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https://www.readbyqxmd.com/read/28641719/surfactant-protein-d-inhibits-interleukin-12p40-production-by-macrophages-through-the-sirp%C3%AE-rock-erk-signaling-pathway
#1
Rui Yamaguchi, Arisa Sakamoto, Takatoshi Yamamoto, Yasuji Ishimaru, Shinji Narahara, Hiroyuki Sugiuchi, Yasuo Yamaguchi
OBJECTIVE: Interleukin (IL)-12 has a pivotal profibrotic role in the development of idiopathic pulmonary fibrosis (IPF). Medical research trials based on IPF registry databases have actively recruited patients. Surfactant protein D (SP-D) is a useful biomarker in patients with IPF. SP-D binds to signal regulatory protein α (SIRPα), which acts as an inhibitory receptor, and this SP-D/SIRPα interaction may have an anti-inflammatory effect. Accordingly, the inhibitory effect of SP-D on IL-12p40 production by lipopolysaccharide (LPS)-stimulated macrophages was investigated...
June 2017: American Journal of the Medical Sciences
https://www.readbyqxmd.com/read/28635301/stem-cell-mediated-paracrine-signaling-alters-fibroplasia-in-human-vocal-fold-fibroblasts-in-vitro
#2
Nao Hiwatashi, Renjie Bing, Iv Kraja, Ryan C Branski
OBJECTIVES: Interactions between mesenchymal stem cells (MSCs) and native vocal fold fibroblasts (VFFs) have not been described in spite of promising preliminary data regarding the effects of MSCs on vocal fold repair in vivo. The current study employed a conditioned media (CM) model to investigate the paracrine effects of bone marrow-derived mesenchymal stem cells (BMSCs) on VFFs. METHODS: Human VFFs were treated with transforming growth factor-β1 (TGF-β1; 10 ng/mL), CM from human BMSCs following 48 hours of TGF-β1 stimulation, or CM+TGF-β1...
June 1, 2017: Annals of Otology, Rhinology, and Laryngology
https://www.readbyqxmd.com/read/28629772/impact-of-the-cardiovascular-system-associated-adipose-tissue-on-atherosclerotic-pathology
#3
REVIEW
Dimitry A Chistiakov, Andrey V Grechko, Veronika A Myasoedova, Alexandra A Melnichenko, Alexander N Orekhov
Cardiac obesity makes an important contribution to the pathogenesis of cardiovascular disease. One of the important pathways of this contribution is the inflammatory process that takes place in the adipose tissue. In this review, we consider the role of the cardiovascular system-associated fat in atherosclerotic cardiovascular pathology and a non-atherosclerotic cause of coronary artery disease, such as atrial fibrillation. Cardiovascular system-associated fat not only serves as the energy store, but also releases adipokines that control local and systemic metabolism, heart/vascular function and vessel tone, and a number of vasodilating and anti-inflammatory substances...
June 8, 2017: Atherosclerosis
https://www.readbyqxmd.com/read/28626076/cardiac-fibroblast-transcriptome-analyses-support-a-role-for-interferogenic-profibrotic-and-inflammatory-genes-in-anti-ssa-ro-associated-congenital-heart-block
#4
Robert M Clancy, Androo J Markham, Tanisha Jackson, Sara E Rasmussen, Miroslav Blumenberg, Jill P Buyon
The signature lesion of SSA/Ro autoantibody-associated congenital heart block (CHB) is fibrosis and a macrophage infiltrate, supporting an experimental focus on cues influencing the fibroblast component. The transcriptomes of human fetal cardiac fibroblasts were analyzed using two complementary approaches. Cardiac injury conditions were simulated in vitro by incubating human fetal cardiac fibroblasts with supernatants from macrophages transfected with the SSA/Ro-associated hY3. The top ten upregulated transcripts in the stimulated fibroblasts reflected a type I interferon (IFN) response (e...
June 16, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28626027/selective-activation-of-epidermal-growth-factor-receptor-in-renal-proximal-tubule-induces-tubulointerstitial-fibrosis
#5
Jessica M Overstreet, Yinqiu Wang, Xin Wang, Aolei Niu, Leslie S Gewin, Bing Yao, Raymond C Harris, Ming-Zhi Zhang
Epidermal growth factor receptor (EGFR) has been implicated in the pathogenesis of diabetic nephropathy and renal fibrosis; however, the causative role of sustained EGFR activation is unclear. Here, we generated a novel kidney fibrotic mouse model of persistent EGFR activation by selectively expressing the EGFR ligand, human heparin-binding EGF-like growth factor (HB-EGF), in renal proximal tubule epithelium. Human HB-EGF expression increased tyrosine kinase phosphorylation of EGFR and the subsequent activation of downstream signaling pathways, including ERK and AKT, as well as the profibrotic TGF-β1/SMAD pathway...
