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Perfluorocarbon Protects against Lipopolysaccharide-Induced Apoptosis of Endothelial Cells in Pulmonary Microvessels.

Bull Exp Biol Med 2021 Feb 16;170(4):410-414. Epub 2021 Mar 16.

Department of Respiratory Diseases, the First Hospital of Qinhuangdao, Qinhuangdao, P.R. China.

This study was aimed to explore the effect and mechanisms of action of perfluorocarbon on LPS-induced apoptosis of pulmonary microvascular endothelial cells (PMVEC) isolated from Sprague-Dawley rats. Apoptosis rates were assessed by flow cytometry. Ultrastructural characteristics of PMVEC were evaluated by transmission electron microscopy. Read More

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February 2021

Tumor necrosis factor-α requires Ezrin to regulate the cytoskeleton and cause pulmonary microvascular endothelial barrier damage.

Microvasc Res 2021 01 30;133:104093. Epub 2020 Sep 30.

Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, PR China. Electronic address:

Acute respiratory distress syndrome (ARDS) is a rapidly progressive disease with unknown pathogenesis. Damage of pulmonary microvascular endothelial cells (PMVECs) caused by inflammatory storm caused by cytokines such as TNF-α is the potential pathogenesis of ARDS. In this study, we examined the role of ezrin and Rac1 in TNF-α-related pathways, which regulates the permeability of PMVECs. Read More

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January 2021

KD025 Shifts Pulmonary Endothelial Cell Bioenergetics and Decreases Baseline Lung Permeability.

Am J Respir Cell Mol Biol 2020 10;63(4):519-530

Department of Physiology and Cell Biology.

KD025 is a ROCK2 inhibitor currently being tested in clinical trials for the treatment of fibrotic lung diseases. The therapeutic effects of KD025 are partly due to its inhibition of profibrotic pathways and fat metabolism. However, whether KD025 affects pulmonary microvascular endothelial cell (PMVEC) function is unknown, despite evidence that alveolar-capillary membrane disruption constitutes major causes of death in fibrotic lung diseases. Read More

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October 2020

Exoenzyme Y induces extracellular active caspase-7 accumulation independent from apoptosis: modulation of transmissible cytotoxicity.

Am J Physiol Lung Cell Mol Physiol 2020 08 24;319(2):L380-L390. Epub 2020 Jun 24.

Department of Physiology and Cell Biology, University of South Alabama, Mobile, Alabama.

Caspase-3 and -7 are executioner caspases whose enzymatic activity is necessary to complete apoptotic cell death. Here, we questioned whether endothelial cell infection leads to caspase-3/7-mediated cell death. Pulmonary microvascular endothelial cells (PMVECs) were infected with (PA103). Read More

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microRNA-223 promotes autophagy to aggravate lung ischemia-reperfusion injury by inhibiting the expression of transcription factor HIF2α.

Am J Physiol Lung Cell Mol Physiol 2020 Apr 8. Epub 2020 Apr 8.

Thoracic Surgery, the First Affiliated Hospital of Nanchang University, China.

Lung ischemia-reperfusion (I/R) injury severely endangers human health, and recent studies have suggested that certain microRNAs (miRNAs) play important roles in this pathological phenomenon. The current study aimed to ascertain the ability of miR-223 to influence lung I/R injury by targeting hypoxia-inducible factor-2α (HIF2α). First, mouse models of lung I/R injury were established: during surgical procedures, pulmonary arteries and veins and unilateral pulmonary portal vessels were blocked and resuming bilateral pulmonary ventilation, followed by restoration of bipulmonary ventilation. Read More

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Protective effects of intermedin/adrenomedullin-2 in a cellular model of human pulmonary arterial hypertension.

Peptides 2020 04 1;126:170267. Epub 2020 Feb 1.

