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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...
October 18, 2016: Microvascular Research
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
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
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...
2016: Scientific Reports
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...
July 24, 2016: Oncotarget
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...
2016: International Journal of Molecular Sciences
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
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
Jun-Tang Li, Wei-Qi Wang, Ling Wang, Ning-Ning Liu, Ya-Li Zhao, Xiao-Shan Zhu, Qin-Qin Liu, Chun-Fang Gao, An-Gang Yang, Lin-Tao Jia
Neutrophil release of NO/ONOO- induces endothelial cell barrier dysfunction in inflammatory acute lung injury (ALI). Previous studies using zymosan-triggered inflammation and ALI model revealed that zymosan promotes inducible NO synthase (iNOS) expression in neutrophils, and that isoflurane inhibits zymosan-induced oxidative stress and iNOS biosynthesis. However, the underlying mechanisms remain largely unknown. We found here that in zymosan-primed neutrophils, iNOS is transcriptionally activated by NF-κB, whose nuclear translocation is triggered by excessive reactive oxygen species (ROS) and consequently activated p38 MAPK...
May 31, 2016: Oncotarget
Diego F Alvarez, Nicole Housley, Anna Koloteva, Chun Zhou, Kristen O'Donnell, Jonathon P Audia
RATIONALE: Dysregulated activation of the Inflammasome-Caspase-1-Interleukin-1β axis elicits damaging hyper-inflammation during critical illnesses such as pneumonia and sepsis. However, in critical illness models of Salmonella infection, burn, or shock, Caspase-1 inhibition worsens outcomes. These paradoxical effects suggest that Caspase-1 drives novel protective responses. Whether the protective effects of Caspase-1 activation involve canonical immune cell and/or non-immune cell responses is unknown...
April 27, 2016: American Journal of Respiratory Cell and Molecular Biology
Zhiyong Wu, Feifeng Dai, Wei Ren, Huagang Liu, Bowen Li, Jinxing Chang
Patients with acute aortic dissection (AAD) usually showed acute lung injury (ALI). However, its pathogenesis is still not well defined. Apoptosis of pulmonary microvascular endothelial cells (PMVECs) is closely related to the alveolus-capillary barrier injury and the increased vascular permeability. In this study, we aim to investigate the human PMVECs (hPMVECs) apoptosis induced by angiotensin II (AngII) and monocyte chemoattractant protein-1 (MCP-1) and their potential interaction in the pathogenesis of AAD complicated with ALI...
2016: American Journal of Translational Research
Guanyu Wang, Jingwen Zhang, Caiming Xu, Xiao Han, Yanyan Gao, Hailong Chen
Acute lung injury (ALI) is a critical complication of the severe acute pancreatitis (SAP), characterized by increased pulmonary permeability with high mortality. Pulmonary microvascular endothelial cells (PMVECs) injury and apoptosis play a key role in ALI. Previous studies indicated that store-operated calcium entry (SOCE) could regulate a variety of cellular processes. The present study was to investigate the effects of SOCE inhibition on ALI induced by SAP in Sprague-Dawley rats, and PMVECs injury induced by lipopolysaccharide (LPS)...
June 2016: Inflammation
Xiao Han, Yuxi Wang, Hailong Chen, Jingwen Zhang, Caiming Xu, Jian Li, Mingyue Li
Acute lung injury (ALI), which is associated with severe acute pancreatitis (SAP), results from damage to the pulmonary microvascular endothelial cells (PMVECs), which in turn leads to high levels of inflammatory cytokines that destroy PMVECs. However, the molecular mechanisms underlying SAP-associated ALI (SAP-ALI) are currently not well understood. Intercellular adhesion molecule-1 (ICAM-1) has been implicated in the persistent migration and accumulation of neutrophils and macrophages, which in turn has been associated with the increased permeability of microvascular endothelial cells...
March 2016: Experimental and Therapeutic Medicine
Sanna Vattulainen-Collanus, Oyediran Akinrinade, Molong Li, Minna Koskenvuo, Caiyun Grace Li, Shailaja P Rao, Vinicio de Jesus Perez, Ke Yuan, Hirofumi Sawada, Juha W Koskenvuo, Cristina Alvira, Marlene Rabinovitch, Tero-Pekka Alastalo
Tie2-promoter-mediated loss of peroxisome proliferator-activated receptor gamma (PPARγ, also known as PPARG) in mice leads to osteopetrosis and pulmonary arterial hypertension. Vascular disease is associated with loss of PPARγ in pulmonary microvascular endothelial cells (PMVEC); we evaluated the role of PPARγ in PMVEC functions, such as angiogenesis and migration. The role of PPARγ in angiogenesis was evaluated in Tie2CrePPARγ(flox/flox) and wild-type mice, and in mouse and human PMVECs. RNA sequencing and bioinformatic approaches were utilized to reveal angiogenesis-associated targets for PPARγ...
