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https://www.readbyqxmd.com/read/29146573/prostanoid-ep4-agonist-l-902-688-activates-ppar%C3%AE-and-attenuates-pulmonary-arterial-hypertension
#1
Hsin-Hsien Li, Hsao-Hsun Hsu, Gwo-Jyh Chang, I-Chen Chen, Wan-Jing Ho, Pei-Chen Hsu, Wei-Jan Chen, Jong-Hwei Su Pang, Chung-Chi Huang, Ying-Ju Lai
Prostacyclin agonists that bind the prostacyclin receptor (IP) to stimulate cyclic adenosine monophosphate (cAMP) synthesis are effective vasodilators for the treatment of idiopathic pulmonary arterial hypertension (IPAH) but this signaling may occur through nuclear peroxisome proliferator-activated receptor-gamma (PPARγ). There is evidence of scant IP and PPARγ expression but stable prostanoid EP4 receptor (EP4) expression in IPAH patients. Both IP and EP4 functionally couple with stimulatory G protein (Gs), which activate signal transduction...
November 16, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29146157/angiotensin-converting-enzyme-2-activation-ameliorates-pulmonary-endothelial-dysfunction-in-rats-with-pulmonary-arterial-hypertension-through-mediating-phosphorylation-of-endothelial-nitric-oxide-synthase
#2
Gang Li, Han Zhang, Lei Zhao, Yaozhong Zhang, Daole Yan, Yinglong Liu
This study aims to investigate the effect of angiotensin-converting enzyme 2 (ACE2) activation on pulmonary endothelial function in the process of preventing pulmonary arterial hypertension (PAH) in rat models and to explore the underlying mechanisms. Specific pathogen free rats were randomly divided into five groups including control group, PAH group, PAH + Resorcinolnaphthalein (Res) group (ACE2 activation), PAH + Res + MLN4760 group (ACE2 inhibition), and PAH + Res + L-NAME group (endothelial nitric oxide synthase [eNOS] inhibition)...
October 28, 2017: Journal of the American Society of Hypertension: JASH
https://www.readbyqxmd.com/read/29142074/stat3-controls-col1a2-enhancer-activation-cooperatively-with-junb-regulates-type-i-collagen-synthesis-post-transcriptionally-and-is-essential-for-lung-myofibroblast-differentiation
#3
Ioannis Papaioannou, Shiwen Xu, Christopher P Denton, David J Abraham, Markella Ponticos
Fibroblast differentiation is key cellular process that underlies the process of fibrosis, a deadly complication of fibrotic diseases like Scleroderma (SSc). This transition coincides with the overproduction of Collagen type I (COL1) and other extracellular matrix proteins. High level expression of the collagen type 1α2 subunit (COL1A2), requires the engagement of a far upstream enhancer, whose activation is strongly dependent on the AP1 factor JunB. We now report that STAT3 also binds the COL1A2 enhancer and is essential for RNA polymerase recruitment, without affecting JunB binding...
November 15, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/29141888/lung-cancer-associated-pulmonary-hypertension-role-of-microenvironmental-inflammation-based-on-tumor-cell-immune-cell-cross-talk
#4
Soni Savai Pullamsetti, Baktybek Kojonazarov, Samantha Storn, Henning Gall, Ylia Salazar, Janine Wolf, Andreas Weigert, Nefertiti El-Nikhely, Hossein Ardeschir Ghofrani, Gabriele A Krombach, Ludger Fink, Stefan Gattenlöhner, Ulf R Rapp, Ralph Theo Schermuly, Friedrich Grimminger, Werner Seeger, Rajkumar Savai
Dyspnea is a frequent, devastating, and poorly understood symptom of advanced lung cancer. In our cohort, among 519 patients who underwent a computed tomography scan for the diagnosis of lung cancer, 250 had a mean pulmonary artery diameter of >28 mm, indicating pulmonary hypertension (PH). In human lung cancer tissue, we consistently observed increased vascular remodeling and perivascular inflammatory cell accumulation (macrophages/lymphocytes). Vascular remodeling, PH, and perivascular inflammatory cell accumulation were mimicked in three mouse models of lung cancer (LLC1, KRas(LA2) , and cRaf-BxB)...
