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https://www.readbyqxmd.com/read/28642034/cyclooxygenase-2-promotes-pulmonary-intravascular-macrophage-accumulation-by-exacerbating-bmp-signaling-in-rat-experimental-hepatopulmonary-syndrome
#1
Chang Liu, Jing Gao, Bing Chen, Lin Chen, Karine Belguise, Weifeng Yu, Kaizhi Lu, Xiaobo Wang, Bin Yi
BACKGROUND AND AIMS: One central factor in hepatopulmonary syndrome (HPS) pathogenesis is intravascular accumulation of activated macrophages in small pulmonary arteries. However, molecular mechanism underlyingthe macrophage accumulation in HPS is unknown. In this study, we aimed to explore whether elevated COX-2 induces the Bone morphogenicprotein-2 (BMP-2)/Crossveinless-2(CV-2) imbalance and then activation of BMP signaling pathway promotes the macrophage accumulation in Common Bile Duct Ligation (CBDL) rat lung...
June 19, 2017: Biochemical Pharmacology
https://www.readbyqxmd.com/read/28601021/aspergillus-fumigatus-induced-early-inflammatory-response-in-pulmonary-microvascular-endothelial-cells-role-of-p38-mapk-and-inhibition-by-silibinin
#2
Jun Song, Weihua Pan, Yue Sun, Jing Han, Weimin Shi, Wanqing Liao
Human invasive pulmonary aspergillosis (IPA) is a serious infectious disease mainly caused by Aspergillus fumigatus (A. fumigatus). Pulmonary microvascular endothelial cells (PMVECs) are important ones in the human lung tissue. However, it remains unclear about the role of PMVECs in IPA. In the present study, we cocultured PMVECs with A. fumigatus. We observed that A. fumigatus induced dose- and time-dependent increases of interleukin 6 (IL-6), interleukin 1β (IL-1β) and intercellular adhesion molecule 1 (ICAM-1) concentration in the cultures...
June 7, 2017: International Immunopharmacology
https://www.readbyqxmd.com/read/28598098/-improving-primary-culture-of-pulmonary-microvascular-endothelial-cells-of-rats
#3
Ling Jiang, Yuan-Dong Hu, Fei-Fei Xu, Ting-Hua Wang
OBJECTIVES: To improve the culturing method of pulmonary microvascular endothelial cells (PMEVCs) of SD rats. METHODS: The culturing processes in regard to obtaining peripheral lung tissue, attaching tissue block,preparing medium and subculturing were modified.These included an injection of heparin sodium before anesthesia, abdominal bleeding, opening of chest when breathing stopped, improvement of operational details, reduction of pollution by adding penicillin and streptomycin, discard of tissues after 48 h of primary culturing, remove of fibroblasts by a second digestion, and identification of cells using a fluorescence microscope for binding with lectin from BSI (FITC-BSI)...
September 2016: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
https://www.readbyqxmd.com/read/28562476/fn14-blockade-on-pulmonary-microvascular-endothelial-cells-improves-the-outcome-of-sepsis-induced-acute-lung-injury
#4
Yun Zou, Suhong Bao, Fang Wang, Long Guo, Jiali Zhu, Jun Wang, Xiaoming Deng, Jinbao Li
Pulmonary microvascular leakage is one of the characteristics of blood-air barrier dysfunction in septic acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Fibroblast growth factor-inducible 14 (Fn14) exerts diverse functions under certain circumstances. However, the role of Fn14 on the integrity of pulmonary microvascular endothelial cells (PMVECs) during sepsis remains unknown. Septic ALI was induced via cecal ligation and puncture (CLP). Fn14 expression on PMVECs was measured 24 h after surgery...
May 30, 2017: Shock
https://www.readbyqxmd.com/read/28526849/interleukin-22-attenuated-angiotensin-ii-induced-acute-lung-injury-through-inhibiting-the-apoptosis-of-pulmonary-microvascular-endothelial-cells
#5
Zhiyong Wu, Zhipeng Hu, Xin Cai, Wei Ren, Feifeng Dai, Huagang Liu, Jinxing Chang, Bowen Li
Apoptosis of pulmonary microvascular endothelial cells (PMVECs) was considered to be closely related to the pathogenesis of acute lung injury (ALI). We aim to investigate whether IL-22 plays protective roles in lung injury through inhibiting the apoptosis of PMVECs. ALI model was induced through subcutaneous infusion of angiotensin II (Ang II). Lung injury and infiltration of inflammatory cells were evaluated by determining the PaO2/FiO2, calculation of dry to weight ratio in lung, and immunohistochemisty analysis...
