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Endoplasmic reticulum stress and acute lung injury

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https://www.readbyqxmd.com/read/28751159/ghrelin-ameliorates-acute-lung-injury-induced-by-oleic-acid-via-inhibition-of-endoplasmic-reticulum-stress
#1
Xiuli Tian, Zhijun Liu, Ting Yu, Haitao Yang, Linlin Feng
AIMS: Acute lung injury (ALI) is associated with excessive mortality and lacks appropriate therapy. Ghrelin is a novel peptide that protects the lung against ALI. This study aimed to investigate whether endoplasmic reticulum stress (ERS) mediates the protective effect of ghrelin on ALI. MAIN METHODS: We used a rat oleic acid (OA)-induced ALI model. Pulmonary impairment was detected by hematoxylin and eosin (HE) staining, lung mechanics, wet/dry weight ratio, and arterial blood gas analysis...
July 24, 2017: Life Sciences
https://www.readbyqxmd.com/read/28675985/hydrogen-alleviates-hyperoxic-acute-lung-injury-related-endoplasmic-reticulum-stress-in-rats-through-upregulation-of-sirt1
#2
Qiang Sun, Wenjie Han, Huijun Hu, Danfeng Fan, Yanbo Li, Yu Zhang, Yan Lv, Mingxin Li, Shuyi Pan
Hyperoxic acute lung injury (HALI) is a major clinical problem for patients undergoing supplemental oxygen therapy. Currently in clinical settings there exist no effective means of prevention or treatment methods. Our previous study found that: hydrogen could reduce HALI, as well as oxidative stress. This research will further explore the mechanism underlying the protective effect of hydrogen on oxygen toxicity. Rats were randomly assigned into three experimental groups and were exposed in a oxygen chamber for 60 continuous hours: 100% balanced air (control); 100% oxygen (HALI); 100% oxygen with hydrogen treatment (HALI + HRS)...
July 21, 2017: Free Radical Research
https://www.readbyqxmd.com/read/28464871/secretion-of-the-endoplasmic-reticulum-stress-protein-grp78-into-the-balf-is-increased-in-cigarette-smokers
#3
Mark O Aksoy, Victor Kim, William D Cornwell, Thomas J Rogers, Beata Kosmider, Karim Bahmed, Carlos Barrero, Salim Merali, Neena Shetty, Steven G Kelsen
BACKGROUND: Identification of biomarkers of cigarette smoke -induced lung damage and early COPD is an area of intense interest. Glucose regulated protein of 78 kD (i.e., GRP78), a multi-functional protein which mediates cell responses to oxidant stress, is increased in the lungs of cigarette smokers and in the serum of subjects with COPD. We have suggested that secretion of GRP78 by lung cells may explain the increase in serum GRP78 in COPD. To assess GRP78 secretion by the lung, we assayed GRP78 in bronchoalveolar lavage fluid (BALF) in chronic smokers and non-smokers...
May 2, 2017: Respiratory Research
https://www.readbyqxmd.com/read/28363030/integrated-stress-response-mediates-epithelial-injury-in-mechanical-ventilation
#4
Tamas Dolinay, Blanca E Himes, Maya Shumyatcher, Gladys Gray Lawrence, Susan S Margulies
Ventilator-induced lung injury (VILI) is a severe complication of mechanical ventilation that can lead to acute respiratory distress syndrome. VILI is characterized by damage to the epithelial barrier with subsequent pulmonary edema and profound hypoxia. Available lung-protective ventilator strategies offer only a modest benefit in preventing VILI because they cannot impede alveolar overdistension and concomitant epithelial barrier dysfunction in the inflamed lung regions. There are currently no effective biochemical therapies to mitigate injury to the alveolar epithelium...
August 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28277743/obesity-induced-endoplasmic-reticulum-stress-causes-lung-endothelial-dysfunction-and-promotes-acute-lung-injury
#5
Dilip Shah, Freddy Romero, Zhi Guo, Jianxin Sun, Jonathan Li, Caleb B Kallen, Ulhas P Naik, Ross Summer
Obesity is a significant risk factor for acute respiratory distress syndrome. The mechanisms underlying this association are unknown. We recently showed that diet-induced obese mice exhibit pulmonary vascular endothelial dysfunction, which is associated with enhanced susceptibility to LPS-induced acute lung injury. Here, we demonstrate that lung endothelial dysfunction in diet-induced obese mice coincides with increased endoplasmic reticulum (ER) stress. Specifically, we observed enhanced expression of the major sensors of misfolded proteins, including protein kinase R-like ER kinase, inositol-requiring enzyme α, and activating transcription factor 6, in whole lung and in primary lung endothelial cells isolated from diet-induced obese mice...