November 15, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/29140397/progress-in-the-understanding-of-the-pathology-of-allergic-asthma-and-the-potential-of-fruit-proanthocyanidins-as-modulators-of-airway-inflammation
#5
REVIEW
Sara L Coleman, Odette M Shaw
Allergic asthma is a chronic inflammatory lung disease characterized by sensitization of the airways, and the development of immunoglobulin E antibodies, to benign antigens. The established pathophysiology of asthma includes recurrent lung epithelial inflammation, excessive mucus production, bronchial smooth muscle hyperreactivity, and chronic lung tissue remodeling, resulting in reversible airflow restriction. Immune cells, including eosinophils and the recently characterized type 2 innate lymphoid cells, infiltrate into the lung tissue as part of the inflammatory response in allergic asthma...
November 15, 2017: Food & Function
https://www.readbyqxmd.com/read/29140131/effects-of-inhaled-corticosteroids-on-the-expression-of-tnf-family-molecules-in-murine-model-of-allergic-asthma
#6
Fei Shi, Yarui Zhang, Chen Qiu, Yi Xiong, Manhui Li, Aijun Shan, Ying Yang, Binbin Li
BACKGROUND: The tumor necrosis factor superfamily member LIGHT (the official gene symbol approved by NCBI Gene Database), an inflammatory factor secreted by T cells after allergen exposure, recently discovered to play crucial roles in asthmatic airway remodeling. However, it is unclear whether LIGHT could be controlled by inhaled corticosteroids, a key component of asthma management. This study was to investigate the effects and potential mechanisms of inhaled budesonide on the expressions of LIGHT and its receptors (LTβR and HVEM) of lung tissues in ovalbumin-sensitized mice...
October 2017: Experimental Lung Research
https://www.readbyqxmd.com/read/29139549/elevated-potassium-outward-currents-in-hyperoxia-treated-atrial-cardiomyocytes
#7
Z Vysotskaya, B Chidipi, J L Rodgers, X Tang, E Samal, N Kolliputi, S Mohapatra, E S Bennett, S K Panguluri
Supplementation of 100% oxygen is a very common intervention in intensive care units (ICU) and critical care centers for patients with dysfunctional lung and lung disorders. Although there is advantage in delivering sufficient levels of oxygen, hyperoxia is reported to be directly associated with increasing in-hospital deaths. Our previous studies reported ventricular and electrical remodeling in hyperoxia treated mouse hearts, and in this article, for the first time, we are investigating the effects of hyperoxia on atrial electrophysiology using whole-cell patch-clamp electrophysiology experiments along with assessment of Kv1...
November 15, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29137886/diesel-exhaust-inhalation-exposure-induces-pulmonary-arterial-hypertension-in-mice
#8
Jing Liu, Xiaoqing Ye, Dapeng Ji, Xiaofei Zhou, Cong Qiu, Weiping Liu, Luyang Yu
Diesel exhaust (DE) is one of the main sources of urban air pollution. An increasing number of evidence showed the association of air pollution with cardiovascular diseases. Pulmonary arterial hypertension (PAH) is one of the most disastrous vascular diseases, which results in right ventricular failure and death. However, the relationship of DE inhalation exposure with PAH is still unknown. In this study, male adult mice were exposed by inhalation to filtered ambient air (negative control), 10% O2 hypoxia (PAH-phenotype positive control), 350 μg/m(3) particulate matter whole DE, or the combination of DE and hypoxic condition...
