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Endoplasmic reticulum stress and pulmonary fibrosis

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https://www.readbyqxmd.com/read/29705800/histone-deacetylases-promote-er-stress-induced-epithelial-mesenchymal-transition-in-human-lung-epithelial-cells
#1
Daishun Liu, Honglan Zhu, Ling Gong, Shenglan Pu, Yang Wu, Wei Zhang, Guichuan Huang
BACKGROUND/AIMS: Epithelial to mesenchymal transition (EMT) is a crucial process involved in pulmonary fibrosis. This study aimed to explore the role of histone deacetylases (HDACs) and endoplasmic reticulum (ER) stress in EMT in human lung epithelial cells. METHODS: Human lung adenocarcinoma A549 cells were treated with bleomycin and tunicamycin to induce EMT. The proliferation of A549 cells was detected by MTT assay. The expression of HDACs and EMT markers was detected by PCR and Western blot analysis...
April 25, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29676583/reticulocalbin-3-deficiency-in-alveolar-epithelium-exacerbated-bleomycin-induced-pulmonary-fibrosis
#2
Jiawei Jin, Xiaoqian Shi, Yongchao Li, Qianyu Zhang, Yu Guo, Chaokun Li, Pingping Tan, Qiuhong Fang, Yingmin Ma, Runlin Z Ma
Reticulocalbin 3 (Rcn3) is an endoplasmic reticulum (ER) lumen protein localized to the secretory pathway. We have reported that Rcn3 plays critical role for alveolar epithelial cell type II (AECII) maturation during perinatal lung development, but its biological role in the adult lung is largely unknown. Herein, we found marked induction of Rcn3 expression in alveolar epithelium during bleomycin-induced pulmonary fibrosis, which is most obvious in AECIIs. To further examine Rcn3 in pulmonary injury-remodeling, we generated transgenic mice to selectively delete Rcn3 in AECIIs in adulthood...
April 20, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29567124/endoplasmic-reticulum-stress-in-pulmonary-fibrosis
#3
REVIEW
Ankita Burman, Harikrishna Tanjore, Timothy S Blackwell
Endoplasmic reticulum (ER) stress is associated with development and progression of fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). ER stress was first implicated in the pathogenesis of IPF >15 years ago with the discovery of disease-causing mutations in surfactant protein C, which result in a misfolded gene product in type II alveolar epithelial cells (AECs). ER stress and the unfolded protein response (UPR) have been linked to lung fibrosis through regulation of AEC apoptosis, epithelial-mesenchymal transition, myofibroblast differentiation, and M2 macrophage polarization...
March 19, 2018: Matrix Biology: Journal of the International Society for Matrix Biology
https://www.readbyqxmd.com/read/29465261/lipid-synthesis-is-required-to-resolve-er-stress-and-limit-fibrotic-responses-in-the-lung
#4
Freddy Romero, Xu Hong, Dilip Shah, Caleb B Kallen, Ivan Rosas, Zhi Guo, DeLeila Schriner, Julie Barta, Hoora Shaghaghi, Jan B Hoek, Clementina Mesaros, Augustine M Choi, Nathaniel W Snyder, Ross Summer
RATIONALE: Endoplasmic reticulum stress is evident in the alveolar epithelium of humans and mice with pulmonary fibrosis but neither the mechanisms causing ER stress nor its contribution to fibrosis are understood. A well-recognized adaptive response to ER stress is that affected cells induce lipid synthesis; however, we recently reported that lipid synthesis was downregulated in the alveolar epithelium in pulmonary fibrosis. OBJECTIVES: To determine whether lipid synthesis is needed to resolve ER stress and limit fibrotic remodeling in the lung...
February 21, 2018: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29323786/pulmonary-endoplasmic-reticulum-stress-scars-smoke-and-suffocation
#5
REVIEW
Jennifer A Dickens, Elke Malzer, Joseph E Chambers, Stefan J Marciniak
Protein misfolding within the endoplasmic reticulum (ER stress) can be a cause or consequence of pulmonary disease. Mutation of proteins restricted to the alveolar type II pneumocyte can lead to inherited forms of pulmonary fibrosis, but even sporadic cases of pulmonary fibrosis appear to be strongly associated with activation of the unfolded protein response and/or the integrated stress response. Inhalation of smoke can impair protein folding and may be an important cause of pulmonary ER stress. Similarly, tissue hypoxia can lead to impaired protein homeostasis (proteostasis)...
