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macrophage fibrosis

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https://www.readbyqxmd.com/read/28826664/aicar-treatment-reduces-interstitial-fibrosis-in-aging-mice-suppression-of-the-inflammatory-fibroblast
#1
Katarzyna A Cieslik, JoAnn Trial, Mark L Entman
In 2030, elderly people will represent 20% of the United States population. Even now, chronic cardiac diseases, especially heart failure with preserved systolic function (HFpEF), are the most expensive DRGs for Medicare. Progressive interstitial fibrosis in the aging heart is well recognized as an important component of HFpEF. Our recent studies suggested an important pathophysiologic role for reduced TGF-β receptor 1 (TGFβR1) signaling in mesenchymal stem cells (MSCs) and their mesenchymal fibroblast progeny in the development of interstitial fibrosis...
August 4, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28822966/inhibitory-actions-of-the-nrg-1-erbb4-pathway-in-macrophages-during-tissue-fibrosis-in-heart-skin-and-lung
#2
Zarha Vermeulen, Anne-Sophie Hervent, Lindsey Dugaucquier, Leni Vandekerckhove, Miche Rombouts, Matthias Beyens, Dorien M Schrijvers, Guido R Y De Meyer, Stuart Maudsley, Gilles W De Keulenaer, Vincent Fm Segers
The neuregulin-1 (NRG-1)/ErbB system is an endothelium-controlled paracrine system modulating cardiac performance and adaptation. Recent studies indicate that NRG-1 has anti-fibrotic effects in the left ventricle (LV), which were explained by direct actions on cardiac fibroblasts. However, the NRG-1/ErbB system also regulates the function of macrophages. In this study, we hypothesized that the anti-fibrotic effect of NRG-1 in the heart is at least partially mediated through inhibitory effects on macrophages...
August 19, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28821730/infiltration-of-m1-but-not-m2-macrophages-is-impaired-after-unilateral-ureter-obstruction-in-nrf2-deficient-mice
#3
Yuji Sogawa, Hajime Nagasu, Shigeki Iwase, Chieko Ihoriya, Seiji Itano, Atsushi Uchida, Kengo Kidokoro, Shun'ichiro Taniguchi, Masafumi Takahashi, Minoru Satoh, Tamaki Sasaki, Takafumi Suzuki, Masayuki Yamamoto, Tiffany Horng, Naoki Kashihara
Chronic inflammation can be a major driver of the failure of a variety of organs, including chronic kidney disease (CKD). The NLR family pyrin domain-containing 3 (NLRP3) inflammasome has been shown to play a pivotal role in inflammation in a mouse kidney disease model. Nuclear factor erythroid 2-related factor 2 (Nrf2), the master transcription factor for anti-oxidant responses, has also been implicated in inflammasome activation under physiological conditions. However, the mechanism underlying inflammasome activation in CKD remains elusive...
August 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28821329/cardiac-progenitor-cell-recruitment-drives-fetal-cardiac-regeneration-by-enhanced-angiogenesis
#4
Carlos Zgheib, Maggie M Hodges, Myron W Allukian, Junwang Xu, Kara L Spiller, Joseph H Gorman, Robert C Gorman, Kenneth W Liechty
BACKGROUND: In contrast to adults, the fetal response to myocardial infarction (MI) is regenerative, requiring the recruitment of cardiac progenitor cells to replace infarcted myocardium. Macrophage contribution to tissue repair depends on their phenotype: M1 are proinflammatory and initiate angiogenesis; M2a are profibrotic and contribute to blood vessels maturation; and M2c are proremodeling and proangiogenesis. The goal of the present study was to expand on this work by examining cardiac progenitor cells recruitment, and the role of macrophages in promoting angiogenesis and cardiac regeneration in the fetal heart after MI...
August 16, 2017: Annals of Thoracic Surgery
https://www.readbyqxmd.com/read/28818858/pai-1-plasminogen-activator-inhibitor-1-expression-renders-alternatively-activated-human-macrophages-proteolytically-quiescent
#5
Philipp J Hohensinner, Johanna Baumgartner, Julia B Kral-Pointner, Pavel Uhrin, Benjamin Ebenbauer, Barbara Thaler, Konstantin Doberer, Stefan Stojkovic, Svitlana Demyanets, Michael B Fischer, Kurt Huber, Gernot Schabbauer, Walter S Speidl, Johann Wojta
OBJECTIVE: Macrophages are versatile immune cells capable of polarizing into functional subsets depending on environmental stimulation. In atherosclerotic lesions, proinflammatory polarized macrophages are associated with symptomatic plaques, whereas Th2 cytokine-polarized macrophages are inversely related with disease progression. To establish a functional cause for these observations, we analyzed extracellular matrix degradation phenotypes in polarized macrophages. APPROACH AND RESULTS: We provide evidence that proinflammatory polarized macrophages rely on membrane-bound proteases including matrix metalloproteinase 14 and the serine protease uPA (urokinase plasminogen activator) together with its receptor uPAR for extracellular matrix degradation...