May 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28473326/reduced-carboxylesterase-1-is-associated-with-endothelial-injury-in-methamphetamine-induced-pulmonary-arterial-hypertension
#6
Mark E Orcholski, Artyom Khurshudyan, Elya A Shamskhou, Ke Yuan, Ian Y Chen, Sean D Kodani, Christophe Morisseau, Bruce D Hammock, Ellen M Hong, Ludmila Alexandrova, Tero-Pekka Alastalo, Gerald Berry, Roham T Zamanian, Vinicio A de Jesus Perez
Pulmonary arterial hypertension is a complication of methamphetamine use (METH-PAH) but the pathogenic mechanisms are unknown. Given that cytochrome P450 2D6 (CYP2D6) and carboxylesterase 1 (CES1) are involved in metabolism of METH and other amphetamine-like compounds, we postulated that loss of function variants could contribute to METH-PAH. While no difference in CYP2D6 expression was seen by lung immunofluorescence, CES1 expression was significantly reduced in endothelium of METH-PAH microvessels. Mass spectrometry analysis showed that healthy pulmonary microvascular endothelial cells (PMVECs) have the capacity to both internalize and metabolize METH...
May 4, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28386354/microrna-1246-mediates-lipopolysaccharide-induced-pulmonary-endothelial-cell-apoptosis-and-acute-lung-injury-by-targeting-angiotensin-converting-enzyme-2
#7
Yue Fang, Fengying Gao, Jing Hao, Zhenwei Liu
In this study, we aimed to identify potential microRNA (miRNA) regulators of angiotensin-converting enzyme 2 (ACE2) and to explore their roles in lipopolysaccharide (LPS)-induced acute lung injury (ALI). The expression of predicted miRNA regulators of ACE2 was examined in LPS-exposed pulmonary microvascular endothelial cells (PMVECs). Gain- and loss-of-function studies were performed to determine the functions of candidate miRNAs in LPS-induced PMVEC apoptosis and inflammatory response. The roles of the miRNAs in LPS-induced lung inflammation and permeability were investigated in a mouse model...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28250575/inhibition-of-murine-pulmonary-microvascular-endothelial-cell-apoptosis-promotes-recovery-of-barrier-function-under-septic-conditions
#8
Lefeng Wang, Sanjay Mehta, Michael Brock, Sean E Gill
Sepsis is characterized by injury of the pulmonary microvasculature and the pulmonary microvascular endothelial cells (PMVEC), leading to barrier dysfunction and acute respiratory distress syndrome (ARDS). Our recent work identified a strong correlation between PMVEC apoptosis and microvascular leak in septic mice in vivo, but the specific role of apoptosis in septic PMVEC barrier dysfunction remains unclear. Thus, we hypothesize that PMVEC apoptosis is likely required for PMVEC barrier dysfunction under septic conditions in vitro...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28228404/endothelial-colony-forming-cells-ameliorate-endothelial-dysfunction-via-secreted-factors-following-ischemia-reperfusion-injury
#9
Jason A Collett, Purvi Mehrotra, Allison Crone, W Christopher Shelley, Mervin C Yoder, David P Basile
Damage to endothelial cells contributes to acute kidney injury (AKI) by leading to impaired perfusion. Endothelial colony-forming cells (ECFC) are endothelial precursor cells with high proliferative capacity, pro-angiogenic activity, and in vivo vessel forming potential. We hypothesized that ECFC may ameliorate the degree of AKI and/or promote repair of the renal vasculature following ischemia-reperfusion (I/R). Rat pulmonary microvascular endothelial cells (PMVEC) with high proliferative potential were compared with pulmonary artery endothelial cells (PAEC) with low proliferative potential in rats subjected to renal I/R...
May 1, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28114372/bubble-induced-endothelial-microparticles-promote-endothelial-dysfunction
#10
Xuhua Yu, Jiajun Xu, Guoyang Huang, Kun Zhang, Long Qing, Wenwu Liu, Weigang Xu
Decompression sickness is a systemic pathophysiological process caused by bubbles and endothelial microparticles (EMPs) are established markers reflecting competency of endothelial function and vascular biology. Here, we investigated the effects of bubble-induced EMPs on endothelial cells in vitro and vivo. Rat pulmonary microvascular endothelial cells (PMVECs) were isolated and stimulated by bubbles and bubble-induced EMPs were collected and incubated with normal PMVECs in vitro. Cell viability and apoptosis were detected using Cell Counting Kit-8 assay and Annexin V FITC/PI double staining, respectively...