School of Medicine, Dentistry and Biomedical Sciences, The Queen's University of Belfast, Northern Ireland, United Kingdom. Electronic address:

Proliferation of pulmonary fibroblasts (PF) and distal migration of smooth muscle cells (PSM) are hallmarks of pulmonary arterial hypertension (PAH). Intermedin/adrenomedullin-2 (IMD/AM2) belongs to the Calcitonin Gene-Related Peptide (CGRP)/Adrenomedullin (AM) superfamily. These peptides act via Calcitonin-Like Receptors (CLR) combined with one of three Receptor activity-modifying proteins (RAMPs). Read More

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Hydrogen treatment prevents lipopolysaccharide-induced pulmonary endothelial cell dysfunction through RhoA inhibition.

Biochem Biophys Res Commun 2020 02 26;522(2):499-505. Epub 2019 Nov 26.

Department of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, 300060, PR China. Electronic address:

Background: Pulmonary microvascular endothelial cells (PMVECs) are initial targets of sepsis-induced acute lung injury (ALI). During the apoptosis of PMVECs, tight junctions (TJ) and adherens junctions (AJ) are firstly damaged. Previous studies have suggested hydrogen treatment can protect lung microvasculature of mice from sepsis-induced endothelial dysfunction and maintain the coherence of pulmonary endothelium, but the underlying mechanism remains unclear. Read More

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February 2020

Hepatocyte-derived exosomal MiR-194 activates PMVECs and promotes angiogenesis in hepatopulmonary syndrome.

Cell Death Dis 2019 11 7;10(11):853. Epub 2019 Nov 7.

Department of Anaesthesia, Southwest Hospital, The Third Military Medical University, Chongqing, China.

Hepatopulmonary syndrome (HPS) is a serious vascular complication in the setting of liver disease. Factors produced by the liver are essential to regulate pulmonary angiogenesis in the pathogenesis of HPS; however, the pathogenic mechanisms of pulmonary angiogenesis are not fully understood. We investigated the role of HPS rat serum exosomes (HEs) and sham-operated rat serum exosomes (SEs) in the regulation of angiogenesis. Read More

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November 2019

MiR145-5p inhibits proliferation of PMVECs via PAI-1 in experimental hepatopulmonary syndrome rat pulmonary microvascular hyperplasia.

Biol Open 2019 Nov 4;8(11). Epub 2019 Nov 4.

Department of Anesthesia, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, China

Hepatopulmonary syndrome (HPS) is a triad of advanced liver disease, intrapulmonary vasodilatation and arterial hypoxemia. Increasing evidence shows that HPS is associated with pulmonary microvascular hyperplasia. The aim of this work was to investigate the underlying mechanism of miR-145 in regulating the proliferation of pulmonary microvascular endothelial cells (PMVECs) and angiogenesis in HPS via plasminogen activator inhibitor-1 (PAI-1). Read More

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November 2019

Autophagy regulates the therapeutic potential of adipose-derived stem cells in LPS-induced pulmonary microvascular barrier damage.

Cell Death Dis 2019 10 23;10(11):804. Epub 2019 Oct 23.

Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Wenzhou City, Zhejiang Province, 325000, PR China.

Adipose-derived stem cells (ADSCs) have been shown to be beneficial in some pulmonary diseases, and the paracrine effect is the major mechanism underlying ADSC-based therapy. Autophagy plays a crucial role in maintaining stem cell homeostasis and survival. However, the role of autophagy in mediating ADSC paracrine effects has not been thoroughly elucidated. Read More

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October 2019

SU5416 attenuated lipopolysaccharide-induced acute lung injury in mice by modulating properties of vascular endothelial cells.

Drug Des Devel Ther 2019 23;13:1763-1772. Epub 2019 May 23.

Department of Respiratory Medicine, Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang, People's Republic of China.

A potent and selective vascular endothelial growth factor receptor (VEGFR) inhibitor SU5416, has been developed for the treatment of solid human tumors. The binding of VEGF to VEGFR plays a crucial role in the pathophysiology of respiratory disorders. However, the impact of SU5416 on lipopolysaccharide (LPS)-induced acute lung injury (ALI) remains unclear. Read More

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December 2019

Krüppel-like factor 6 mediates pulmonary angiogenesis in rat experimental hepatopulmonary syndrome and is aggravated by bone morphogenetic protein 9.