November 11, 2017: Environmental Pollution
https://www.readbyqxmd.com/read/29133079/baicalein-attenuates-monocrotaline-induced-pulmonary-arterial-hypertension-by-inhibiting-vascular-remodeling-in-rats
#9
Ruizan Shi, Zehui Wei, Diying Zhu, Naijie Fu, Wang Chang, Sha Yin, Yueqin Liang, Jianfeng Xing, Xuening Wang, Yan Wang
BACKGROUND: Pulmonary arterial hypertension (PAH) is a devastating cardiopulmonary disorder characterized by elevated pulmonary arterial pressure (PAP) and right ventricular hypertrophy (RVH) driven by progressive vascular remodeling. Reversing adverse vascular remodeling is an important concept in the treatment of PAH. Endothelial injury, inflammation, and oxidative stress are three main contributors to pulmonary vascular remodeling. Baicalein is a natural flavonoid that has been shown to possess anti-proliferative, anti-inflammatory, anti-oxidative, and cardioprotective properties...
November 10, 2017: Pulmonary Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/29126429/rna-sequencing-analysis-of-lung-primary-fibroblast-response-to-eosinophil-degranulation-products-predicts-downstream-effects-on-inflammation-tissue-remodeling-and-lipid-metabolism
#10
Stephane Esnault, Ksenija Bernau, Elizabeth E Torr, Yury A Bochkov, Nizar N Jarjour, Nathan Sandbo
BACKGROUND: The association of eosinophils with inflammation and tissue remodeling is at least partially due to their release of toxic granule proteins and other mediators, including cytokines. Tissue remodeling and consequent functional defects are affected by activity of connective tissue fibroblasts. Exaggerated fibroblast activation, accumulation and change of phenotype may lead to fibrosis and loss of tissue function. So far, little information has been reported on how eosinophils affect inflammation and tissue remodeling via the activation of fibroblasts...
November 10, 2017: Respiratory Research
https://www.readbyqxmd.com/read/29125826/lysyl-oxidases-regulate-fibrillar-collagen-remodelling-in-idiopathic-pulmonary-fibrosis
#11
Gavin Tjin, Eric S White, Alen Faiz, Delphine Sicard, Daniel J Tschumperlin, Annabelle Mahar, Eleanor P W Kable, Janette K Burgess
Idiopathic pulmonary fibrosis (IPF) is a progressive scarring disease of the lung with few effective therapeutic options. Structural remodelling of the extracellular matrix [i.e. collagen cross-linking mediated by the lysyl oxidase (LO) family of enzymes (LOX, LOXL1-4)] might contribute to disease pathogenesis and represent a therapeutic target. This study aimed to further our understanding of the mechanisms by which LO inhibitors might improve lung fibrosis. Lung tissues from IPF and non-IPF subjects were examined for collagen structure (second harmonic generation imaging) and LO gene (microarray analysis) and protein (immunohistochemistry and western blotting) levels...
November 1, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/29118335/adam9-promotes-lung-cancer-progression-through-vascular-remodeling-by-vegfa-angpt2-and-plat
#12
Chen-Yuan Lin, Chia-Fong Cho, Shih-Ting Bai, Jing-Pei Liu, Ting-Ting Kuo, Li-Ju Wang, Yu-Sen Lin, Ching-Chan Lin, Liang-Chuan Lai, Tzu-Pin Lu, Chih-Ying Hsieh, Chin-Nan Chu, Da-Chuan Cheng, Yuh-Pyng Sher
Lung cancer has a very high prevalence of brain metastasis, which results in a poor clinical outcome. Up-regulation of a disintegrin and metalloproteinase 9 (ADAM9) in lung cancer cells is correlated with metastasis to the brain. However, the molecular mechanism underlying this correlation remains to be elucidated. Since angiogenesis is an essential step for brain metastasis, microarray experiments were used to explore ADAM9-regulated genes that function in vascular remodeling. The results showed that the expression levels of vascular endothelial growth factor A (VEGFA), angiopoietin-2 (ANGPT2), and tissue plasminogen activator (PLAT) were suppressed in ADAM9-silenced cells, which in turn leads to decreases in angiogenesis, vascular remodeling, and tumor growth in vivo...