2017: PloS One
https://www.readbyqxmd.com/read/27982686/the-expression-levels-of-notch-related-signaling-molecules-in-pulmonary-microvascular-endothelial-cells-in-bleomycin-induced-rat-pulmonary-fibrosis
#11
Qian Yin, Weihua Wang, Guangbin Cui, Haiyan Nan, Linfeng Yan, Wenhu Zhang, Song Zhang, Jingguo Wei
Previous studies have suggested that the Notch signaling pathway plays a very important role in the proliferation and differentiation of pulmonary microvascular endothelial cells (PMVECs). Therefore, we aimed to investigate the expression level of Notch-related signaling molecules in PMVECs in bleomycin (BLM)-induced rat pulmonary fibrosis. Immunohistochemistry, immunofluorescence, Western blotting, and real-time PCR were used to analyze the differences in protein and mRNA expression levels of Notch-related signaling molecules, i...
May 4, 2017: Physiological Research
https://www.readbyqxmd.com/read/27830014/ve-cadherin-involved-in-the-pulmonary-microvascular-endothelial-cell-barrier-injury-induced-by-angiotensin-ii-through-modulating-the-cellular-apoptosis-and-skeletal-rearrangement
#12
Zhiyong Wu, Huagang Liu, Wei Ren, Feifeng Dai, Jinxing Chang, Bowen Li
OBJECTIVE: Angiotensin II (AngII) involved in the pathogenesis of pulmonary injury through impairing the integrity of pulmonary microvascular endothelial barrier, but the mechanism is still not clear. We aim to determine the roles of VE-cadherin, playing crucial roles in the adhesion of the vascular endothelial barrier and the barrier function, in the pulmonary microvascular endothelial cell (PMVEC) barrier injury mediated by AngII. METHODS: Mice acute lung injury (ALI) model was induced through pumping of AngII...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27769693/cdc42-regulates-lps-induced-proliferation-of-primary-pulmonary-microvascular-endothelial-cells-via-erk-pathway
#13
Jiawen Lv, Junchao Zeng, Wen Zhao, Yuanxiong Cheng, Lin Zhang, Shaoxi Cai, Guodong Hu, Yinghua Chen
BACKGROUND: After stimulation due to injury, cell division cycle protein 42 (Cdc42) restores and enhances barrier functions by strengthening intercellular adherens junctions; however, its influence on cell proliferation after injury remains unknown. OBJECTIVE: In this study, we sought to investigate the effect of stimulation using small doses of lipopolysaccharide (LPS) on the proliferation of pulmonary microvascular endothelial cells (PMVECs). METHODS: We stimulated PMVECs with different doses of LPS and evaluated the effects on cell proliferation...
January 2017: Microvascular Research
https://www.readbyqxmd.com/read/27765042/circulating-microparticles-in-severe-pulmonary-arterial-hypertension-increase-intercellular-adhesion-molecule-1-expression-selectively-in-pulmonary-artery-endothelium
#14
Leslie A Blair, April K Haven, Natalie N Bauer
BACKGROUND: Microparticles (MPs) stimulate inflammatory adhesion molecule expression in systemic vascular diseases, however it is unknown whether circulating MPs stimulate localized ICAM-1 expression in the heterogeneically distinct pulmonary endothelium during pulmonary arterial hypertension (PAH). Pulmonary vascular lesions with infiltrating inflammatory cells in PAH form in the pulmonary arteries and arterioles, but not the microcirculation. Therefore, we sought to determine whether circulating MPs from PAH stimulate pulmonary artery endothelial cell-selective ICAM-1 expression...
October 20, 2016: Respiratory Research
https://www.readbyqxmd.com/read/27565063/blockade-of-cxc-chemokine-receptor-3-on-endothelial-cells-protects-against-sepsis-induced-acute-lung-injury
#15
Xuejiao Zhu, Yun Zou, Bing Wang, Jiali Zhu, Yi Chen, Lei Wang, Jinbao Li, Xiaoming Deng
BACKGROUND: CXCR3, a G-protein coupled chemokine receptor, has been shown to play a critical role in recruiting inflammatory cells into lungs in several studies. However, its roles in polymicrobial septic acute lung injury (ALI) is yet unknown. Therefore, the purpose of this study was to elucidate the protective effects of CXCR3 blockade on pulmonary microvascular endothelial cells (PMVECs) in septic ALI and explore potential mechanisms. MATERIALS AND METHODS: ALI was induced by polymicrobial sepsis through cecal ligation and puncture surgery...