Biol Open 2019 Jun 26;8(6). Epub 2019 Jun 26.

Department of Anaesthesia, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038 China

Hepatopulmonary syndrome (HPS) is a serious pulmonary vascular disease derived from chronic liver disease, and its key pathogenesis is angiogenesis. Krüppel-like factor 6 (KLF6) mediates physiological repair and remodeling during vascular injury. However, the role of KLF6 in pulmonary microvascular endothelial cells (PMVECs) during angiogenesis of HPS and its underlying mechanism in HPS have not been investigated. Read More

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Loss of cell polarity regulated by PTEN/Cdc42 enrolled in the process of Hepatopulmonary Syndrome.

J Cell Mol Med 2019 08 29;23(8):5542-5552. Epub 2019 May 29.

Department of Anaesthesia, Southwest Hospital, The Third Military Medical University (Army Medical University), Chongqing, China.

One central factor in hepatopulmonary syndrome (HPS) pathogenesis is pulmonary vascular remodelling (PVR) which involves dysregulation of proliferation and migration in pulmonary microvascular endothelial cells (PMVECs). Growing evidence suggests that Apical/basolateral polarity plays an important role in cell proliferation, migration, adhesion and differentiation. In this study, we explored whether cell polarity is involved and critical in experimental HPS rats that are induced by common bile duct ligation (CBDL). Read More

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Inhibition of mitochondrial autophagy protects donor lungs for lung transplantation against ischaemia-reperfusion injury in rats via the mTOR pathway.

J Cell Mol Med 2019 05 19;23(5):3190-3201. Epub 2019 Mar 19.

Department of Thoracic Surgery, the First Affiliated Hospital of Nanchang University, Nanchang, P.R. China.

Impaired mitochondrial function is a key factor attributing to lung ischaemia-reperfusion (IR) injury, which contributes to major post-transplant complications. Thus, the current study was performed to investigate the role of mitochondrial autophagy in lung I/R injury and the involvement of the mTOR pathway. We established rat models of orthotopic left lung transplantation to investigate the role of mitochondrial autophagy in I/R injury following lung transplantation. Read More

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miR-33 and RIP140 participate in LPS-induced acute lung injury

Turk J Med Sci 2019 Feb 11;49(1):422-428. Epub 2019 Feb 11.

Background/aim: Pulmonary microvascular endothelial cells (PMVECs) play a pivotal role in the process of acute lung injury (ALI), which can be induced by lipopolysaccharide (LPS). Numerous reports have indicated that both miR-33 and RIP140 are involved in the inflammatory response in macrophages. In this study, we sought to investigate whether miR-33 and RIP140 participate in ALI induced by LPS. Read More

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February 2019

Loss of Endothelium-Derived Wnt5a Is Associated With Reduced Pericyte Recruitment and Small Vessel Loss in Pulmonary Arterial Hypertension.

Circulation 2019 04;139(14):1710-1724

Division of Pulmonary and Critical Care Medicine (K.Y., E.A.S., M.E.O., A.N., V.A.d.J.P.), Stanford University, Palo Alto, CA.

Background: Pulmonary arterial hypertension (PAH) is a life-threatening disorder of the pulmonary circulation associated with loss and impaired regeneration of microvessels. Reduced pericyte coverage of pulmonary microvessels is a pathological feature of PAH and is caused partly by the inability of pericytes to respond to signaling cues from neighboring pulmonary microvascular endothelial cells (PMVECs). We have shown that activation of the Wnt/planar cell polarity pathway is required for pericyte recruitment, but whether production and release of specific Wnt ligands by PMVECs are responsible for Wnt/planar cell polarity activation in pericytes is unknown. Read More

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Phosphorylated ERM Mediates Lipopolysaccharide Induced Pulmonary Microvascular Endothelial Cells Permeability Through Negatively Regulating Rac1 Activity.

Arch Bronconeumol 2019 06 15;55(6):306-311. Epub 2018 Nov 15.

Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, China.

Introduction: 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.