January 11, 2018: FEBS Journal
https://www.readbyqxmd.com/read/29238093/circhipk2-mediated-%C3%AF-1r-promotes-endoplasmic-reticulum-stress-in-human-pulmonary-fibroblasts-exposed-to-silica
#6
Zhouli Cao, Qingling Xiao, Xiaoniu Dai, Zewei Zhou, Rong Jiang, Yusi Cheng, Xiyue Yang, Huifang Guo, Jing Wang, Zhaoqing Xi, Honghong Yao, Jie Chao
Silicosis is characterized by fibroblast accumulation and excessive deposition of extracellular matrix. Although the roles of SiO2 -induced chemokines and cytokines released from alveolar macrophages have received significant attention, the direct effects of SiO2 on protein production and functional changes in pulmonary fibroblasts have been less extensively studied. Sigma-1 receptor, which has been associated with cell proliferation and migration in the central nervous system, is expressed in the lung, but its role in silicosis remains unknown...
December 13, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/29161089/protein-folding-and-the-challenges-of-maintaining-endoplasmic-reticulum-proteostasis-in-idiopathic-pulmonary-fibrosis
#7
Freddy Romero, Ross Summer
Alveolar epithelial type II (AEII) cells are "professional" secretory cells that synthesize and secrete massive quantities of proteins to produce pulmonary surfactant and maintain airway immune defenses. To facilitate this high level of protein synthesis, AEII cells are equipped with an elaborate endoplasmic reticulum (ER) structure and possess an abundance of the machinery needed to fold, assemble, and secrete proteins. However, conditions that suddenly increase the quantity of new proteins entering the ER or that impede the capacity of the ER to fold proteins can cause misfolded or unfolded proteins to accumulate in the ER lumen, also called ER stress...
November 2017: Annals of the American Thoracic Society
https://www.readbyqxmd.com/read/29079731/involvement-of-er-stress-pi3k-akt-activation-and-lung-fibroblast-proliferation-in-bleomycin-induced-pulmonary-fibrosis
#8
Han-Shui Hsu, Chen-Chi Liu, Jiun-Han Lin, Tien-Wei Hsu, Jyuan-Wei Hsu, Kelly Su, Shih-Chieh Hung
Pulmonary fibrosis is characterized by fibroblast proliferation and extracellular matrix remodelling, leading to respiratory insufficiency. The mechanisms underlying this progressive and devastating disease remain unclear. Conditions that can impair the function of the endoplasmic reticulum (ER) cause accumulation of unfolded or misfolded proteins, resulting in ER stress and activation of the unfolded protein response (UPR). ER stress has been implicated in many conditions including cancer, diabetes, obesity, and inflammation...
October 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28798253/cyp2e1-regulates-the-development-of-radiation-induced-pulmonary-fibrosis-via-er-stress-and-ros-dependent-mechanisms
#9
Beomseok Son, TaeWoo Kwon, Sungmin Lee, IkJoon Han, Wanyeon Kim, HyeSook Youn, BuHyun Youn
Radiation-induced pulmonary fibrosis (RIPF) is one of the most common side effects of lung cancer radiotherapy. This study was conducted to identify the molecular mechanism responsible for RIPF. We revealed that the transcriptional level of cytochrome P450 2E1 (CYP2E1) was elevated by examining expression profile analysis of RIPF mouse models. We also confirmed that CYP2E1 regulated levels of endoplasmic reticulum (ER) stress and reactive oxygen species (ROS) in alveolar epithelial type II (AE2) cells and lung fibroblasts...
November 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28677092/amelioration-of-bleomycin-induced-pulmonary-fibrosis-by-chlorogenic-acid-through-endoplasmic-reticulum-stress-inhibition
#10
Yi-Chun Wang, Jing Dong, Jing Nie, Ji-Xiang Zhu, Hui Wang, Qiong Chen, Jun-Yi Chen, Jia-Mei Xia, Wei Shuai
To investigate the inhibitory effects of chlorogenic acid on pulmonary fibrosis and the internal mechanisms in vivo and in vitro. 30 male BALB/C mice were randomized into 5 groups: control group, pulmonary fibrosis model group, low, middle and high dose of chlorogenic acid groups. Mice in pulmonary fibrosis model group were administered 5.0 mg/kg bleomycin with intracheal instillation and mice in 3 chlorogenic acid groups were treated with chlorogenic acid every day for 28 days after bleomycin administration...
September 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28659504/endoplasmic-reticulum-stress-in-lung-disease
#11
REVIEW
Stefan J Marciniak
Exposure to inhaled pollutants, including fine particulates and cigarette smoke is a major cause of lung disease in Europe. While it is established that inhaled pollutants have devastating effects on the genome, it is now recognised that additional effects on protein folding also drive the development of lung disease. Protein misfolding in the endoplasmic reticulum affects the pathogenesis of many diseases, ranging from pulmonary fibrosis to cancer. It is therefore important to understand how cells respond to endoplasmic reticulum stress and how this affects pulmonary tissues in disease...