February 15, 2016: Journal of Cell Science
Haiyan Ge, Huili Zhu, Nuo Xu, Dan Zhang, Jiaxian Ou, Guifang Wang, Xiaocong Fang, Jian Zhou, Yuanlin Song, Chunxue Bai
Aquaporin (AQP) 1, a water channel protein expressed widely in vascular endothelia, has been shown to regulate cell migration, angiogenesis, and organ regeneration. Even though its role in the pathogenesis of lung ischemia-reperfusion (IR) injury has been defined, the functional role of AQP1 during long-term IR resolution remains to be clarified. Here, we found that AQP1 expression was increased at late time points (7-14 d) after IR and colocalized with endothelial cell (EC) marker CD31. Compared with IR in wild-type mice, IR in Aqp1(-/-) mice had significantly enhanced leukocyte infiltration, collagen deposition, and microvascular permeability, as well as inhibited angiogenic factor expression...
June 2016: American Journal of Respiratory Cell and Molecular Biology
Min Shao, Song-Tao Tang, Bao Liu, Hua-Qing Zhu
The pathology of acute respiratory distress syndrome (ARDS) is closely associated with the failure of alveolar‑capillary barrier integrity and alveolar filling by high protein pulmonary edema, resulting from hyperpermeability. High mobility group box 1 (HMGB1) is a novel late mediator of sepsis, which is specifically involved in endotoxin‑induced acute lung injury and sepsis‑associated lethality. Although the role of HMGB1 in endothelial cell cytoskeletal rearrangement and vascular permeability have been investigated preliminarily, the molecular mechanisms remain to be fully elucidated...
January 2016: Molecular Medicine Reports
Liguo Wang, Liwei Zhuang, Haifang Rong, Yuening Guo, Xiaohua Ling, Ruifeng Wang, Xin Yu, Wei Zhang
Hepatopulmonary syndrome (HPS) is one of the reasons for the mortality of patients with perioperative liver disease. Intrapulmonary vascular dilatation is the most important mechanism underlying HPS, and it primarily occurs due to cell proliferation. Inhibiting the proliferation of pulmonary microvascular endothelial cells (PMVECs) may provide a novel strategy to prevent HPS. MicroRNAs (miRNAs) regulate gene expression and are crucial in cell proliferation. To investigate the mechanism underlying the proliferation of PMVECs in HPS, PMVECs were isolated from rat models of HPS...
December 2015: Molecular Medicine Reports
Yukie Saito, Yousuke Fujii, Masato Yashiro, Mitsuru Tsuge, Nobuyuki Nosaka, Nobuko Yamashita, Mutsuko Yamada, Hirokazu Tsukahara, Tsuneo Morishima
Lung hyperpermeability affects the development of acute respiratory distress syndrome (ARDS), but therapeutic strategies for the control of microvascular permeability have not been established. We examined the effects of edaravone, dexamethasone, and N-monomethyl-L-arginine (L-NMMA) on permeability changes in human pulmonary microvascular endothelial cells (PMVEC) under a hypercytokinemic state. Human PMVEC were seeded in a Boyden chamber. After monolayer confluence was achieved, the culture media were replaced respectively by culture media containing edaravone, dexamethasone, and L-NMMA...
2015: Acta Medica Okayama
Jordan Nickols, Boniface Obiako, K C Ramila, Kevin Putinta, Sarah Schilling, Sarah L Sayner
Bacteria-induced sepsis is a common cause of pulmonary endothelial barrier dysfunction and can progress toward acute respiratory distress syndrome. Elevations in intracellular cAMP tightly regulate pulmonary endothelial barrier integrity; however, cAMP signals are highly compartmentalized: whether cAMP is barrier-protective or -disruptive depends on the compartment (plasma membrane or cytosol, respectively) in which the signal is generated. The mammalian soluble adenylyl cyclase isoform 10 (AC10) is uniquely stimulated by bicarbonate and is expressed in pulmonary microvascular endothelial cells (PMVECs)...
December 15, 2015: American Journal of Physiology. Lung Cellular and Molecular Physiology
Yongmei Cao, Zhen Jiang, Zhen Zeng, Yujing Liu, Yuchun Gu, Yingying Ji, Yupeng Zhao, Yingchuan Li
Pulmonary arterial hypertension (PAH) is a life-threatening disorder that ultimately causes heart failure. While the underlying causes of this condition are not well understood, previous studies suggest that the anti-apoptotic nature of pulmonary microvascular endothelial cells (PMVECs) in hypoxic environments contributes to PAH pathogenesis. In this study, we focus on the contribution of Bcl-2 and hypoxia response element (HRE) to apoptosis-resistant endothelial cells and investigate the mechanism. PMVECs obtained from either normal rats or apoptosis-resistant PMVECs obtained from PAH rats were transduced with recombinant lentiviral vectors carrying either Bcl-2-shRNA or HRE combined Bcl-2-shRNA, and then cultured these cells for 24 h under hypoxic (5% O2) or normoxic (21% O2) conditions...
January 2016: Apoptosis: An International Journal on Programmed Cell Death
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