scholarly journals Small Interfering RNA Efficiently Suppresses Adhesion Molecule Expression on Pulmonary Microvascular Endothelium

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Tobias Walker ◽  
Julian Siegel ◽  
Andrea Nolte ◽  
Silke Hartmann ◽  
Angela Kornberger ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Microvascular Endothelial Cells ◽  
Adhesion Molecule Expression ◽  
Small Interfering Rnas ◽  
Sirna Transfection ◽  
Microvascular Endothelium ◽  
Microvascular Endothelial

Background. Adhesion molecules are known to influence postoperative organ function, they are hardly involved in the inflammatory response following the ischemia-reperfusion injury. We sought to investigate the potency of small interfering RNAs to suppress adhesion molecule expression in human pulmonary microvascular endothelial cells.Methods. Human lung microvascular endothelial cells were transfected with specific siRNA followed by a stimulation of the cells with an inflammatory cytokine. Adhesion molecule expression was determined by FACS-analysis, and reduction of intracellular mRNA was determined by qRT-PCR. Furthermore, the attachment of isolated neutrophils on the endothelial layer was determined after siRNA transfection.Results. In summary, siRNA transfection significantly decreased the percentage positive cells in a single cocktail transfection of each adhesion molecule investigated. Adhering neutrophils were diminished as well.Conclusion. siRNA might be a promising tool for the effective suppression of adhesion molecule expression on pulmonary microvascular cells, potentially minimizing leukocyte-endothelial depending interactions of a pulmonary allograft.

Methylene blue modulates adhesion molecule expression on microvascular endothelial cells

2014 ◽  
Vol 63 (8) ◽  
pp. 649-656 ◽  
Author(s):  
Isabella Werner ◽  
Fengwei Guo ◽  
Ulrich A. Stock ◽  
Michèle Lupinski ◽  
Patrick Meybohm ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Microvascular Endothelial Cells ◽  
Adhesion Molecule Expression ◽  
Microvascular Endothelial

scholarly journals Exosomes Derived from CXCR4-Overexpressing BMSC Promoted Activation of Microvascular Endothelial Cells in Cerebral Ischemia/Reperfusion Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Xutong Li ◽  
Ye Zhang ◽  
Yong Wang ◽  
Dan Zhao ◽  
Chengcheng Sun ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Reperfusion Injury ◽  
Vascular Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Tube Formation ◽  
Microvascular Endothelial Cells ◽  
Significant Difference ◽  
Microvascular Endothelial

Background. Ischemic stroke is a severe acute cerebrovascular disease which can be improved with neuroprotective therapies at an early stage. However, due to the lack of effective neuroprotective drugs, most stroke patients have varying degrees of long-term disability. In the present study, we investigated the role of exosomes derived from CXCR4-overexpressing BMSCs in restoring vascular function and neural repair after ischemic cerebral infarction. Methods. BMSCs were transfected with lentivirus encoded by CXCR4 (BMSCCXCR4). Exosomes derived from BMSCCXCR4 (ExoCXCR4) were isolated and characterized by transmission electron microscopy and dynamic light scattering. Western blot and qPCR were used to analyze the expression of CXCR4 in BMSCs and exosomes. The acute middle cerebral artery occlusion (MCAO) model was prepared, ExoCXCR4 were injected into the rats, and behavioral changes were analyzed. The role of ExoCXCR4 in promoting the proliferation and tube formation for angiogenesis and protecting brain endothelial cells was determined in vitro. Results. Compared with the control groups, the ExoCXCR4 group showed a significantly lower mNSS score at 7 d, 14 d, and 21 d after ischemia/reperfusion ( P < 0.05 ). The bEnd.3 cells in the ExoCXCR4 group have stronger proliferation ability than other groups ( P < 0.05 ), while the CXCR4 inhibitor can reduce this effect. Exosomes control (ExoCon) can significantly promote the migration of bEnd.3 cells ( P < 0.05 ), while there was no significant difference between the ExoCXCR4 and ExoCon groups ( P > 0.05 ). ExoCXCR4 can further promote the proliferation and tube formation for the angiogenesis of the endothelium compared with ExoCon group ( P < 0.05 ). In addition, cobalt chloride (COCl2) can increase the expression of β-catenin and Wnt-3, while ExoCon can reduce the expression of these proteins ( P < 0.05 ). ExoCXCR4 can further attenuate the activation of Wnt-3a/β-catenin pathway ( P < 0.05 ). Conclusions. In ischemia/reperfusion injury, ExoCXCR4 promoted the proliferation and tube formation of microvascular endothelial cells and play an antiapoptotic role via the Wnt-3a/β-catenin pathway.