November 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29117177/barrier-tissue-macrophages-functional-adaptation-to-environmental-challenges
#13
REVIEW
Allan McI Mowat, Charlotte L Scott, Calum C Bain
Macrophages are found throughout the body, where they have crucial roles in tissue development, homeostasis and remodeling, as well as being sentinels of the innate immune system that can contribute to protective immunity and inflammation. Barrier tissues, such as the intestine, lung, skin and liver, are exposed constantly to the outside world, which places special demands on resident cell populations such as macrophages. Here we review the mounting evidence that although macrophages in different barrier tissues may be derived from distinct progenitors, their highly specific properties are shaped by the local environment, which allows them to adapt precisely to the needs of their anatomical niche...
November 7, 2017: Nature Medicine
https://www.readbyqxmd.com/read/29116547/the-bpd-trio-interaction-of-dysregulated-pdgf-vegf-and-tgf-signaling-in-neonatal-chronic-lung-disease
#14
REVIEW
Prajakta Oak, Anne Hilgendorff
The development of neonatal chronic lung disease (nCLD), i.e., bronchopulmonary dysplasia (BPD) in preterm infants, significantly determines long-term outcome in this patient population. Risk factors include mechanical ventilation and oxygen toxicity impacting on the immature lung resulting in impaired alveolarization and vascularization. Disease development is characterized by inflammation, extracellular matrix remodeling, and apoptosis, closely intertwined with the dysregulation of growth factor signaling...
November 7, 2017: Molecular and Cellular Pediatrics
https://www.readbyqxmd.com/read/29115924/transcription-factor-e2f1-promotes-emt-by-regulating-zeb2-in-small-cell-lung-cancer
#15
Tingting Wang, Xufang Chen, Weiwei Qiao, Lijun Kong, Daqing Sun, Zunling Li
BACKGROUND: Epithelial-mesenchymal transition (EMT) is an early event in tumour invasion and metastasis, and widespread and distant metastasis at early stages is the typical biological behaviour in small cell lung cancer (SCLC). Our previous reports showed that high expression of the transcription factor E2F1 was involved in the invasion and metastasis of SCLC, but the role of E2F1 in the process of EMT in SCLC is unknown. METHODS: Immunohistochemistry was performed to evaluate the expressions of EMT related markers...
November 7, 2017: BMC Cancer
https://www.readbyqxmd.com/read/29115563/ormdl3-may-participate-in-the-pathogenesis-of-bronchial-epithelial%C3%A2-mesenchymal-transition-in-asthmatic-mice-with-airway-remodeling
#16
Qi Cheng, Yunxiao Shang
Asthma is a common chronic respiratory disease in children that is caused by a complex interaction between genetic and environmental factors. Orosomucoid‑like 3 (ORMDL3) is a candidate gene that has been strongly associated with asthma; however, the underlying mechanisms are unknown. ORMDL3 regulates the expression of metalloproteinases and transforming growth factor‑β, and ORMDL3 transgenic mice exhibit increased airway remodeling. Therefore, ORMDL3 may be associated with airway remodeling. The present study attempted to examine the associations between ORMDL3 and the severity of airway remodeling in asthmatic mice, and also to determine whether ORMDL3 induces epithelial‑mesenchymal transition (EMT) in the bronchial epithelium...