June 16, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28598023/nintedanib-reduces-ventilation-augmented-bleomycin-induced-epithelial-mesenchymal-transition-and-lung-fibrosis-through-suppression-of-the-src-pathway
#6
Li-Fu Li, Kuo-Chin Kao, Yung-Yang Liu, Chang-Wei Lin, Ning-Hung Chen, Chung-Shu Lee, Chih-Wei Wang, Cheng-Ta Yang
Mechanical ventilation (MV) used in patients with acute respiratory distress syndrome (ARDS) can increase lung inflammation and pulmonary fibrogenesis. Src is crucial in mediating the transforming growth factor (TGF)-β1-induced epithelial-mesenchymal transition (EMT) during the fibroproliferative phase of ARDS. Nintedanib, a multitargeted tyrosine kinase inhibitor that directly blocks Src, has been approved for the treatment of idiopathic pulmonary fibrosis. The mechanisms regulating interactions among MV, EMT and Src remain unclear...
June 9, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28585302/rictor-mtorc2-promotes-macrophage-activation-and-kidney-fibrosis
#7
Jiafa Ren, Jianzhong Li, Ye Feng, Bingyan Shu, Yuan Gui, Wei Wei, Weichun He, Junwei Yang, Chunsun Dai
Mammalian target of rapamycin (mTOR) signaling controls many essential cellular functions. However, the role for Rictor/mTORC2 in regulating macrophage activation and kidney fibrosis remains largely unknown. We report here that Rictor/mTORC2 was activated in macrophages from the fibrotic kidneys of mice. Ablation of Rictor in macrophages diminished kidney fibrosis, inflammatory cell accumulation, macrophage proliferation and polarization after unilateral ureter obstruction (UUO) or ischemia/reperfusion injury (IRI)...
June 6, 2017: Journal of Pathology
https://www.readbyqxmd.com/read/28562065/role-of-platelet-derived-tgf-%C3%AE-1-and-ros-in-radiation-induced-organ-fibrosis
#8
Jasimuddin Ahamed, Jeffrey Laurence
SIGNIFICANCE: This review evaluates the role of platelet-derived TGF-β1 in oxidative stress-linked pathologic fibrosis, with an emphasis on the heart and kidney, using ionizing radiation as a clinically relevant stimulus. Current radiation-induced organ fibrosis interventions focus on pan-neutralization of transforming growth factor (TGF)-β1 or use of anti-oxidants and anti-proliferative agents, with limited clinical efficacy. Recent Advances: Pathologic fibrosis represents excessive accumulation of collagen and other extracellular matrix (ECM) components following dysregulation of a balance between ECM synthesis and degradation...
May 31, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28546006/atrial-myofibroblast-activation-and-connective-tissue-formation-in-a-porcine-model-of-atrial-fibrillation-and-reduced-left-ventricular-function
#9
Patrick Lugenbiel, Fabian Wenz, Katharina Govorov, Pascal Syren, Hugo A Katus, Dierk Thomas
AIMS: Atrial fibrillation (AF) is associated with fibrosis that slows electrical conduction and causes perpetuation of the arrhythmia. The molecular characterization of AF pathophysiology may provide novel therapeutic options. This study was designed to elucidate profibrotic signaling and myofibroblast activation in a porcine model of atrial tachypacing-induced AF and reduced left ventricular function. MATERIALS AND METHODS: Ten domestic pigs were randomized to sinus rhythm (SR) or AF groups...
July 15, 2017: Life Sciences
https://www.readbyqxmd.com/read/28486700/dysregulation-of-the-adam17-notch-signalling-pathways-in-endometriosis-from-oxidative-stress-to-fibrosis
#10
Iñaki González-Foruria, Pietro Santulli, Sandrine Chouzenoux, Francisco Carmona, Charles Chapron, Frédéric Batteux
STUDY QUESTION: Is oxidative stress associated with the A disintegrin and metalloproteases (ADAM) metallopeptidase domain 17 (ADAM17)/Notch signalling pathway and fibrosis in the development of endometriosis? SUMMARY ANSWER: Oxidative stress is correlated with hyperactivation of the ADAM17/Notch signalling pathway and a consequent increase in fibrosis in patients with endometriosis. WHAT IS KNOWN ALREADY: It is nowadays accepted that oxidative stress plays an important role in the onset and progression of endometriosis...