June 30, 2017: European Respiratory Review: An Official Journal of the European Respiratory Society
https://www.readbyqxmd.com/read/28498407/respiratory-syncytial-virus-infection-accelerates-lung-fibrosis-through-the-unfolded-protein-response-in-a-bleomycin-induced-pulmonary-fibrosis-animal-model
#12
Lina Wang, Wei Cheng, Zhimin Zhang
Emerging evidence has demonstrated that endoplasmic reticulum stress (ER) is involved in the pathogenesis of idiopathic pulmonary fibrosis, however, the underlying mechanism remains unclear. Viral infection often triggers a hyperinflammatory response by an expansion of the ER. The present study was designed to observe the role of respiratory syncytial virus infection (RSV)‑induced ER stress on lung fibrosis. In order to determine the role of ER stress on the onset and progression of pulmonary fibrosis, mice received an intratracheal combined injection of RSV and bleomycin on day 0...
July 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28337301/endoplasmic-reticulum-stress-a-new-wrestler-in-the-pathogenesis-of-idiopathic-pulmonary-fibrosis
#13
Lei Zhang, Yi Wang, Nuruliarizki Shinta Pandupuspitasari, Guorao Wu, Xudong Xiang, Quan Gong, Weining Xiong, Cong-Yi Wang, Ping Yang, Boxu Ren
Idiopathic pulmonary fibrosis (IPF) has attracted extensive attention for its unexplained progressive lung scarring, short median survival and its unresponsiveness to traditional therapies. Despite extensive studies, the mechanisms underlying IPF pathoetiologies, however, remain poorly understood. Recent advances delineated a potential function of endoplasmic reticulum (ER) stress in meeting the need of fibrotic response, which pinpointed a critical role for the unfolded protein response (UPR) pathways in IPF pathogenesis...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28157203/hepatocyte-growth-factor-secreted-by-bone-marrow-stem-cell-reduce-er-stress-and-improves-repair-in-alveolar-epithelial-ii-cells
#14
Izabela Nita, Katrin Hostettler, Luca Tamo, Michaela Medová, Giuseppe Bombaci, Jun Zhong, Ramanjaneyulu Allam, Yitzhak Zimmer, Michael Roth, Thomas Geiser, Amiq Gazdhar
Idiopathic Pulmonary Fibrosis (IPF) is a progressive, irreversible lung disease with complex pathophysiology. Evidence of endoplasmic reticulum (ER) stress has been reported in alveolar epithelial cells (AEC) in IPF patients. Secreted mediators from bone marrow stem cells (BMSC-cm) have regenerative properties. In this study we investigate the beneficial effects of BMSC-cm on ER stress response in primary AEC and ER stressed A549 cells. We hypothesize that BMSC-cm reduces ER stress. Primary AEC isolated from IPF patients were treated with BMSC-cm...
February 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28056498/bone-marrow-stem-cell-therapy-partially-ameliorates-pathological-consequences-in-livers-of-mice-expressing-mutant-human-%C3%AE-1-antitrypsin
#15
COMPARATIVE STUDY
Prakash Baligar, Veena Kochat, Shailendra K Arindkar, Zaffar Equbal, Snehashish Mukherjee, Swati Patel, Perumal Nagarajan, Sujata Mohanty, Jeffrey H Teckman, Asok Mukhopadhyay
Alpha-1-antitrypsin (AAT) deficiency (AATD) is a genetic disease, caused by mutation of the AAT gene. Accumulation of mutated AAT protein aggregates in hepatocytes leads to endoplasmic reticulum stress, resulting in impairment of liver functions and, in some cases, hepatocellular carcinoma, whereas decline of AAT levels in sera is responsible for pulmonary emphysema. In advanced liver disease, the only option for treatment is liver transplantation, whereas AAT replacement therapy is therapeutic for emphysema...
April 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/27799632/pulmonary-fibrosis-in-the-era-of-stratified-medicine
#16
REVIEW
Susan K Mathai, Chad A Newton, David A Schwartz, Christine Kim Garcia
Both common and rare variants contribute to the genetic architecture of pulmonary fibrosis. Genome-wide association studies have identified common variants, or those with a minor allele frequency of >5%, that are linked to pulmonary fibrosis. The most widely replicated variant (rs35705950) is located in the promoter region of the MUC5B gene and has been strongly associated with idiopathic pulmonary fibrosis (IPF) and familial interstitial pneumonia (FIP) across multiple different cohorts. However, many more common variants have been identified with disease risk and in aggregate account for approximately one-third of the risk of IPF...