August 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28245985/4-pba-inhibits-lps-induced-inflammation-through-regulating-er-stress-and-autophagy-in-acute-lung-injury-models
#6
Meichun Zeng, Wenhua Sang, Sha Chen, Ran Chen, Hailin Zhang, Feng Xue, Zhengmao Li, Yu Liu, Yongsheng Gong, Hongyu Zhang, Xiaoxia Kong
Acute lung injury (ALI) is a common clinical disorder that causes substantial health problems worldwide. An excessive inflammatory response is the central feature of ALI, but the mechanism is still unclear, especially the role of endoplasmic-reticulum (ER) stress and autophagy. To identify the cellular mechanism of lung inflammation during lipopolysaccharide (LPS)-induced mouse model of ALI, we investigated the influence of classic ER stress inhibitor 4-phenyl butyric acid (4-PBA) on ER stress and autophagy, which partially affect the activation of inflammation, both in LPS-induced ALI mouse model and human alveolar epithelial cell model...
April 5, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/28205623/preventive-effects-of-carnosine-on-lipopolysaccharide-induced-lung-injury
#7
Ken-Ichiro Tanaka, Toshifumi Sugizaki, Yuki Kanda, Fumiya Tamura, Tomomi Niino, Masahiro Kawahara
Acute respiratory distress syndrome (ARDS) is a potentially devastating form of acute lung injury, which involves neutrophilic inflammation and pulmonary cell death. Reactive oxygen species (ROS) play important roles in ARDS development. New compounds for inhibiting the onset and progression of ARDS are required. Carnosine (β-alanyl-L-histidine) is a small di-peptide with numerous activities, including antioxidant effects, metal chelation, proton buffering capacity and the inhibition of protein carbonylation and glycoxidation...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28128330/cold-inducible-rna-binding-protein-cirp-causes-sepsis-associated-acute-lung-injury-via-induction-of-endoplasmic-reticulum-stress
#8
Mohammad Moshahid Khan, Weng-Lang Yang, Max Brenner, Alexandra Cerutti Bolognese, Ping Wang
Cold-inducible RNA-binding protein (CIRP), released into the circulation during sepsis, causes lung injury via an as yet unknown mechanism. Since endoplasmic reticulum (ER) stress is associated with acute lung injury (ALI), we hypothesized that CIRP causes ALI via induction of ER stress. To test this hypothesis, we studied the lungs of wild-type (WT) and CIRP knockout (KO) mice at 20 h after induction of sepsis by cecal ligation and puncture (CLP). WT mice had significantly more severe ALI than CIRP KO mice...
January 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/27894854/decreased-level-of-endogenous-ghrelin-is-involved-in-the-progression-of-lung-injury-induced-by-oleic-acid
#9
Zhijun Liu, Ting Yu, Haitao Yang, Xiuli Tian, Linlin Feng
AIMS: Acute lung injury (ALI) is associated with excessive mortality and lacks appropriate therapy. Ghrelin is a novel peptide that protects the lung against ALI. This study aimed to investigate the role of endogenous ghrelin in the pathogenesis of ALI. MAIN METHODS: We used a rat oleic acid (OA)-induced ALI model. Pulmonary impairment was detected by hematoxylin and eosin (HE) staining, lung mechanics, wet/dry weight ratio, and arterial blood gas analysis. Plasma and lung content of ghrelin was examined by ELISA, and mRNA expression of ghrelin was measured by quantitative real-time PCR...
November 25, 2016: Life Sciences
https://www.readbyqxmd.com/read/27442881/toll-like-receptor-4-ablation-rescues-against-paraquat-triggered-myocardial-dysfunction-role-of-er-stress-and-apoptosis
#10
Yonghong Lei, Xue Li, Fang Yuan, Lu Liu, Juan Zhang, Yanping Yang, Jieqiong Zhao, Yan Han, Jun Ren, Xiaobing Fu
Paraquat is a nitrogen herbicide imposing severe organ toxicity in human leading to acute lung injury and heart failure. The present study was designed to examine the impact of ablation of the innate proinflammatory mediator toll-like receptor 4 (TLR4) in paraquat-induced cardiac contractile dysfunction and the underlying mechanisms involved with a focus on endoplasmic reticulum (ER) stress and apoptosis. Adult male wild-type (WT) and TLR4 knockout (TLR4(-/-) ) mice were challenged with paraquat (45 mg/kg, i...
