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Search results for: Human Cardiac Microvascular Endothelial Cells

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#32602017   2020/06/29 To Up

Protective effects of acetylcholine on hypoxia-induced endothelial-to-mesenchymal transition in human cardiac microvascular endothelial cells.

Endothelial-to-mesenchymal transition (EndMT) has been reported as a key factor in myocardial fibrosis. Acetylcholine (ACh), a neurotransmitter of the vagus nerve, has been confirmed to exert cardio-protective properties with unclear mechanisms. In this study, the specific markers of cell injury, EndMT, inflammation, and autophagy were measured. We found that treatment with ACh prevented hypoxia-induced cell viability reduction and apoptosis in human cardiac microvascular endothelial cells (HCMECs). Additionally, our results indicate that pre-treatment with ACh significantly suppresses hypoxia-induced EndMT and NF-κB activation in HCMECs. ACh also reduced hypoxia-inducible factor (HIF)-1ɑ protein levels under hypoxia. Knock down of HIF-1ɑ enhanced the inhibitory effect of ACh on NF-κB activation. The NF-κB-specific small molecule inhibitor BAY 11-7082, prostaglandin E2, and LY294002 prevented hypoxia-induced EndMT. Moreover, our data show that hypoxia triggers autophagy in HCMECs, and ACh significantly upregulates autophagy activity. Pre-treatment of HCMECs with 3-methyladenine or chloroquine partially reversed ACh-induced EndMT inhibition. These results suggest that ACh may confer protection against hypoxia-induced EndMT through the inhibition of NF-κB and the induction of autophagy.
Zhiyang Li, Xuelian Li, Yeqian Zhu, Qiushi Chen, Bingong Li, Fengxiang Zhang

2337 related Products with: Protective effects of acetylcholine on hypoxia-induced endothelial-to-mesenchymal transition in human cardiac microvascular endothelial cells.

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#32579402   2020/06/24 To Up

Vascular Permeability Disruption Explored in the Proteomes of Mouse Lungs and Human Microvascular Cells following Acute Bromine Exposure.

Bromine (Br) is an organohalide found in nature and is integral to many manufacturing processes. Br is toxic to living organisms and high concentrations can prove fatal. To meet industrial demand large amounts of purified Br are produced, transported, and stored worldwide providing a multitude of interfaces for potential human exposure through either accidents or terrorism. To identify the key mechanisms associated with acute Br exposure, we havesurveyed the lung proteomes of C57BL/6 male mice and human lung derived microvascular endothelial cells (HMEC's) at 24 hrs following exposure to Br in concentrations likely to be encountered in the vicinity of industrial accidents. Global discovery proteomics applications, combined with systems biology analysis identified robust and highly significant changes in proteins associated with three biological processes: 1. exosome secretion, 2. inflammation, and 3. vascular permeability. We focused on the latter, conducting physiological studies on isolated perfused lungs harvested from mice 24 hrs post Br exposure. These experiments revealed significant increases in the filtration coefficient (Kf) indicating increased permeability of the pulmonary vasculature. Similarly, confluent monolayers of Br and Br-lipid treated HMEC's exhibited differential levels of ZO-1 that found to be dissociated from cell wall localization, an increase in phosphorylation and internalization of E-cadhedrin, as well as increased actin stress fiber formation, all of which are consistent with increased permeability. Taken as a whole, our discovery proteomics and systems analysis workflow, combined with physiological measurements of permeability, revealed both profound and novel biological changes that contribute to our current understanding of Br toxicity.
Dylan R Addis, Saurabh Aggarwal, Stephen F Doran, Ming-Yuan Jian, Israr Ahmad, Kyoko Kojima, David A Ford, Sadis Matalon, James A Mobley

2701 related Products with: Vascular Permeability Disruption Explored in the Proteomes of Mouse Lungs and Human Microvascular Cells following Acute Bromine Exposure.

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#32548106   2020/05/29 To Up

Molecular and Biomechanical Clues From Cardiac Tissue Decellularized Extracellular Matrix Drive Stromal Cell Plasticity.