May 9, 2017: Molecular Human Reproduction
https://www.readbyqxmd.com/read/28469078/mir-21-is-associated-with-fibrosis-and-right-ventricular-failure
#11
Sushma Reddy, Dong-Qing Hu, Mingming Zhao, Eddie Blay, Nefthi Sandeep, Sang-Ging Ong, Gwanghyun Jung, Kristina B Kooiker, Michael Coronado, Giovanni Fajardo, Daniel Bernstein
Combined pulmonary insufficiency (PI) and stenosis (PS) is a common long-term sequela after repair of many forms of congenital heart disease, causing progressive right ventricular (RV) dilation and failure. Little is known of the mechanisms underlying this combination of preload and afterload stressors. We developed a murine model of PI and PS (PI+PS) to identify clinically relevant pathways and biomarkers of disease progression. Diastolic dysfunction was induced (restrictive RV filling, elevated RV end-diastolic pressures) at 1 month after generation of PI+PS and progressed to systolic dysfunction (decreased RV shortening) by 3 months...
May 4, 2017: JCI Insight
https://www.readbyqxmd.com/read/28469072/uncoupling-of-the-profibrotic-and-hemostatic-effects-of-thrombin-in-lung-fibrosis
#12
Barry S Shea, Clemens K Probst, Patricia L Brazee, Nicholas J Rotile, Francesco Blasi, Paul H Weinreb, Katharine E Black, David E Sosnovik, Elizabeth M Van Cott, Shelia M Violette, Peter Caravan, Andrew M Tager
Fibrotic lung disease, most notably idiopathic pulmonary fibrosis (IPF), is thought to result from aberrant wound-healing responses to repetitive lung injury. Increased vascular permeability is a cardinal response to tissue injury, but whether it is mechanistically linked to lung fibrosis is unknown. We previously described a model in which exaggeration of vascular leak after lung injury shifts the outcome of wound-healing responses from normal repair to pathological fibrosis. Here we report that the fibrosis produced in this model is highly dependent on thrombin activity and its downstream signaling pathways...
May 4, 2017: JCI Insight
https://www.readbyqxmd.com/read/28424623/notch-signaling-in-ischemic-damage-and-fibrosis-evidence-and-clues-from-the-heart
#13
REVIEW
Silvia Nistri, Chiara Sassoli, Daniele Bani
Notch signaling is a major intercellular coordination mechanism highly conserved throughout evolution. In vertebrates, Notch signaling is physiologically involved in embryo development, including mesenchymal cell commitment, formation of heart tissues and angiogenesis. In post-natal life, Notch signaling is maintained as a key mechanism of cell-cell communication and its dysregulations have been found in pathological conditions such as ischemic and fibrotic diseases. In the heart, Notch takes part in the protective response to ischemia, being involved in pre- and post-conditioning, reduction of reperfusion-induced oxidative stress and myocardial damage, and cardiomyogenesis...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28409352/epithelial-to-mesenchymal-transition-emt-and-endothelial-to-mesenchymal-transition-endmt-role-and-implications-in-kidney-fibrosis
#14
Ana S Cruz-Solbes, Keith Youker
Tubulointerstitial injury is one of the hallmarks of renal disease. In particular, interstitial fibrosis has a prominent role in the development and progression of kidney injury. Collagen-producing fibroblasts are responsible for the ECM deposition. However, the origin of those activated fibroblasts is not clear. This chapter will discuss in detail the concept of epithelial to mesenchymal transition (EMT) and endothelial to mesenchymal transition (EndMT) in the context of fibrosis and kidney disease. In short, EMT and EndMT involve a change in cell shape, loss of polarity and increased motility associated with increased collagen production...
2017: Results and Problems in Cell Differentiation
https://www.readbyqxmd.com/read/28405618/efficacy-of-alk5-inhibition-in-myelofibrosis
#15
Lanzhu Yue, Matthias Bartenstein, Wanke Zhao, Wanting Tina Ho, Ying Han, Cem Murdun, Adam W Mailloux, Ling Zhang, Xuefeng Wang, Anjali Budhathoki, Kith Pradhan, Franck Rapaport, Huaquan Wang, Zonghong Shao, Xiubao Ren, Ulrich Steidl, Ross L Levine, Zhizhuang Joe Zhao, Amit Verma, Pearlie K Epling-Burnette
Myelofibrosis (MF) is a bone marrow disorder characterized by clonal myeloproliferation, aberrant cytokine production, extramedullary hematopoiesis, and bone marrow fibrosis. Although somatic mutations in JAK2, MPL, and CALR have been identified in the pathogenesis of these diseases, inhibitors of the Jak2 pathway have not demonstrated efficacy in ameliorating MF in patients. TGF-β family members are profibrotic cytokines and we observed significant TGF-β1 isoform overexpression in a large cohort of primary MF patient samples...