August 17, 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/28817691/rac2-is-required-for-alternative-macrophage-activation-and-bleomycin-induced-pulmonary-fibrosis-a-macrophage-autonomous-phenotype
#6
Shweta Joshi, Alok R Singh, Simon S Wong, Muamera Zulcic, Min Jiang, Annie Pardo, Moises Selman, James S Hagood, Donald L Durden
Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by cellular phenotype alterations and deposition of extracellular matrix proteins. The alternative activation of macrophages in the lungs has been associated as a major factor promoting pulmonary fibrosis, however the mechanisms underlying this phenomenon are poorly understood. In the present study, we have defined a molecular mechanism by which signals transmitted from the extracellular matrix via the α4β1 integrin lead to the activation of Rac2 which regulates alternative macrophage differentiation, a signaling axis within the pulmonary macrophage compartment required for bleomycin induced pulmonary fibrosis...
2017: PloS One
https://www.readbyqxmd.com/read/28815768/micro-vesicles-derived-from-human-wharton-s-jelly-mesenchymal-stromal-cells-mitigate-renal-ischemia-reperfusion-injury-in-rats-after-cardiac-death-renal-transplantation
#7
Xiaoqiang Wu, Tianzhong Yan, Zhiwei Wang, Xuan Wu, Guanghui Cao, Chan Zhang, Xiangyong Tian, Junpeng Wang
OBJECTIVES: The purpose of the present study was to investigate the possible therapeutic effects of the human Wharton-Jelly mesenchymal stromal cells derived micro-vesicles (hWJMSCs-MVs) on renal ischemia-reperfusion injury (IRI) after cardiac death (CD) renal transplantation in rats. METHODS: MVs were injected intravenously in rats immediately after renal transplantation. The animals were sacrificed at 24 h, 48 h, 1 and 2 weeks post-transplantation. ELISA was used to determine the von Willebrand Factor (vWF), tumore necrosis factor (TNF)-α and interleukin (IL)-10 levels in the serum...
August 16, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28814429/nintedanib-macrophage-activation-and-ameliorates-vascular-and-fibrotic-manifestations-in-the-fra2-mouse-model-of-systemic-sclerosis
#8
Jingang Huang, Christiane Maier, Yun Zhang, Alina Soare, Clara Dees, Christian Beyer, Ulrike Harre, Chih-Wei Chen, Oliver Distler, Georg Schett, Lutz Wollin, Jörg H W Distler
BACKGROUND: Nintedanib is an inhibitor targeting platelet-derived growth factor receptor, fibroblast growth factor receptor and vascular endothelial growth factor receptor tyrosine kinases that has recently been approved for the treatment of idiopathic pulmonary fibrosis. The aim of this study was to analyse the effects of nintedanib in the fos-related antigen-2 (Fra2) mouse model of systemic sclerosis (SSc). METHODS: The effects of nintedanib on pulmonary arterial hypertension with proliferation of pulmonary vascular smooth muscle cells (PVSMCs) and luminal occlusion, on microvascular disease with apoptosis of microvascular endothelial cells (MVECs) and on fibroblast activation with myofibroblast differentiation and accumulation of extracellular matrix were analysed...
August 16, 2017: Annals of the Rheumatic Diseases
https://www.readbyqxmd.com/read/28812526/parvovirus-infection-is-associated-with-myocarditis-and-myocardial-fibrosis-in-young-dogs
#9
Jordan Ford, Laura McEndaffer, Randall Renshaw, Alex Molesan, Kathleen Kelly
Perinatal parvoviral infection causes necrotizing myocarditis in puppies, which results in acute high mortality or progressive cardiac injury. While widespread vaccination has dramatically curtailed the epidemic of canine parvoviral myocarditis, we hypothesized that canine parvovirus 2 (CPV-2) myocardial infection is an underrecognized cause of myocarditis, cardiac damage, and/or repair by fibrosis in young dogs. In this retrospective study, DNA was extracted from formalin-fixed, paraffin-embedded tissues from 40 cases and 41 control dogs under 2 years of age from 2007 to 2015...
January 1, 2017: Veterinary Pathology
https://www.readbyqxmd.com/read/28811075/regulatory-t-cell-deficient-scurfy-mice-exhibit-a-th2-m2-like-inflammatory-response-in-the-skin
#10
Stefanie Haeberle, Verena Raker, Jessica Haub, Yong O Kim, Shih-Yen Weng, Osman K Yilmaz, Alexander Enk, Kerstin Steinbrink, Detlef Schuppan, Eva N Hadaschik
BACKGROUND: Scurfy mice have a functional defect in regulatory T cells (Treg), which leads to lethal multi-organ inflammation. The missing Treg function results in uncontrolled autoimmune cellular and humoral inflammatory responses. We and others have previously shown that during the course of disease scurfy mice develop severe skin inflammation and autoantibodies including anti-nuclear autoantibodies (ANA). OBJECTIVE: Autoimmune skin inflammation and ANA are hallmarks for the diagnosis of autoimmune connective tissue diseases; therefore we analyzed scurfy mice for typical signs of these diseases...