February 2017: Environmental Toxicology
https://www.readbyqxmd.com/read/26807721/deletion-of-ask1-protects-against-hyperoxia-induced-acute-lung-injury
#11
Jutaro Fukumoto, Ruan Cox, Itsuko Fukumoto, Young Cho, Prasanna Tamarapu Parthasarathy, Lakshmi Galam, Richard F Lockey, Narasaiah Kolliputi
Apoptosis signal-regulating kinase 1 (ASK1), a member of the MAPK kinase kinase kinase (MAP3K) family, is activated by various stimuli, which include oxidative stress, endoplasmic reticulum (ER) stress, calcium influx, DNA damage-inducing agents and receptor-mediated signaling through tumor necrosis factor receptor (TNFR). Inspiration of a high concentration of oxygen is a palliative therapy which counteracts hypoxemia caused by acute lung injury (ALI)-induced pulmonary edema. However, animal experiments so far have shown that hyperoxia itself could exacerbate ALI through reactive oxygen species (ROS)...
2016: PloS One
https://www.readbyqxmd.com/read/26661653/suramin-protects-from-cisplatin-induced-acute-kidney-injury
#12
Tess V Dupre, Mark A Doll, Parag P Shah, Cierra N Sharp, Alex Kiefer, Michael T Scherzer, Kumar Saurabh, Doug Saforo, Deanna Siow, Lavona Casson, Gavin E Arteel, Alfred Bennett Jenson, Judit Megyesi, Rick G Schnellmann, Levi J Beverly, Leah J Siskind
Cisplatin, a commonly used cancer chemotherapeutic, has a dose-limiting side effect of nephrotoxicity. Approximately 30% of patients administered cisplatin suffer from kidney injury, and there are limited treatment options for the treatment of cisplatin-induced kidney injury. Suramin, which is Federal Drug Administration-approved for the treatment of trypanosomiasis, improves kidney function after various forms of kidney injury in rodent models. We hypothesized that suramin would attenuate cisplatin-induced kidney injury...
February 1, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/26658190/lung-epithelial-cell-derived-extracellular-vesicles-activate-macrophage-mediated-inflammatory-responses-via-rock1-pathway
#13
H-G Moon, Y Cao, J Yang, J H Lee, H S Choi, Y Jin
Despite decades of research, the pathogenesis of acute respiratory distress syndrome (ARDS) remains poorly understood, thus impeding the development of effective treatment. Diffuse alveolar damage (DAD) and lung epithelial cell death are prominent features of ARDS. Lung epithelial cells are the first line of defense after inhaled stimuli, such as in the case of hyperoxia. We hypothesized that lung epithelial cells release 'messenger' or signaling molecules to adjacent or distant macrophages, thereby initiating or propagating inflammatory responses after noxious insult...
December 10, 2015: Cell Death & Disease
https://www.readbyqxmd.com/read/26652754/nogo-b-receptor-modulates-pulmonary-artery-smooth-muscle-cell-function-in-developing-lungs
#14
Kent S Tadokoro, Ujala Rana, Xigang Jing, G Ganesh Konduri, Qing R Miao, Ru-Jeng Teng
Nogo-B and its receptor (NgBR) are involved in blood vessel growth in developing lungs, but their role in pulmonary artery smooth muscle cell (PASMC) growth is unknown. We hypothesized that NgBR regulates growth of PASMCs by modulating the function of endoplasmic reticulum (ER) and formation of reactive oxygen species (ROS). In utero constriction of the ductus arteriosus created pulmonary hypertension in fetal lambs (hypertensive fetal lamb [HTFL]). PASMCs isolated 8 days after surgery were assessed for the alteration of protein levels by immunoblots and ROS formation by dihydroethidium and Cell ROX deep red fluorescence...
June 2016: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/26475925/endoplasmic-reticulum-stress-of-neutrophils-is-required-for-ischemia-reperfusion-induced-acute-lung-injury
#15
Rong Hu, Zhi-Feng Chen, Jia Yan, Qi-Fang Li, Yan Huang, Hui Xu, Xiao-Ping Zhang, Hong Jiang
Diverse clinical factors, including intestinal ischemia, contribute to acute lung injury (ALI), which has up to a 40% mortality rate. During the development of lung injury an immune response is elicited that exacerbates the lung insult. Neutrophils have been well studied in mediating the pulmonary insults through an assortment of mechanisms, such as release of granule contents and production of proinflammatory cytokines due to the overactivation of complement and cytokines. In this study, we found that enhanced endoplasmic reticulum (ER) stress was observed in infiltrated neutrophils in the early stage of an ALI mice model...