November 6, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29115380/combination-treatment-of-adipose-derived-stem-cells-and-adiponectin-attenuates-pulmonary-arterial-hypertension-in-rats-by-inhibiting-pulmonary-arterial-smooth-muscle-cell-proliferation-and-regulating-the-ampk-bmp-smad-pathway
#17
Li Luo, Wuhong Zheng, Guili Lian, Huaning Chen, Ling Li, Changsheng Xu, Liangdi Xie
The present study aimed to assess the effects of therapy with adiponectin (APN) gene-modified adipose-derived stem cells (ADSCs) on pulmonary arterial hypertension (PAH) in rats and the underlying cellular and molecular mechanisms. ADSCs were successfully isolated from the rats and characterized. ADSCs were effectively infected with the green fluorescent protein (GFP)-empty (ADSCs-V) or the APN-GFP (ADSCs-APN) lentivirus and the APN expression was evaluated by ELISA. Sprague-Dawley rats were administered monocrotaline (MCT) to develop PAH...
October 31, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29113816/hdac2-suppresses-il17a-mediated-airway-remodeling-in-human-and-experimental-modeling-of-copd
#18
Tianwen Lai, Baoping Tian, Chao Cao, Yue Hu, Jiesen Zhou, Yong Wang, Yanping Wu, Zhouyang Li, Xuchen Xu, Min Zhang, Feng Xu, Yuan Cao, Min Chen, Dong Wu, Bin Wu, Chen Dong, Wen Li, Songmin Ying, Zhihua Chen, Huahao Shen
BACKGROUND: Airway remodeling is a central feature of chronic obstructive pulmonary disease (COPD), but the mechanisms underlying its development have not been fully elucidated. OBJECTIVE: To determine whether histone deacetylase (HDAC) 2 protects against cigarette smoke (CS)-induced airway remodeling through IL17A-dependent mechanisms. METHODS: Sputum samples and lung tissues were obtained from control subjects and patients with COPD. The relationships between HDAC2, IL17A, and airway remodeling were investigated...
November 4, 2017: Chest
https://www.readbyqxmd.com/read/29111316/concentrations-of-sp-a-and-hsp70-are-associated-with-polarization-of-macrophages-in-pleural-effusions-of-non-small-cell-lung-cancer
#19
Mariusz Kaczmarek, Malgorzata Lagiedo, Agnieszka Masztalerz, Magdalena Kozlowska, Agata Nowicka, Beata Brajer, Halina Batura-Gabryel, Jan Sikora
Damage-associated molecular pattern (DAMP) molecules can initiate an immune response through Toll-like receptors (TLRs). DAMPs are released from cells as a response to the extracellular danger and can be by-products of tissue damage. In cancer microenvironment necrotic cells release debris which has potency to become DAMPs. Non-small cell lung cancer (NSCLC) is often accompanied by pleural effusion (PE), which contains a variety of DAMPs. Surfactant protein A (SP-A) and heat shock protein 70 (Hsp70) are important DAMPs in the respiratory tract...
October 27, 2017: Immunobiology
https://www.readbyqxmd.com/read/29108819/pulmonary-vascular-remodeling-patterns-and-expression-of-general-control-nonderepressible-2-gcn2-in-pulmonary-veno-occlusive-disease
#20
Esther J Nossent, Fabrice Antigny, David Montani, Harm Jan Bogaard, Maria Rosa Ghigna, Mélanie Lambert, Vincent Thomas de Montpréville, Barbara Girerd, Xavier Jaïs, Laurent Savale, Olaf Mercier, Elie Fadel, Florent Soubrier, Olivier Sitbon, Gérald Simonneau, Anton Vonk Noordegraaf, Marc Humbert, Frédéric Perros, Peter Dorfmüller
BACKGROUND: Heritable pulmonary veno-occlusive disease (PVOD) is linked to mutations in the eukaryotic initiation factor 2 alpha kinase 4 (EIF2AK4) gene, leading to a loss of general control nonderepressible 2 (GCN2). The role of GCN2 expression in pulmonary vascular remodeling remains obscure. We sought to identify specific histologic and biologic features in heritable PVOD. METHODS: Clinical data and lung histology of 24 PVOD patients (12 EIF2AK4 mutation carriers, 12 non-carriers) were submitted to systematic histologic analysis and semiautomated morphometry...
October 4, 2017: Journal of Heart and Lung Transplantation
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