July 13, 2017: Journal of Dermatological Science
https://www.readbyqxmd.com/read/28808355/new-markers-of-inflammation-and-tubular-damage-in-children-with-chronic-kidney-disease
#11
Kinga Musiał, Agnieszka Bargenda, Dorota Drożdż, Danuta Zwolińska
INTRODUCTION AND AIMS: Monocyte chemoattractant protein- (MCP-) 1, macrophage colony-stimulating factor (MCSF), and neopterin are connected with monocyte migration and transition into macrophages, leading to fibrosis and tubular damage in the course of CKD. The aim of the study was to analyze the applicability of urinary fractional excretion (FE) of MCP1, MCSF, and neopterin, as markers of inflammation and tubular damage, in children with CKD. METHODS: The study group consisted of 61 children with CKD stages 1-5 and 23 age-matched controls...
2017: Disease Markers
https://www.readbyqxmd.com/read/28808187/g-aminobutyric-acid-promotes-methionine-choline-deficient-diet-induced-nonalcoholic-steatohepatitis
#12
Yoon Seok Roh, Ara Cho, Zixiong Zhou, Hyuneui Jeong, Jeong-Eun Park, Youn-Soo Cha, Suk-Heung Oh, Chae-Woong Lim, Bumseok Kim
Nonalcoholic steatohepatitis (NASH) is one of the most common liver diseases and a major cause of liver fibrosis worldwide. G-Aminobutyric acid (GABA) is one of the most abundant inhibitory neurotransmitters in the central nervous system. Recently, it has been reported that GABAergic signaling pathways are found in various non-neuronal tissues including the immune system and play a functional role. In the present study, we investigated whether administration of GABA has effects on NASH through its immunomodulatory effects...
October 17, 2016: Journal of Biomedical Research
https://www.readbyqxmd.com/read/28808179/aggf1-attenuates-hepatic-inflammation-and-activation-of-hepatic-stellate-cells-by-repressing-ccl2-transcription
#13
Wenping Xu, Sheng Zeng, Min Li, Zhiwen Fan, Bisheng Zhou
Liver injury represents a continuum of pathophysiological processes involving a complex interplay between hepatocytes, macrophages, and hepatic stellate cells. The mechanism whereby these intercellular interactions contribute to liver injury and fibrosis is not completely understood. We report here that angiogenic factor with G patch and FHA domains 1 (Aggf1) was downregulated in the livers of cirrhotic patients compared to healthy controls and in primary hepatocytes in response to carbon tetrachloride (CCl4) stimulation...
October 17, 2016: Journal of Biomedical Research
https://www.readbyqxmd.com/read/28804725/meprin-metalloprotease-deficiency-associated-with-higher-mortality-rates-and-more-severe-diabetic-kidney-injury-in-mice-with-stz-induced-type-1-diabetes
#14
John E Bylander, Faihaa Ahmed, Sabena M Conley, Jean-Marie Mwiza, Elimelda Moige Ongeri
Meprins are membrane-bound and secreted metalloproteinases consisting of α and/or β subunits that are highly expressed in kidney epithelial cells and are differentially expressed in podocytes and leukocytes (macrophages and monocytes). Several studies have implicated meprins in the progression of diabetic nephropathy (DN) and fibrosis-associated kidney disease. However, the mechanisms by which meprins modulate DN are not understood. To delineate the role of meprins in DN, we subjected meprin αβ knockout (αβKO) mice and their wild-type (WT) counterparts to streptozotocin-induced type 1 diabetes...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28803898/electrospun-fibrous-membranes-featuring-sustained-release-of-ibuprofen-reduce-adhesion-and-improve-neurological-function-following-lumbar-laminectomy
#15
Shen Liu, Guoqing Pan, Guangwang Liu, José das Neves, Sa Song, Shuai Chen, Bangjun Cheng, Zhiyong Sun, Bruno Sarmento, Wenguo Cui, Cunyi Fan
Electrospun fibrous membranes provide suitable physical anti-adhesion barriers for reducing tissue anti-adhesion following surgery. However, often during the biodegradation process, these barriers trigger inflammation and cause a foreign body reaction with subsequent decrease in anti-adhesion efficacy. Here, a facile strategy comprising the incorporation of ibuprofen (IBU) into implantable membranes and its sustained release was proposed in order to improve anti-adhesion effects and neurological outcomes, namely to prevent failed back surgery syndrome (FBSS)...