November 15, 2015: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/26438401/blockade-of-kca3-1-potassium-channels-protects-against-cisplatin-induced-acute-kidney-injury
#16
Cheng-Lung Chen, Jiunn-Wang Liao, Oliver Yoa-Pu Hu, Li-Heng Pao
Tubular cell apoptosis significantly contributes to cisplatin-induced acute kidney injury (AKI) pathogenesis. Although KCa3.1, a calcium-activated potassium channel, participates in apoptosis, its involvement in cisplatin-induced AKI is unknown. Here, we found that cisplatin treatment triggered an early induction of KCa3.1 expression associated with HK-2 cell apoptosis, the development of renal tubular damage, and apoptosis in mice. Treatment with the highly selective KCa3.1 blocker TRAM-34 suppressed cisplatin-induced HK-2 cell apoptosis...
September 2016: Archives of Toxicology
https://www.readbyqxmd.com/read/26279443/lipopolysaccharide-induces-autophagic-cell-death-through-the-perk-dependent-branch-of-the-unfolded-protein-response-in-human-alveolar-epithelial-a549-cells
#17
Shaoying Li, Liang Guo, Pin Qian, Yunfeng Zhao, Ao Liu, Fuyun Ji, Liutong Chen, Xueling Wu, Guisheng Qian
BACKGROUND: Alveolar epithelial cell death plays a critical role in the pathogenesis of lipopolysaccharide (LPS)-induced acute lung injury. Increased autophagy has a dual effect on cell survival. However, it is not known whether autophagy promotes death or survival in human alveolar epithelial cells exposed to LPS. METHODS: Genetic and pharmacological approaches were used to evaluate the effect of autophagy on A549 cell viability upon LPS exposure. The endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways were examined with immunoblotting studies to further explore underlying mechanisms...
2015: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/25878598/ulinastatin-suppresses-endoplasmic-reticulum-stress-and-apoptosis-in-the-hippocampus-of-rats-with-acute-paraquat-poisoning
#18
Hai-Feng Li, Shi-Xing Zhao, Bao-Peng Xing, Ming-Li Sun
Lung injury is the main manifestation of paraquat poisoning. Few studies have addressed brain damage after paraquat poisoning. Ulinastatin is a protease inhibitor that can effectively stabilize lysosomal membranes, prevent cell damage, and reduce the production of free radicals. This study assumed that ulinastatin would exert these effects on brain tissues that had been poisoned with paraquat. Rat models of paraquat poisoning were intraperitoneally injected with ulinastatin. Simultaneously, rats in the control group were administered normal saline...
March 2015: Neural Regeneration Research
https://www.readbyqxmd.com/read/25862813/intestinal-epithelial-tlr-4-activation-is-required-for-the-development-of-acute-lung-injury-after-trauma-hemorrhagic-shock-via-the-release-of-hmgb1-from-the-gut
#19
Chhinder P Sodhi, Hongpeng Jia, Yukihiro Yamaguchi, Peng Lu, Misty Good, Charlotte Egan, John Ozolek, Xiaorong Zhu, Timothy R Billiar, David J Hackam
The mechanisms that lead to the development of remote lung injury after trauma remain unknown, although a central role for the gut in the induction of lung injury has been postulated. We hypothesized that the development of remote lung injury after trauma/hemorrhagic shock requires activation of TLR4 in the intestinal epithelium, and we sought to determine the mechanisms involved. We show that trauma/hemorrhagic shock caused lung injury in wild-type mice, but not in mice that lack TLR4 in the intestinal epithelium, confirming the importance of intestinal TLR4 activation in the process...
May 15, 2015: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/25802570/regulatory-effects-of-hydrogen-sulfide-on-alveolar-epithelial-cell-endoplasmic-reticulum-stress-in-rats-with-acute-lung-injury
#20
Zhi-Wei Liu, Hai-Ying Wang, Lan Guan, Bin Zhao
BACKGROUND: The present study was undertaken to examine the regulatory effect of hydrogen sulfide (H2S) on endoplasmic reticulum stress in alveolar epithelial cells of rats with acute lung injury (ALI) induced by oleic acid (OA). METHODS: Seventy-two male Sprague Dawley (SD) rats were divided into control group, oleic acid-induced ALI group (OA group), oleic acid-induced ALI with sodium hydrosulfide (NaHS) pretreatment group (OA+NaHS group), and sodium hydrosulfide treatment group (NaHS group)...
2015: World Journal of Emergency Medicine
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