Abstract 532: Protein Analysis of Tongxinluo-modulated Cytokines in Cardiac Microvascular Endothelial Cells via Tandem Mass Tag Quantitative Proteomics After Ischemia/Reperfusion Injury

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Qing Li ◽  
Yuejin Yang
Keyword(s):  
Endothelial Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Tissue Growth ◽  
Microvascular Endothelial Cells ◽  
Heme Oxygenase 1 ◽  
Differential Proteins ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

Background: Proteomics is a potential tool to study the large-scale expression, function and interaction of the complement of proteins in an organism. In this study, we used the TMT-labeled proteomics to detect the various cytokines in an in vitro model of cardiac microvascular endothelial cells (CMECs) ischemia/reperfusion injury with Tongxinluo(TXL) treatment. Our aims are to investigate whether TXL could modulate the secretion function of CMECs, and to synthetically analysis the underlying mechanism of the regulation. Methods: Human CMECs were exposed to different concentrations of TXL, and incubated to scavenge free oxygen for 2 h of hypoxia and were moved to normal conditions for 2 h of reoxygenation. Cell apoptosis was assessed by flow cytometric analysis. CMECs were divided into three groups for TMT-labeled proteomics analysis: CMECs in normal condition (Group N), CMECs in hypoxia and serum deprivation condition (Group HR), CMECs treatment with TXL in hypoxia and serum condition(Group HR+TXL) . We utilized bioinformatics analysis to identify differential proteins. Results: TXL concentration-dependently decreased apoptosis of CMECs. The optimal concentration of TXL to have the maximum protection for CMECs was 800 μg/mL. Both hypoxia/reoxygenation and TXL treatment significantly changed the cytokines level of CMECs. 32 differential proteins between group N and group HR were detected. TXL treatment up-regulated 6 cytokines and down-regulated 6 cytokines in ischemia/reperfusion injury. These proteins mainly had vital functions such as cell proliferation, stress response, regulation of multicelluler organismal metabolic process. We evaluated several proteins played important roles in ischemia/reperfusion injury including Human Heme Oxygenase 1 (HMOX1), angiopoietin 2 (ANGPT2), sequestosome 1 (SQSTM1), and connective tissue growth factor (CTGF). Conclusion: The study presented differential proteins responsible for ischemia/reperfusion injury through TMT-labeled proteomic analysis. We assessed some vital proteins including their characters and roles. These findings may provide new mechanisms of TXL treatment in acute myocardial diseases.

scholarly journals Astragalus Polysaccharide Suppresses the Expression of Adhesion Molecules through the Regulation of the p38 MAPK Signaling Pathway in Human Cardiac Microvascular Endothelial Cells after Ischemia-Reperfusion Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Zhu Hai-Yan ◽  
Gao Yong-Hong ◽  
Wang Zhi-Yao ◽  
Xu Bing ◽  
Wu Ai-Ming ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Reperfusion Injury ◽  
P38 Mapk ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mapk Signaling ◽  
Microvascular Endothelial Cells ◽  
Astragalus Polysaccharide ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

Astragalus polysaccharide is a major component of radix astragali, a vital qi-reinforcing herb medicine with favorable immune-regulating effects. In a previous animal experiment, we demonstrated that astragalus polysaccharide effectively alleviates ischemia-reperfusion injury (IRI) of cardiac muscle through the regulation of the inflammatory reactions. However, the relationship between this herb and the cohesion molecules on the cell surface remains controversial. In this study, human cardiac microvascular endothelial cells (HCMECs) were used to validate the protective effects of astragalus under an IRI scheme simulated through hypoxia/reoxygenation in vitro. The results indicated that astragalus polysaccharide inhibited the cohesion between HCMECs and polymorphonuclear leukocyte (PMN) during IRI through the downregulation of p38 MAPK signaling and the reduction of cohesive molecule expression in HCMECs.

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