August 10, 2017: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/28801314/macrophage-migration-inhibitory-factor-limits-renal-inflammation-and-fibrosis-by-counteracting-tubular-cell-cycle-arrest
#16
Sonja Djudjaj, Ina V Martin, Eva M Buhl, Nina J Nothofer, Lin Leng, Marta Piecychna, Jürgen Floege, Jürgen Bernhagen, Richard Bucala, Peter Boor
Renal fibrosis is a common underlying process of progressive kidney diseases. We investigated the role of macrophage migration inhibitory factor (MIF), a pleiotropic proinflammatory cytokine, in this process. In mice subjected to unilateral ureteral obstruction, genetic deletion or pharmacologic inhibition of MIF aggravated fibrosis and inflammation, whereas treatment with recombinant MIF was beneficial, even in established fibrosis. In two other models of progressive kidney disease, global Mif deletion or MIF inhibition also worsened fibrosis and inflammation and associated with worse kidney function...
August 11, 2017: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/28799535/hygroscopic-sonographically-detectable-clips-form-characteristic-breast-and-lymph-node-pseudocysts
#17
Moshe Carmon, Sofia Zilber, David Gekhtman, Oded Olsha, Tal Hadar, Eliahu Golomb
The use of hygroscopic sonographically detectable clips (HSDCs) has dramatically increased during the last years, especially in breast cancer patients who undergo neoadjuvant chemotherapy. The aims of this study are to define the appearance of HSDC sites in histopathological specimens, and to enable pathologists to recognize these sites and differentiate them from other lesions. We examined 124 breast cancer specimens in which the application of HSDCs was documented, 88 breast tissues and 36 lymph nodes, and analyzed the appearance of the clip site in these tissues...
August 11, 2017: Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc
https://www.readbyqxmd.com/read/28799208/ccr2-monocytic-myeloid-derived-immunosuppressive-cells-m-mdsc-inhibit-collagen-degradation-and-promote-lung-fibrosis-by-producing-tgf-%C3%AE-1
#18
Astrid Lebrun, Sandra Lo Re, Mathilde Chantry, Xavier Izquierdo Carerra, Francine Uwambayinema, Doriana Ricci, Raynal Devosse, Saloua Ibouraadaten, Lisa Brombin, Mihaly Palmai-Pallag, Yousof Yakoub, Manolis Pasparakis, Dominique Lison, François Huaux
Monocytes infiltrating scar tissue are predominantly viewed as progenitor cells. Here, we show that tissue CCR2(+) monocytes possess specific immunosuppressive and pro-fibrotic functions. CCR2(+) monocytic cells are acutely recruited to the lung before the onset of silica-induced fibrosis in mice. These tissue monocytes are defined as monocytic-Myeloid-Derived Suppressor Cells (M-MDSC) because they significantly suppress T lymphocyte proliferation in vitro. M-MDSC collected from silica-treated mice also express TGF-β1, which stimulates lung fibroblasts to release TIMP-1, an inhibitor of metalloproteinase collagenolytic activity...
August 11, 2017: Journal of Pathology
https://www.readbyqxmd.com/read/28798256/metabolic-characterization-and-rna-profiling-reveal-glycolytic-dependence-of-pro-fibrotic-phenotype-of-alveolar-macrophages-in-lung-fibrosis
#19
Na Xie, Huachun Cui, Jing Ge, Sami Banerjee, Sijia Guo, Shubham Dubey, Edward Abraham, Rui-Ming Liu, Gang Liu
Metabolic reprogramming has been intrinsically linked to macrophage activation. Alveolar macrophages are known to play an important role in the pathogenesis of pulmonary fibrosis. However, systematic characterization of expression profile in these cells is still lacking. Furthermore, main metabolic programs and their regulation of cellular phenotype are completely unknown. In this study, we comprehensively analyzed the expression profile and main metabolic programs in alveolar macrophages from mice with or without experimental pulmonary fibrosis...
August 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28798254/oxygen-dependent-changes-in-lung-development-do-not-affect-epithelial-infection-with-influenza-a-virus
#20
William Domm, Min Yee, Ravi S Misra, Robert Gelein, Aitor Nogales, Luis Martinez Sobrido, Michael A O'Reilly
Infants born prematurely often require supplemental oxygen that contributes to aberrant lung development and increased pulmonary morbidity following a respiratory viral infection. We have been using a mouse model to understand how early-life hyperoxia affects the adult lung response to influenza A virus (IAV) infection. Prior studies showed how neonatal hyperoxia (100% oxygen) increased sensitivity of adult mice to infection with influenza A virus (IAV (A/Hong Kong/X31) H3N2) as defined by persistent inflammation, pulmonary fibrosis, and mortality...
August 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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