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https://www.readbyqxmd.com/read/29656123/selenium-supplementation-prevents-metabolic-and-transcriptomic-responses-to-cadmium-in-mouse-lung
#1
Xin Hu, Joshua D Chandler, Jolyn Fernandes, Michael L Orr, Li Hao, Karan Uppal, David C Neujahr, Dean P Jones, Young-Mi Go
BACKGROUND: The protective effect of selenium (Se) on cadmium (Cd) toxicity is well documented, but underlying mechanisms are unclear. METHODS: Male mice fed standard diet were given Cd (CdCl2 , 18 μmol/L) in drinking water with or without Se (Na2 SeO4, 20 μmol/L) for 16 weeks. Lungs were analyzed for Cd concentration, transcriptomics and metabolomics. Data were analyzed with biostatistics, bioinformatics, pathway enrichment analysis, and combined transcriptome-metabolome-wide association study...
April 12, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29625182/idiopathic-pulmonary-fibrosis-epithelial-mesenchymal-interactions-and-emerging-therapeutic-targets
#2
REVIEW
Justin C Hewlett, Jonathan A Kropski, Timothy S Blackwell
Idiopathic pulmonary fibrosis (IPF) is a chronic fibrotic disease of the lung that is marked by progressive decline in pulmonary function and ultimately respiratory failure. Genetic and environmental risk factors have been identified that indicate injury to, and dysfunction of the lung epithelium is central to initiating the pathogenic process. Following injury to the lung epithelium, growth factors, matrikines and extracellular matrix driven signaling together activate a variety of repair pathways that lead to inflammatory cell recruitment, fibroblast proliferation and expansion of the extracellular matrix, culminating in tissue fibrosis...
April 3, 2018: Matrix Biology: Journal of the International Society for Matrix Biology
https://www.readbyqxmd.com/read/29599211/experimental-right-ventricular-hypertension-induces-regional-%C3%AE-1-integrin-mediated-transduction-of-hypertrophic-and-profibrotic-right-and-left-ventricular-signaling
#3
Mei Sun, Ryo Ishii, Kenichi Okumura, Adrienn Krauszman, Siegfried Breitling, Olga Gomez, Aleksander Hinek, Stellar Boo, Boris Hinz, Kim A Connelly, Wolfgang M Kuebler, Mark K Friedberg
BACKGROUND: Development of right ventricular (RV) hypertension eventually contributes to RV and left ventricular (LV) myocardial fibrosis and dysfunction. The molecular mechanisms are not fully elucidated. METHODS AND RESULTS: Pulmonary artery banding was used to induce RV hypertension in rats in vivo. Then, we evaluated cardiac function and regional remodeling 6 weeks after pulmonary artery banding. To further elucidate mechanisms responsible for regional cardiac remodeling, we also mimicked RV hypertensive stress by cyclic mechanical stretching applied to confluent cultures of cardiac fibroblasts, isolated from the RV free wall, septal hinge points, and LV free wall...
March 29, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29563334/allele-specific-differences-in-transcriptome-mirnome-and-mitochondrial-function-in-two-hypertrophic-cardiomyopathy-mouse-models
#4
Styliani Vakrou, Ryuya Fukunaga, D Brian Foster, Lars Sorensen, Yamin Liu, Yufan Guan, Kirubel Woldemichael, Roberto Pineda-Reyes, Ting Liu, Jill C Tardiff, Leslie A Leinwand, Carlo G Tocchetti, Theodore P Abraham, Brian O'Rourke, Miguel A Aon, M Roselle Abraham
Hypertrophic cardiomyopathy (HCM) stems from mutations in sarcomeric proteins that elicit distinct biophysical sequelae, which in turn may yield radically different intracellular signaling and molecular pathologic profiles. These signaling events remain largely unaddressed by clinical trials that have selected patients based on clinical HCM diagnosis, irrespective of genotype. In this study, we determined how two mouse models of HCM differ, with respect to cellular/mitochondrial function and molecular biosignatures, at an early stage of disease...
March 22, 2018: JCI Insight
https://www.readbyqxmd.com/read/29557906/autocrine-activation-of-fibroblasts-by-induction-of-il-11-expression-is-a-common-pathway-of-profibrotic-factors
#5
Matthias Mack
No abstract text is available yet for this article.
