, which is able to express on monocytes, converting them into endothelial progenitor cells. Conclusions: Monocytes as endothelial progenitor cells contribute to the regeneration and restoration of endothelial function in its dysfunction that develops in GP and abdominal sepsis. In consequence of developing immunosuppression and suppression of monocyte function in the stage of septic shock, the process of renewal of endothelial cells is weakened, the secretion of pro-inflammatory cytokines, in particular TNF-α, decreases, which can contribute to an increase in mortality in septic shock. Keywords: Monocytes, abdominal sepsis, septic shock, endothelial dysfunction, progenitor cells.


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