Methods: Rat PMVECs were isolated and monolayered cultured, then challenged with different doses of LPS (0. Read More

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Differential Mechanisms of Septic Human Pulmonary Microvascular Endothelial Cell Barrier Dysfunction Depending on the Presence of Neutrophils.

Front Immunol 2018 2;9:1743. Epub 2018 Aug 2.

Centre for Critical Illness Research, Lawson Health Research Institute, London, ON, Canada.

Sepsis is characterized by injury of pulmonary microvascular endothelial cells (PMVEC) leading to barrier dysfunction. Multiple mechanisms promote septic PMVEC barrier dysfunction, including interaction with circulating leukocytes and PMVEC apoptotic death. Our previous work demonstrated a strong correlation between septic neutrophil (PMN)-dependent PMVEC apoptosis and pulmonary microvascular albumin leak in septic mice ; however, this remains uncertain in human PMVEC. Read More

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October 2019

A Vinyl Ether-Functional Polycarbonate as a Template for Multiple Postpolymerization Modifications.

Macromolecules 2018 May 16;51(9):3233-3242. Epub 2018 Apr 16.

Department of Chemistry, Department of Chemical Engineering, Department of Materials Science & Engineering, and Laboratory for Synthetic-Biologic Interactions, Texas A&M University, P.O. Box 30012, 3255 TAMU, College Station, Texas 77842-3012, United States.

A highly-reactive vinyl ether-functionalized aliphatic polycarbonate and its block copolymer were developed as templates for multiple post-polymerization conjugation chemistries. The vinyl ether-functional six-membered cyclic carbonate monomer was synthesized by a well-established two-step procedure starting from 2,2-bis(hydroxymethyl)propionic acid. An organobase-catalyzed ring-opening polymerization of the synthesized monomer afforded polycarbonates with pendant vinyl ether functionalities (PMVEC). Read More

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BML-111 alleviates acute lung injury through regulating the expression of lncRNA MALAT1.

Arch Biochem Biophys 2018 07 25;649:15-21. Epub 2018 Apr 25.

Department of Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China. Electronic address:

BML-111 is a lipoxin receptor agonist that plays a vital role on inflammation. MALAT1 is reported to mediate lung injury. ALI rat model was established using the method of venous cannula. Read More

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MicroRNA-339-3p alleviates inflammation and edema and suppresses pulmonary microvascular endothelial cell apoptosis in mice with severe acute pancreatitis-associated acute lung injury by regulating Anxa3 via the Akt/mTOR signaling pathway.

J Cell Biochem 2018 08 25;119(8):6704-6714. Epub 2018 Apr 25.

Intensive Care Unit, Shengjing Hospital of China Medical University, Shenyang, P.R. China.

Severe acute pancreatitis (SAP) is a disease with a high mortality. Patients with SAP may also be complicated with acute lung injury (ALI). So far the therapy for SAP-ALI is still limited. Read More

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Carbonic anhydrase IX is a critical determinant of pulmonary microvascular endothelial cell pH regulation and angiogenesis during acidosis.

Am J Physiol Lung Cell Mol Physiol 2018 07 5;315(1):L41-L51. Epub 2018 Apr 5.

Department of Physiology and Cell Biology, University of South Alabama , Mobile, Alabama.

Carbonic anhydrase IX (CA IX) is highly expressed in rapidly proliferating and highly glycolytic cells, where it serves to enhance acid-regulatory capacity. Pulmonary microvascular endothelial cells (PMVECs) actively utilize aerobic glycolysis and acidify media, whereas pulmonary arterial endothelial cells (PAECs) primarily rely on oxidative phosphorylation and minimally change media pH. Therefore, we hypothesized that CA IX is critical to PMVEC angiogenesis because of its important role in regulating pH. Read More

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A Novel Finding: Macrophages Involved in Inflammation Participate in Acute Aortic Dissection Complicated with Acute Lung Injury.

Curr Mol Med 2017 ;17(8):568-579

Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.

Background: Little is known about the pathogenesis of acute lung injury (ALI) complicated with acute aortic dissection (AAD).