March 20, 2018: Transplantation
https://www.readbyqxmd.com/read/29525327/obesity-related-heart-failure-with-a-preserved-ejection-fraction-the-mechanistic-rationale-for-combining-inhibitors-of-aldosterone-neprilysin-and-sodium-glucose-cotransporter-2
#6
REVIEW
Milton Packer, Dalane W Kitzman
Obesity-related heart failure with a preserved ejection fraction (HFpEF) is an important phenotype prevalent in the community, especially in people with metabolic disorders (e.g., dyslipidemia, diabetes). These individuals exhibit a marked expansion of plasma volume, but ventricular distensibility is limited, most likely as a result of cardiac microvascular rarefaction acting in concert with myocardial and pericardial fibrosis. Consequently, the increase in plasma volume causes a disproportionate increase in cardiac filling pressures, leading to heart failure, even though systolic ejection is not impaired...
March 7, 2018: JACC. Heart Failure
https://www.readbyqxmd.com/read/29518614/central-role-of-dysregulation-of-tgf-%C3%AE-smad-in-ckd-progression-and-potential-targets-of-its-treatment
#7
REVIEW
Lin Chen, Tian Yang, De-Wen Lu, Hui Zhao, Ya-Long Feng, Hua Chen, Dan-Qian Chen, Nosratola D Vaziri, Ying-Yong Zhao
Chronic kidney disease (CKD) has emerged as a major cause of morbidity and mortality worldwide. Interstitial fibrosis, glomerulosclerosis and inflammation play the central role in the pathogenesis and progression of CKD to end stage renal disease (ESRD). Transforming growth factor-β1 (TGF-β1) is the central mediator of renal fibrosis and numerous studies have focused on inhibition of TGF-β1 and its downstream targets for treatment of kidney disease. However, blockade of TGF-β1 has not been effective in the treatment of CKD patients...
March 5, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29506624/ccn3-a-key-matricellular-protein-distinctly-inhibits-tgf%C3%AE-1-mediated-smad1-5-8-signalling-in-human-podocyte-culture
#8
Tarunkumar Hemraj Madne, Mark Edward Carl Dockrell
Growth factors like TGFβ and CTGF (CCN2) plays a vital role in various cellular functions. TGFβ and CTGF are overexpressed in renal fibrosis. CTGF act as profibrotic stimuli to TGFβ. CCN3 is a member of CCN family which also comprises CCN1 (CYR61), CCN2 (CTGF), CCN4 (WISP-1), CCN5 (WISP-2) and CCN6 (WISP-3). CCN3 has been shown to antagonise CTGF. In this study, we investigated the role of CCN3 in TGFβ1-mediated signalling in human podocytes culture. This study describes the novel function of CCN3 in regulation of TGFβ1 mediated non-canonical Smad signalling in human podocytes culture...
February 28, 2018: Cellular and Molecular Biology
https://www.readbyqxmd.com/read/29500512/mesenchymal-stem-cells-inhibit-hypoxia-induced-inflammatory-and-fibrotic-pathways-in-bladder-smooth-muscle-cells
#9
Bridget Wiafe, Adetola Adesida, Thomas Churchill, Peter Metcalfe
PURPOSE: Partial bladder outlet obstruction is a multifactorial urological condition in which hypoxia plays a significant role. We recently investigated hypoxia's role as a single stressor and found that hypoxia induced an intense inflammatory and profibrotic switch in bladder smooth muscle cells (bSMCs). With the immunomodulatory capacity of mesenchymal stem cells (MSCs), we aimed to investigate if the hypoxia-signaling pathways can be mitigated using MSCs. METHODS: Bladder smooth muscle cells were cultured in 3% oxygen tension for 72 h with either the direct or indirect co-culture with bone marrow derived MSCs...
March 2, 2018: World Journal of Urology
https://www.readbyqxmd.com/read/29497173/pirfenidone-reduces-profibrotic-responses-in-human-dermal-myofibroblasts-in-vitro
#10
Caroline L Hall, Adrienne R Wells, Kai P Leung
Pirfenidone (PFD) is a synthetic small molecule inhibitor with demonstrated anti-inflammatory and antifibrotic properties in vitro and in vivo. The exact mechanism(s) of PFD action remain unclear, due in part to the broad effects of this drug on the complex processes involved in inflammation and fibrosis. While PFD is FDA-approved for the treatment of idiopathic pulmonary fibrosis, the efficacy of this compound for the treatment of dermal fibrosis has not yet been fully characterized. Dermal fibrosis is the pathological formation of excess fibrous connective tissue of the skin, usually the result of traumatic cutaneous injury...