April 6, 2017: JCI Insight
https://www.readbyqxmd.com/read/28396839/inhibition-of-the-tgf%C3%AE-signalling-pathway-by-cgmp-and-cgmp-dependent-kinase-i-in-renal-fibrosis
#16
Elisabeth Schinner, Veronika Wetzl, Andrea Schramm, Frieder Kees, Peter Sandner, Johannes-Peter Stasch, Franz Hofmann, Jens Schlossmann
Agents that enhance production of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) ameliorate the progression of renal fibrosis. However, the molecular mechanism of this process is not fully understood. We hypothesize that the antifibrotic effects of cGMP and cGMP-dependent kinase I (cGKI) are mediated via regulation of the TGFβ signalling pathway, both via ERK and the Smad-dependent route. Kidney fibrosis was induced by unilateral ureter obstruction (UUO) in wild-type and cGKI-deficient (cGKI-KO) mice...
April 2017: FEBS Open Bio
https://www.readbyqxmd.com/read/28387853/cxcl8-antagonist-improves-diabetic-nephropathy-in-male-mice-with-diabetes-and-attenuates-high-glucose-induced-mesangial-injury
#17
Siyuan Cui, Yujie Zhu, Jianling Du, Muhammad Noman Khan, Bing Wang, Jing Wei, Jya-Wei Cheng, John R Gordon, Yutian Mu, Fang Li
Inflammation is recognized as a crucial contribution to diabetic nephropathy (DN). CXCL8 binds to its CXC chemokine receptors (CXCR1 and CXCR2) for recruiting neutrophil infiltration and initiates tissue inflammation. Therefore, we explored the effect of CXCR1 and CXCR2 inhibition on DN. This was achieved by CXCL8(3-72)K11R/G31P (G31P), an antagonist of CXCL8 that has exhibited therapeutic efficacy in inflammatory diseases and malignancies. In this study, we found that renal leukocyte accumulation and rapid increases of CXCL8 occurred in high-fat diet/streptozocin-induced diabetic mice...
June 1, 2017: Endocrinology
https://www.readbyqxmd.com/read/28382387/high-soluble-endoglin-levels-do-not-induce-changes-in-structural-parameters-of-mouse-heart
#18
Jana Rathouska, Petra Fikrova, Alena Mrkvicova, Katerina Blazickova, Michala Varejckova, Eva Dolezelova, Ivana Nemeckova, Barbora Vitverova, Lenka Peslova, Eunate Gallardo-Vara, Miguel Pericacho, Petr Nachtigal
A soluble form of endoglin (sEng) released into the circulation was suggested to be a direct inducer of endothelial dysfunction, inflammation and contributed to the development of hypertension by interfering with TGF-β signaling in cardiovascular pathologies. In the present study, we assessed the hypothesis that high sEng level-induced hypertension via a possible sEng interference with TGF-β signaling pathways may result in inflammatory, structural or fibrotic changes in hearts of Sol-Eng+ mice (mice with high levels of soluble endoglin) fed either chow or high-fat diet...
April 5, 2017: Heart and Vessels
https://www.readbyqxmd.com/read/28363295/biological-principles-of-scar-and-contracture
#19
REVIEW
Peter O Kwan, Edward E Tredget
Hypertrophic scar and contracture in burn patients is a complex process. Contributing factors include critical injury depth and activation of key cell subpopulations, including deep dermal fibroblasts, myofibroblasts, fibrocytes, and T-helper cells, which cause scarring rather than regeneration. These cells influence each other via cellular profibrotic and antifibrotic signals, which help to determine the outcome. These cells also both modify and interact with extracellular matrix of the wound, ultimately forming hypertrophic scar...
May 2017: Hand Clinics
https://www.readbyqxmd.com/read/28358366/forkhead-box-a3-attenuated-the-progression-of-fibrosis-in-a-rat-model-of-biliary-atresia
#20
Rui Dong, Yifan Yang, Zhen Shen, Chao Zheng, Zhu Jin, Yanlei Huang, Zhien Zhang, Shan Zheng, Gong Chen
Biliary atresia is a rare, devastating disease of infants where a fibroinflammatory process destroys the bile ducts, leading to fibrosis and biliary cirrhosis, and death if untreated. The cause and pathogenesis remain largely unknown. We tried to investigate factors involved in biliary atresia, especially forkhead box A3 (Foxa3), which might exert a role in the treatment of liver disease. We used RNA sequencing to sequence the whole transcriptomes of livers from six biliary atresia and six choledochal cysts patients...
March 30, 2017: Cell Death & Disease
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