Objective: We aim to investigate the roles of macrophages-derived matrix metalloproteinase 9 (MMP9) in the development of ALI complicated with AAD and factors involved in the recruitment of macrophages.

Methods: This study included three parts: (i) Determination of serum MMPs, angiotensin II (AngII) and MCP-1 in patients with AAD complicated with ALI or AAD only, non-ruptured chronic aortic aneurysm patients or healthy volunteers using ELISA method. Read More

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[Pathogenic role of leukotriene B4 in pulmonary microvascular endothelial cell hyper- permeability induced by one lung ventilation in rabbits].

Nan Fang Yi Ke Da Xue Xue Bao 2017 Nov;37(11):1523-1528

Department of Anesthesiology, The First People's Hospital of Yunnan Province, Kunming 650032, China. E-mail:

Objective: To elucidate the pathogenic role of leukotriene B4 (LTB4) in increased pulmonary microvascular endothelial cell permeability induced by one lung ventilation (OLV) in rabbits.

Methods: Forty-eight healthy Japanese white rabbits were randomly divided into control group (group C), saline pretreatment group (group S), bestatin (a leukotriene A4 hydrolase (LTA4H) inhibitor) plus saline pretreatment group (group B), OLV group (group O), saline pretreatment plus OLV group (group SO) and bestatin plus saline pretreatment with OLV group (group BO). ELISA was used to detect LTB4 content in the lung tissues, and LTA4H and phospholipase Cεl (PLCEl) expressions were examined by Western blotting and quantitative PCR. Read More

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November 2017

Peroxiredoxin 6 phospholipid hydroperoxidase activity in the repair of peroxidized cell membranes.

Redox Biol 2018 04 12;14:41-46. Epub 2017 Aug 12.

Institute for Environmental Medicine, Department of Physiology, Perelman School of Medicine of the University of Pennsylvania, Philadelphia, PA 19104, USA.

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 A and the GSH peroxidase activities of Prdx6 are required for a maximal rate of recovery. Like other peroxiredoxins, Prdx6 can reduce HO and short chain hydroperoxides, but in addition can directly reduce phospholipid hydroperoxides. Read More

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Single cell cloning generates lung endothelial colonies with conserved growth, angiogenic, and bioenergetic characteristics.

Pulm Circ 2017 Oct-Dec;7(4):777-792. Epub 2017 Sep 12.

1 5557 Department of Physiology and Cell Biology, University of South Alabama, Mobile, AL, USA.

Pulmonary artery, capillary, and vein endothelial cells possess distinctive structures and functions, which represent a form of vascular segment specific macroheterogeneity. However, within each of these segmental populations, individual cell functional variability represents a poorly characterized microheterogeneity. Here, we hypothesized that single cell clonogenic assays would reveal microheterogeneity among the parent cell population and enable isolation of highly representative cells with committed parental characteristics. Read More

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September 2017

JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 On Aortic Dissection with Acute Lung Injury.

Dis Markers 2017 30;2017:1917804. Epub 2017 Jul 30.

Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.

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. Read More

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Interleukin 22 attenuated angiotensin II induced acute lung injury through inhibiting the apoptosis of pulmonary microvascular endothelial cells.

Sci Rep 2017 05 19;7(1):2210. Epub 2017 May 19.

Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, China.

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). Read More

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Reduced carboxylesterase 1 is associated with endothelial injury in methamphetamine-induced pulmonary arterial hypertension.

Am J Physiol Lung Cell Mol Physiol 2017 08 4;313(2):L252-L266. Epub 2017 May 4.

Division of Pulmonary and Critical Care Medicine, Stanford University Medical Center, Stanford, California;

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. Read More

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microRNA-1246 mediates lipopolysaccharide-induced pulmonary endothelial cell apoptosis and acute lung injury by targeting angiotensin-converting enzyme 2.

Am J Transl Res 2017 15;9(3):1287-1296. Epub 2017 Mar 15.

Department of Respiratory Medicine, Shanghai General Hospital, Shanghai Jiaotong University Shanghai, China.

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. Read More

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