Decellularized-organ-derived extracellular matrix (dECM) has been used for many years in tissue engineering and regenerative medicine. The manufacturing of hydrogels from dECM allows to make use of the pro-regenerative properties of the ECM and, simultaneously, to shape the material in any necessary way. The objective of the present project was to investigate differences between cardiovascular tissues (left ventricle, mitral valve, and aorta) with respect to generating dECM hydrogels and their interaction with cells in 2D and 3D. The left ventricle, mitral valve, and aorta of porcine hearts were decellularized using a series of detergent treatments (SDS, Triton-X 100 and deoxycholate). Mass spectrometry-based proteomics yielded the ECM proteins composition of the dECM. The dECM was digested with pepsin and resuspended in PBS (pH 7.4). Upon warming to 37°C, the suspension turns into a gel. Hydrogel stiffness was determined for samples with a dECM concentration of 20 mg/mL. Adipose tissue-derived stromal cells (ASC) and a combination of ASC with human pulmonary microvascular endothelial cells (HPMVEC) were cultured, respectively, on and in hydrogels to analyze cellular plasticity in 2D and vascular network formation in 3D. Differentiation of ASC was induced with 10 ng/mL of TGF-β1 and SM22α used as differentiation marker. 3D vascular network formation was evaluated with confocal microscopy after immunofluorescent staining of PECAM-1. In dECM, the most abundant protein was collagen VI for the left ventricle and mitral valve and elastin for the aorta. The stiffness of the hydrogel derived from the aorta (6,998 ± 895 Pa) was significantly higher than those derived from the left ventricle (3,384 ± 698 Pa) and the mitral valve (3,233 ± 323 Pa) (One-way ANOVA, = 0.0008). Aorta-derived dECM hydrogel drove non-induced (without TGF-β1) differentiation, while hydrogels derived from the left ventricle and mitral valve inhibited TGF-β1-induced differentiation. All hydrogels supported vascular network formation within 7 days of culture, but ventricular dECM hydrogel demonstrated more robust vascular networks, with thicker and longer vascular structures. All the three main cardiovascular tissues, myocardium, valves, and large arteries, could be used to fabricate hydrogels from dECM, and these showed an origin-dependent influence on ASC differentiation and vascular network formation.
Gabriel Romero Liguori, Tácia Tavares Aquinas Liguori, Sérgio Rodrigues de Moraes, Viktor Sinkunas, Vincenzo Terlizzi, Joris A van Dongen, Prashant K Sharma, Luiz Felipe Pinho Moreira, Martin Conrad Harmsen

1899 related Products with: Molecular and Biomechanical Clues From Cardiac Tissue Decellularized Extracellular Matrix Drive Stromal Cell Plasticity.

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#32545307   2020/06/11 To Up

IRE1 Endoribonuclease Activity Modulates Hypoxic HIF-1α Signaling in Human Endothelial Cells.

While the role of hypoxia and the induction of the hypoxia inducible factors (HIFs) and the unfolded protein response (UPR) pathways in the cancer microenvironment are well characterized, their roles and relationship in normal human endothelium are less clear. Here, we examined the effects of IRE1 on HIF-1α protein levels during hypoxia in primary human umbilical vein endothelial cells (HUVECs). The results demonstrated that HIF-1α levels peaked at 6 h of hypoxia along with two of their target genes, and , whereas at up to 12 h of hypoxia the mRNA levels of markers of the UPR, , , , and , did not increase, suggesting that the UPR was not activated. Interestingly, the siRNA knockdown of IRE1 or inhibition of endonuclease activity with 4µ8C during hypoxia significantly reduced HIF-1α protein without affecting mRNA expression. The inhibition of the endonuclease activity with 4µ8C in two other primary endothelial cells during hypoxia, human cardiac microvascular endothelial cells and human aortic endothelial cells showed the same reduction in the HIF-1α protein. Surprisingly, the siRNA knockdown of during hypoxia did not decrease the HIF1α protein levels, indicating that the IRE1-mediated effect on stabilizing the HIF1α protein levels was XBP1s-independent. The studies presented here, therefore, provide evidence that IRE1 activity during hypoxia increases the protein levels of HIF1α in an XBP1s-independent manner.
Adrianna Moszyńska, James F Collawn, Rafal Bartoszewski

1388 related Products with: IRE1 Endoribonuclease Activity Modulates Hypoxic HIF-1α Signaling in Human Endothelial Cells.

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#32531895   2020/06/10 To Up

MnTBAP Reverses Pulmonary Vascular Remodeling and Improves Cardiac Function in Experimentally Induced Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by obstructed pulmonary vasculatures. Current therapies for PAH are limited and only alleviate symptoms. Reduced levels of BMPR2 are associated with PAH pathophysiology. Moreover, reactive oxygen species, inflammation and autophagy have been shown to be hallmarks in PAH. We previously demonstrated that MnTBAP, a synthetic metalloporphyrin with antioxidant and anti-inflammatory activity, inhibits the turn-over of BMPR2 in human umbilical vein endothelial cells. Therefore, we hypothesized that MnTBAP might be used to treat PAH. Human pulmonary artery endothelial cells (PAECs), as well as pulmonary microvascular endothelial (MVECs) and smooth muscle cells (MVSMCs) from PAH patients, were treated with MnTBAP. In vivo, either saline or MnTBAP was given to PAH rats induced by Sugen 5416 and hypoxia (SuHx). On PAECs, MnTBAP was found to increase BMPR2 protein levels by blocking autophagy. Moreover, MnTBAP increased BMPR2 levels in pulmonary MVECs and MVSMCs isolated from PAH patients. In SuHx rats, MnTBAP reduced right ventricular (RV) afterload by reversing pulmonary vascular remodeling, including both intima and media layers. Furthermore, MnTBAP improved RV function and reversed RV dilation in SuHx rats. Taken together, these data highlight the importance of MnTBAP as a potential therapeutic treatment for PAH.
Maria Catalina Gomez-Puerto, Xiao-Qing Sun, Ingrid Schalij, Mar Orriols, Xiaoke Pan, Robert Szulcek, Marie-José Goumans, Harm-Jan Bogaard, Qian Zhou, Peter Ten Dijke

2545 related Products with: MnTBAP Reverses Pulmonary Vascular Remodeling and Improves Cardiac Function in Experimentally Induced Pulmonary Arterial Hypertension.