March 1, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/29490938/lipoxins-regulate-the-early-growth-response-1-network-and-reverse-diabetic-kidney-disease
#11
Eoin P Brennan, Muthukumar Mohan, Aaron McClelland, Christos Tikellis, Mark Ziemann, Antony Kaspi, Stephen P Gray, Raelene Pickering, Sih Min Tan, Syed Tasadaque Ali-Shah, Patrick J Guiry, Assam El-Osta, Karin Jandeleit-Dahm, Mark E Cooper, Catherine Godson, Phillip Kantharidis
Background The failure of spontaneous resolution underlies chronic inflammatory conditions, including microvascular complications of diabetes such as diabetic kidney disease. The identification of endogenously generated molecules that promote the physiologic resolution of inflammation suggests that these bioactions may have therapeutic potential in the context of chronic inflammation. Lipoxins (LXs) are lipid mediators that promote the resolution of inflammation. Methods We investigated the potential of LXA4 and a synthetic LX analog (Benzo-LXA4 ) as therapeutics in a murine model of diabetic kidney disease, ApoE-/- mice treated with streptozotocin...
February 28, 2018: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/29485009/oral-submucous-fibrosis-as-an-overhealing-wound-implications-in-malignant-transformation
#12
Mohit Sharma, Smitha Sammith Shetty, Raghu Radhakrishnan
BACKGROUND: Oral submucous fibrosis is an oral potentially malignant disorder with high incidence of malignant transformation and rising global prevalence. However, the genesis of oral submucous fibrosis is still unclear despite superfluity of literature. In the background of ineffective treatment, it is necessary to decode its onset and progression before designing customized treatment regimens. OBJECTIVE: The objective of this article is to decipher the pathogenesis of oral submucous fibrosis in order to identify novel drug targets...
February 26, 2018: Recent Patents on Anti-cancer Drug Discovery
https://www.readbyqxmd.com/read/29481398/%C3%AE-catenin-dependent-wnt-signaling-a-pathway-in-acute-cutaneous-wounding
#13
Antoine L Carre, Michael S Hu, Aaron W James, Kenichiro Kawai, Michael G Galvez, Michael T Longaker, H Peter Lorenz
BACKGROUND: Acute wound healing is a dynamic process that results in the formation of scar tissue. The mechanisms of this process are not well understood; numerous signaling pathways are thought to play a major role. Here, the authors have identified β-catenin-dependent Wnt signaling as an early acute-phase reactant in acute wound healing and scar formation. METHODS: The authors created 6-mm full-thickness excisional cutaneous wounds on adult β-catenin-dependent Wnt signal (BAT-gal) reporter mice...
March 2018: Plastic and Reconstructive Surgery
https://www.readbyqxmd.com/read/29438665/cartilage-intermediate-layer-protein-1-alleviates-pressure-overload-induced-cardiac-fibrosis-via-interfering-tgf-%C3%AE-1-signaling
#14
Cheng-Lin Zhang, Qian Zhao, Hui Liang, Xue Qiao, Jin-Yu Wang, Dan Wu, Li-Ling Wu, Li Li
Cardiac fibrosis is characterized by excessive deposition of extracellular matrix (ECM) proteins in the myocardium and results in decreased ventricular compliance and diastolic dysfunction. Cartilage intermediate layer protein-1 (CILP-1), a novel identified cardiac matricellular protein, is upregulated in most conditions associated with cardiac remodeling, however, whether CILP-1 is involved in pressure overload-induced fibrotic response is unknown. Here, we investigated whether CILP-1 was critically involved in the fibrotic remodeling induced by pressure overload...
February 10, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29427621/brg1-promotes-liver-fibrosis-via-activation-of-hepatic-stellate-cells
#15
Haijie Li, Jingqin Lan, Caishun Han, Kaixuan Guo, Guihua Wang, Junbo Hu, Jianping Gong, Xuelai Luo, Zhixin Cao
Liver fibrosis, an important health concern associated to chronic liver injury that provides a permissive environment for cancer development, is characterized by the persistent deposition of extracellular matrix components mainly derived from activated hepatic stellate cells (HSCs). Brg1, the core subunit of the SWI/SNF chromatin remodeling complex, has been proved to associated with nonalcoholic steatohepatitis which may progress to cirrhosis. Herein, we determined whether Brg1 regulates liver fibrosis and examined its mechanism by focusing on HSCs activation...
