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https://www.readbyqxmd.com/read/29118909/role-of-autophagy-and-its-signaling-pathways-in-ischemia-reperfusion-injury
#1
Shaohua Dai, Qirong Xu, Sheng Liu, Bentong Yu, Jichun Liu, Jian Tang
This study was conducted to investigate the mechanism of autophagy and its signaling pathways in ischemia/reperfusion injury (IRI). Pulmonary microvascular endothelial cells (PMVECs) were used to construct I/R models. The cells were then treated with autophagy inhibitor 3-MA and infected with adenovirus expressing Beclin 1-shRNA. The expression of CD31, LC3-II, Bcl-2, Bax, LC3-II, Beclin 1, AKT, p-AKT, AMPK and p-AMPK, apoptosis, cell viability and migration ability were determined. Over 95% isolated PMVECs were positive for CD31...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/29115603/amelioration-of-lung-ischemia%C3%A2-reperfusion-injury-by-jnk-and-p38-small-interfering-rnas-in-rat-pulmonary-microvascular-endothelial-cells-in-an-ischemia%C3%A2-reperfusion-injury-lung-transplantation-model
#2
Juan Wang, Jing Tan, Yanhong Liu, Linlin Song, Di Li, Xiaoguang Cui
The inhibition of mitogen‑activated protein kinases (MAPKs), including c‑Jun NH2‑terminal protein kinase (JNK), p38 MAPK (p38) and extracellular signal‑regulated protein kinase 1/2 (ERK1/2), have an important effect on lung ischemia‑reperfusion injury (IRI) during lung transplantation (LT). However, the way in which combined MAPK inhibition exerts optimal protective effects on lung IRI remains to be elucidated. Therefore, the present study evaluated the therapeutic efficacy of the inhibition of MAPKs in rat pulmonary microvascular endothelial cells (PMVECs) in an IRI model of LT...
November 6, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28936960/-role-of-phosphorylated-moesin-in-the-injury-of-pulmonary-microvascular-endothelial-cells-of-rats-and-its-mechanism
#3
Gang Wang, Gengyun Sun
OBJECTIVE: To investigate the role of phosphorylated Moesin (p-Moesin) in the injury of pulmonary microvascular endothelial cells (PMVECs) of rats induced by tumor necrosis factor-α (TNF-α), and to approach the impact of Rac1 signal pathway on Moesin phosphorylation. METHODS: PMVECs of rats were cultured in vitro and passed on to the third generation, and the TNF-α time-effect experiment, dose-effect experiment and Rac1 signaling pathway intervention experiment were performed respectively...
September 2017: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
https://www.readbyqxmd.com/read/28870649/lipopolysaccharide-impairs-permeability-of-pulmonary-microvascular-endothelial-cells-via-connexin40
#4
Hua-Song Zhou, Meng Li, Bing-Dong Sui, Lei Wei, Rui Hou, Wen-Sheng Chen, Qiang Li, Sheng-Hui Bi, Jin-Zhou Zhang, Ding-Hua Yi
The endotoxin lipopolysaccharide (LPS)-induced pulmonary endothelial barrier disruption is a key pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). However, the molecular mechanisms underlying LPS-impaired permeability of pulmonary microvascular endothelial cells (PMVECs) are not fully understood. Gap junctions, particularly Connexin40 (Cx40), are necessary for the maintenance of normal vascular function. In this study, we for the first time investigated the role of Cx40 in LPS-impaired permeability of PMVECs and provided potential therapeutic approaches based on mechanistic findings of Cx40 regulation by LPS stimuli...
January 2018: Microvascular Research
https://www.readbyqxmd.com/read/28865296/peroxiredoxin-6-phospholipid-hydroperoxidase-activity-in-the-repair-of-peroxidized-cell-membranes
#5
Aron B Fisher, Jose P Vasquez-Medina, Chandra Dodia, Elena M Sorokina, Jian-Qin Tao, Sheldon I Feinstein
Although lipid peroxidation associated with oxidative stress can result in cellular death, sub-lethal lipid peroxidation can gradually resolve with return to the pre-exposure state. We have shown that resolution of lipid peroxidation is greatly delayed in lungs or cells that are null for peroxiredoxin 6 (Prdx6) and that both the phospholipase A2 and the GSH peroxidase activities of Prdx6 are required for a maximal rate of recovery. Like other peroxiredoxins, Prdx6 can reduce H2O2 and short chain hydroperoxides, but in addition can directly reduce phospholipid hydroperoxides...