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#32506850   // To Up

"Effects of extracts from Renshen (Radix Ginseng), Sanqi (Radix Notoginseng), and Chuanxiong (Rhizoma Chuanxiong) on F-actin in senescent microvascular endothelial cells".

To investigate the effects of extracts from Renshen (Radix Ginseng), Sanqi (Radix Notoginseng), and Chuanxiong (Rhizoma Chuanxiong) on the endothelial actin cytoskeleton in senescent human cardiac microvascular endothelial cells (HCMECs), and to propose the possible mechanism underlying the actions.
Qiang Wang, Jing Yang, Yan Lei, Chengkui Xiu, Yanming Huo, Hang Shi

1908 related Products with: "Effects of extracts from Renshen (Radix Ginseng), Sanqi (Radix Notoginseng), and Chuanxiong (Rhizoma Chuanxiong) on F-actin in senescent microvascular endothelial cells".

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#32484440   2020/06/02 To Up

Shear stress activates ADAM10 sheddase to regulate Notch1 via the Piezo1 force sensor in endothelial cells.

Mechanical force is a determinant of Notch signalling but the mechanism of force detection and its coupling to Notch are unclear. We propose a role for Piezo1 channels, which are mechanically-activated non-selective cation channels. In cultured microvascular endothelial cells, Piezo1 channel activation by either shear stress or a chemical agonist Yoda1 activated a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10), a Ca-regulated transmembrane sheddase that mediates S2 Notch1 cleavage. Consistent with this observation, we found Piezo1-dependent increase in the abundance of Notch1 intracellular domain (NICD) that depended on ADAM10 and the downstream S3 cleavage enzyme, γ-secretase. Conditional endothelial-specific disruption of Piezo1 in adult mice suppressed the expression of multiple Notch1 target genes in hepatic vasculature, suggesting constitutive functional importance in vivo. The data suggest that Piezo1 is a mechanism conferring force sensitivity on ADAM10 and Notch1 with downstream consequences for sustained activation of Notch1 target genes and potentially other processes.
Vincenza Caolo, Marjolaine Debant, Naima Endesh, T Simon Futers, Laeticia Lichtenstein, Fiona Bartoli, Gregory Parsonage, Elizabeth Av Jones, David J Beech

1960 related Products with: Shear stress activates ADAM10 sheddase to regulate Notch1 via the Piezo1 force sensor in endothelial cells.

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#32483641   // To Up

Effects of Preoperative WBC Count on Post-CABG Surgery Clinical Outcome.

White blood cells (WBCs) play a major role in inflammation, with effects on the vascular wall, the microvascular blood flow, and endothelial cells and endothelial function. Previous studies have shown that a high WBC count may increase the risk of cardiovascular complication rate and mortality after coronary artery bypass graft (CABG) surgery. The aim of the study was to evaluate the association between preoperative WBC count and the post-CABG clinical outcome.
Alexander Aizenshtein, Erez Kachel, Grosman Rimon Liza, Basem Hijazi, Arnon Blum

1518 related Products with: Effects of Preoperative WBC Count on Post-CABG Surgery Clinical Outcome.

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#32434208   2020/05/20 To Up

Overexpression of microRNA-136-3p Alleviates Myocardial Injury in Coronary Artery Disease via the Rho A/ROCK Signaling Pathway.

Coronary artery disease (CAD) is a cardiovascular disease that poses a fatal threat to human health, and the identification of potential biomarkers may help to delineate its pathophysiological mechanisms. Accumulating evidence has implicated microRNAs (miRNAs) in the pathogenesis and development of cardiovascular diseases. The present study aims to identify the expression of miRNA-136-3p (miR-136-3p) in CAD and further investigate its functional relevance in myocardial injury both in vitro and in vivo.
Yongbo Lin, Hanliang Dan, Jinguo Lu

1635 related Products with: Overexpression of microRNA-136-3p Alleviates Myocardial Injury in Coronary Artery Disease via the Rho A/ROCK Signaling Pathway.

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#32407984   2020/05/11 To Up

Nicorandil reversed homocysteine-induced coronary microvascular dysfunction via regulating PI3K/Akt/eNOS pathway.

Nicorandil exerts a protective effect against coronary microvascular dysfunction in acute myocardial infarction (AMI) patients. However, the mechanism and effect of nicorandil in hyperhomocysteinemia (HHcy) AMI patients remain unclear.
Biming Zhan, Zongyu Xu, Yang Zhang, Kefei Wan, Hanyue Deng, Dimeng Wang, Huihui Bao, Qinghua Wu, Xiaohong Hu, Hong Wang, Xiao Huang, Xiaoshu Cheng

2909 related Products with: Nicorandil reversed homocysteine-induced coronary microvascular dysfunction via regulating PI3K/Akt/eNOS pathway.

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