December 2016: Thorax
https://www.readbyqxmd.com/read/27135434/grp78-and-chop-modulate-macrophage-apoptosis-and-the-development-of-bleomycin-induced-pulmonary-fibrosis
#17
Ehab A Ayaub, Philipp S Kolb, Zahraa Mohammed-Ali, Victor Tat, James Murphy, Pierre-Simon Bellaye, Chiko Shimbori, Felix J Boivin, Rocky Lai, Edward G Lynn, Šárka Lhoták, Darren Bridgewater, Martin Rj Kolb, Mark D Inman, Jeffrey G Dickhout, Richard C Austin, Kjetil Ask
Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) have been associated with fibrotic lung disease, although exactly how they modulate this process remains unclear. Here we investigated the role of GRP78, the main UPR regulator, in an experimental model of lung injury and fibrosis. Grp78(+/-) , Chop(-/-) and wild type C57BL6/J mice were exposed to bleomycin by oropharyngeal intubation and lungs were examined at days 7 and 21. We demonstrate here that Grp78(+/-) mice were strongly protected from bleomycin-induced fibrosis, as shown by immunohistochemical analysis, collagen content and lung function measurements...
August 2016: Journal of Pathology
https://www.readbyqxmd.com/read/26883801/chop-deficiency-protects-mice-against-bleomycin-induced-pulmonary-fibrosis-by-attenuating-m2-macrophage-production
#18
Yingying Yao, Yi Wang, Zhijun Zhang, Long He, Jianghui Zhu, Meng Zhang, Xiaoyu He, Zhenshun Cheng, Qilin Ao, Yong Cao, Ping Yang, Yunchao Su, Jianping Zhao, Shu Zhang, Qilin Yu, Qin Ning, Xudong Xiang, Weining Xiong, Cong-Yi Wang, Yongjian Xu
C/EBP homologous protein (Chop) has been shown to have altered expression in patients with idiopathic pulmonary fibrosis (IPF), but its exact role in IPF pathoaetiology has not been fully addressed. Studies conducted in patients with IPF and Chop(-/-) mice have dissected the role of Chop and endoplasmic reticulum (ER) stress in pulmonary fibrosis pathogenesis. The effect of Chop deficiency on macrophage polarization and related signalling pathways were investigated to identify the underlying mechanisms. Patients with IPF and mice with bleomycin (BLM)-induced pulmonary fibrosis were affected by the altered Chop expression and ER stress...
May 2016: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/26545899/camkii-inhibition-in-type-ii-pneumocytes-protects-from-bleomycin-induced-pulmonary-fibrosis-by-preventing-ca2-dependent-apoptosis
#19
Christopher J Winters, Olha Koval, Shubha Murthy, Chantal Allamargot, Sara C Sebag, John D Paschke, Omar A Jaffer, A Brent Carter, Isabella M Grumbach
The calcium and calmodulin-dependent kinase II (CaMKII) translates increases in intracellular Ca(2+) into downstream signaling events. Its function in pulmonary pathologies remains largely unknown. CaMKII is a well-known mediator of apoptosis and regulator of endoplasmic reticulum (ER) Ca(2+). ER stress and apoptosis of type II pneumocytes lead to aberrant tissue repair and progressive collagen deposition in pulmonary fibrosis. Thus we hypothesized that CaMKII inhibition alleviates fibrosis in response to bleomycin by attenuating apoptosis and ER stress of type II pneumocytes...
January 1, 2016: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/26359372/aberrant-expression-and-activity-of-histone-deacetylases-in-sporadic-idiopathic-pulmonary-fibrosis
#20
Martina Korfei, Sylwia Skwarna, Ingrid Henneke, BreAnne MacKenzie, Oleksiy Klymenko, Shigeki Saito, Clemens Ruppert, Daniel von der Beck, Poornima Mahavadi, Walter Klepetko, Saverio Bellusci, Bruno Crestani, Soni Savai Pullamsetti, Ludger Fink, Werner Seeger, Oliver Holger Krämer, Andreas Guenther
BACKGROUND: Activation and differentiation of fibroblasts into contractile protein-expressing myofibroblasts and their acquired apoptosis-resistant phenotype are critical factors towards the development of idiopathic pulmonary fibrosis (IPF), a fatal disease characterised by distorted pulmonary structure and excessive extracellular matrix (ECM) deposition. The molecular mechanisms underlying these processes in IPF remain incompletely understood. We investigated the possible implication of aberrant overexpression and activity of histone deacetylases (HDACs) in IPF...
November 2015: Thorax
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