August 12, 2017: Redox Biology
https://www.readbyqxmd.com/read/28858723/epigallocatechin-3-gallate-inhibits-tlr4-signaling-through-the-67-kda-laminin-receptor-and-effectively-alleviates-acute-lung-injury-induced-by-h9n2-swine-influenza-virus
#6
Ming-Ju Xu, Bao-Jian Liu, Cun-Lian Wang, Guo-Hua Wang, Yong Tian, Shao-Hua Wang, Jun Li, Pei-Yao Li, Rui-Hua Zhang, Dong Wei, Shu-Fei Tian, Tong Xu
Epigallocatechin-3-gallate (EGCG) was found to inhibit the Toll-like receptor 4 (TLR4) pathway involved in influenza virus pathogenesis. Here, the effect of EGCG on TLR4 in an H9N2 virus-induced acute lung injury mouse model was investigated. BALB/c mice were inoculated intranasally with A/Swine/Hebei/108/2002 (H9N2) virus or noninfectious allantoic fluid, and treated with EGCG and E5564 or normal saline orally for 5 consecutive days. PMVECs were treated with EGCG or anti-67kDa laminin receptor (LR). Lung physiopathology, inflammation, oxidative stress, viral replication, and TLR4/NF-κB/Toll-interacting protein (Tollip) pathway in lung tissue and/or PMVECs were investigated...
November 2017: International Immunopharmacology
https://www.readbyqxmd.com/read/28827891/jak2-stat3-pathway-was-associated-with-the-protective-effects-of-il-22-on-aortic-dissection-with-acute-lung-injury
#7
Wei Ren, Zhiwei Wang, Zhiyong Wu, Zhipeng Hu, Feifeng Dai, Jinxing Chang, Bowen Li, Huagang Liu, Yongle Ruan
Patients with aortic dissection (AD) may present acute lung injury (ALI) that may affect the prognosis. In this study, we aim to investigate the roles and mechanism of IL-22 in the pathogenesis of AD complicated with ALI. Six hundred and twenty-one AD patients were included, and the incidence of ALI and pulmonary CT findings were analyzed. Mouse ALI model was established through AngII, and then IL-22 injection and AG490 were given. The pathological changes, infiltration of inflammatory cells, and expression of STAT3 were determined...
2017: Disease Markers
https://www.readbyqxmd.com/read/28776666/potential-role-of-the-jagged1-notch1-signaling-pathway-in-the-endothelial-myofibroblast-transition-during-blm-induced-pulmonary-fibrosis
#8
Qian Yin, Weihua Wang, Guangbin Cui, Linfeng Yan, Song Zhang
Endothelial cell myofibroblast transition (EndoMT) is found during the process of bleomycin (BLM)-induced pulmonary fibrosis in rats, and plays a very important role in sustaining inflammation and collagen secretion. Moreover, some studies have suggested that the Notch1 signaling pathway may be involved in the expression of α-smooth muscle actin (α-SMA) in pulmonary microvascular endothelial cells (PMVECs), a protein marker of EndoMT. Therefore, we aimed to investigate the expression level of α-SMA and Notch1-related signaling molecules in PMVECs from BLM-induced rats and determine the relationship between the Notch1 signaling pathway and the expression of α-SMA in PMVECs...
August 4, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28743337/-effect-of-multidrug-resistant-associated-protein-4-overexpression-on-lipopolysaccharide-induced-vascular-endothelial-hyperpermeability-and-its-mechanism
#9
Wenfang Xia, Huanming Zhang, Yanlei Zheng, Qingshan Zhou, Bin Su
OBJECTIVE: To investigate the effect of multidrug resistance protein 4 (MRP4) overexpression on lipopolysaccharide (LPS)-induced vascular endothelial hyperpermeability of rat pulmonary micro-vascular endothelial cells (PMVECs) and its molecule mechanism. METHODS: Three to six passages of PMVECs were cultured in vitro, and they were divided into three groups: the cells in LPS group were only challenged by LPS 10 μg/mL after being cultured in serum-free medium for 24 hours; the cells in Ad-shRNA and Ad-MRP4 groups were infected with the empty virus control or recombinant adenovirus expressing MRP4 for 2 hours, and then were cultured in serum-free medium for 24 hours followed by stimulation of LPS 10 μg/mL...
July 2017: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
https://www.readbyqxmd.com/read/28642034/cyclooxygenase-2-promotes-pulmonary-intravascular-macrophage-accumulation-by-exacerbating-bmp-signaling-in-rat-experimental-hepatopulmonary-syndrome
#10
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 underlying the macrophage accumulation in HPS is unknown. In this study, we aimed to explore whether elevated COX-2 induces the Bone morphogenic protein-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...
August 15, 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
#11
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
#12
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
#13
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
#14
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
#15
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. Although 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...
August 1, 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
#16
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
#17
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
#18
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
#19
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
#20
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
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