August 2016: Journal of Surgical Research
https://www.readbyqxmd.com/read/27480323/inhibition-of-autophagy-ameliorates-pulmonary-microvascular-dilation-and-pmvecs-excessive-proliferation-in-rat-experimental-hepatopulmonary-syndrome
#16
Duo Xu, Bing Chen, Jianteng Gu, Lin Chen, Karine Belguise, Xiaobo Wang, Bin Yi, Kaizhi Lu
Hepatopulmonary syndrome (HPS) is a defective liver-induced pulmonary vascular disorder with massive pulmonary microvascular dilation and excessive proliferation of pulmonary microvascular endothelial cells (PMVECs). Growing evidence suggests that autophagy is involved in pulmonary diseases, protectively or detrimentally. Thus, it is interesting and important to explore whether autophagy might be involved in and critical in HPS. In the present study, we report that autophagy was activated in common bile duct ligation (CBDL) rats and cultured pulmonary PMVECs induced by CBDL rat serum, two accepted in vivo and in vitro experimental models of HPS...
August 2, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27463003/%C3%AE-2-adrenoreceptor-modulated-fak-pathway-induced-by-dexmedetomidine-attenuates-pulmonary-microvascular-hyper-permeability-following-kidney-injury
#17
Qian Chen, Bin Yi, Jianbo Ma, Jiaoling Ning, Lingzhi Wu, Daqing Ma, Kaizhi Lu, Jianteng Gu
Renal ischemia-reperfusion (rI/R) could cause remote acute lung injury (ALI) and combination of these two organ injuries can remarkably increase the mortality. This study aims to determine whether dexmedetomidine, an α2-adrenoreceptor agonist sedative, can ameliorate pulmonary microvascular hyper-permeability following rI/R injury and explore the underlying mechanisms. In vivo, C57BL/6J mice received dexmedetomidine (25µg/kg, i.p.) in the absence or presence of α2-adrenergic antagonist atipamezole (250µg/kg, i...
August 30, 2016: Oncotarget
https://www.readbyqxmd.com/read/27455237/the-effects-of-aquaporin-1-in-pulmonary-edema-induced-by-fat-embolism-syndrome
#18
Yiwei Zhang, Kun Tian, Yan Wang, Rong Zhang, Jiawei Shang, Wei Jiang, Aizhong Wang
This study was designed to investigate the role of aquaporin1 (AQP1) in the pathologic process of pulmonary edema induced by fat embolism syndrome (FES) and the effects of a free fatty acid (FFA) mixture on AQP1 expression in pulmonary microvascular endothelial cells (PMVECs). In vivo, edema was more serious in FES mice compared with the control group. The expression of AQP1 and the wet-to-dry lung weight ratio (W/D) in the FES group were significantly increased compared with the control group. At the same time, inhibition of AQP1 decreased the pathological damage resulting from pulmonary edema...
July 21, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27259686/contribution-of-concentration-sensitive-sodium-channels-to-the-absorption-of-alveolar-fluid-in-mice
#19
Teruki Hagiwara, Shigeru Yoshida
The concentration-sensitive sodium channel (Nac) is activated by an increase in the extracellular sodium concentration. Although the expression of Nac in alveolar type II epithelial cells (AEC II) has been reported previously, the physiological role of Nac in the lung has not been established. We characterized Nac expression and examined amiloride-insensitive sodium transport mediated by Nac in mouse lung. Immunofluorescence studies revealed that Nac did not colocalize with either aquaporin 5 or cystic fibrosis transmembrane conductance regulator, but partially colocalized with the epithelial sodium channel γ-subunit...
September 2016: Respiratory Physiology & Neurobiology
https://www.readbyqxmd.com/read/27178323/the-phospholipase-a2-activity-of-peroxiredoxin-6-modulates-nadph-oxidase-2-activation-via-lysophosphatidic-acid-receptor-signaling-in-the-pulmonary-endothelium-and-alveolar-macrophages
#20
José Pablo Vázquez-Medina, Chandra Dodia, Liwei Weng, Clementina Mesaros, Ian A Blair, Sheldon I Feinstein, Shampa Chatterjee, Aron B Fisher
Peroxiredoxin 6 (Prdx6) is essential for activation of NADPH oxidase type 2 (NOX2) in pulmonary microvascular endothelial cells (PMVECs), alveolar macrophages (AMs), and polymorphonuclear leukocytes. Angiotensin II and phorbol ester increased superoxide/H2O2 generation in PMVECs, AMs, and isolated lungs from wild-type (WT) mice, but had much less effect on cells or lungs from Prdx6-null or Prdx6-D140A-knock-in mice that lack the phospholipase A2 activity (PLA2) of Prdx6; addition of either lysophosphatidylcholine (LPC) or lysophosphatidic acid (LPA) to cells restored their oxidant generation...
August 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
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