February 7, 2018: Experimental Cell Research
https://www.readbyqxmd.com/read/29417309/il-33-can-promote-the-process-of-pulmonary-fibrosis-by-inducing-the-imbalance-between-mmp-9-and-timp-1
#16
Liyan Wu, Zujin Luo, Jinxu Zheng, Peng Yao, Zhenyan Yuan, Xiaohong Lv, Jing Zhao, Min Wang
IL-33 played an important role in inflammatory diseases as evidenced by their high levels of expression in diseased tissues. Previous studies showed that IL-33/ST2L signal transduction pathway participated in epithelial-mesenchymal transition (EMT) of A549 cells. Cytokine IL-1β can increase the expression of MMPs by activating NF-kB. The excessive or inappropriate expression of MMP-9 may randomly and non-selectively destroy the extracellular matrix. TIMP-1 (tissue inhibitor of MMP-9) effects on ebb and flow of ECM by inhibiting activation of MMP-9...
February 7, 2018: Inflammation
https://www.readbyqxmd.com/read/29411011/activation-of-the-nfat-calcium-signaling-pathway-in-human-lamina-cribrosa-cells-in-glaucoma
#17
Mustapha Irnaten, Alexander Zhdanov, Deirdre Brennan, Thomas Crotty, Abbot Clark, Dmitri Papkovsky, Colm O'Brien
Purpose: Optic nerve cupping in glaucoma is characterized by remodeling of the extracellular matrix (ECM) and fibrosis in the lamina cribrosa (LC). We have previously shown that glaucoma LC cells express raised levels of ECM genes and have elevated intracellular calcium ([Ca2+]i). Raised [Ca2+]i is known to promote proliferation, activation, and contractility in fibroblasts via the calcineurin-NFAT (nuclear factor of activated T-cells) signaling pathway. In this study, we examine NFAT expression in normal and glaucoma LC cells, and investigate the effect of cyclosporin A (CsA, a known inhibitor of NFAT activity) on [Ca2+]i and ECM gene expression in normal and glaucoma LC cells...
February 1, 2018: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/29401161/the-cellular-response-of-keloids-and-hypertrophic-scars-to-botulinum-toxin-a-a-comprehensive-literature-review
#18
Evan Austin, Eugene Koo, Jared Jagdeo
BACKGROUND: Keloids and hypertrophic scars are conditions of pathologic scarring characterized by fibroblast hyperproliferation and excess collagen deposition. These conditions significantly impact patients by causing psychosocial, functional, and aesthetic distress. Current treatment modalities have limitations. Clinical evidence indicates that botulinum toxin A (BoNT-A) may prevent and treat keloids and hypertrophic scars. OBJECTIVE: To examine investigated cellular pathways involved in BoNT-A therapeutic modulation of keloids and hypertrophic scars...
February 2018: Dermatologic Surgery: Official Publication for American Society for Dermatologic Surgery [et Al.]
https://www.readbyqxmd.com/read/29375046/one-session-of-exercise-regulates-cathepsin-b-activity-in-the-livers-of-trained-and-untrained-rats
#19
A Wyczalkowska-Tomasik, B Czarkowska-Paczek, J Piekarczyk-Persa, M Zendzian-Piotrowska
Physical exercise causes adaptive changes, mainly in muscles, but it also influences other organs, including liver. Most changes are beneficial; however, strenuous exercise is a strong stressor, and it can result in splanchnic hypoperfusion with subsequent disturbances in liver homeostasis and energy. Cathepsin B is a protease linked to protein turnover and extracellular matrix degradation. It is also involved in autophagy and the activation of proinflammatory and profibrotic pathways. This study investigated the influences of one session of exercise and endurance training on the mRNA, protein level, and activity of cathepsin B in rat liver...
October 2017: Journal of Physiology and Pharmacology: An Official Journal of the Polish Physiological Society
https://www.readbyqxmd.com/read/29367207/non-alcoholic-steatohepatitis-pathogenesis-sublethal-hepatocyte-injury-as-a-driver-of-liver-inflammation
#20
REVIEW
Samar H Ibrahim, Petra Hirsova, Gregory J Gores
A subset of patients with non-alcoholic fatty liver disease develop an inflammatory condition, termed non-alcoholic steatohepatitis (NASH). NASH is characterised by hepatocellular injury, innate immune cell-mediated inflammation and progressive liver fibrosis. The mechanisms whereby hepatic inflammation occurs in NASH remain incompletely understood, but appear to be linked to the proinflammatory microenvironment created by toxic lipid-induced hepatocyte injury, termed lipotoxicity. In this review, we discuss the signalling pathways induced by sublethal hepatocyte lipid overload that contribute to the pathogenesis of NASH...
May 2018: Gut
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