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https://www.readbyqxmd.com/read/28924605/pai-1-is-a-critical-regulator-of-fgf23-homeostasis
#1
Mesut Eren, Aaron T Place, Paul M Thomas, Panagiotis Flevaris, Toshio Miyata, Douglas E Vaughan
Elevated levels of fibroblast growth factor 23 (FGF23), a bone-derived phosphaturic hormone, are associated with a number of pathologic conditions including chronic kidney disease, cardiac hypertrophy, and congestive heart failure. Currently, there are no specific treatments available to lower plasma FGF23 levels. We have recently reported that genetic plasminogen activator inhibitor-1 (PAI-1) deficiency provided a significant reduction in circulating FGF23 levels while simultaneously prolonging the life span of Klotho-deficient mice...
September 2017: Science Advances
https://www.readbyqxmd.com/read/28923627/associations-among-cardio-ankle-vascular-index-carotid-intima-media-thickness-and-fibroblast-growth-factor-21-levels-in-kidney-transplant-patients
#2
T Trakarnvanich, S Prommool, S Kurathong, T Teepprasan, Y Wang
BACKGROUND: Cardiovascular disease is the major cause of death in patients with chronic kidney disease, even after renal transplantation. Cardio-ankle vascular index (CAVI) provides an indicator of arterial stiffness, whereas fibroblast growth factor-21 (FGF-21) levels may provide a biomarker for atherosclerotic disease. We investigated the association between CAVI and FGF-21 and their relationships to carotid intima-media thickness (IMT) and other cardiovascular risk factors. METHODS: This study included 90 renal transplant patients...
October 2017: Transplantation Proceedings
https://www.readbyqxmd.com/read/28923350/ascorbate-starvation-alters-endoplasmic-reticulum-resident-enzymes-in-cardiac-fibroblasts-priming-them-for-increased-procollagen-secretion
#3
Randy T Cowling, Joong Il Park, Ayodeji E Sotimehin, Barry H Greenberg
Since ascorbate is unnecessary for cell growth and survival, cardiac fibroblasts are routinely cultured without it. However, ascorbate is necessary for optimal collagen synthesis, so we hypothesized that its presence would influence cell phenotype. Cardiac fibroblasts cultured without ascorbate had increased intracellular levels of procollagens, with procollagen α1(III) showing the largest accumulation. Endoplasmic reticulum (ER)-resident proteins that are known to bind single-stranded procollagens were also elevated...
September 15, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28920705/human-endothelial-progenitor-cell-derived-exosomes-increase-proliferation-and-angiogenesis-in-cardiac-fibroblasts-by-promoting-the-mesenchymal-endothelial-transition-and-reducing-high-mobility-group-box-1-protein-b1-expression
#4
Xiao Ke, Dahao Yang, Jiawen Liang, Xing Wang, Shaoyun Wu, Xiaoqing Wang, Chengheng Hu
Myocardial fibrosis is a characteristic feature of cardiomyopathies. However, no effective strategies to attenuate cardiac fibrosis are currently available. Late-stage endothelial progenitor cells (EPCs) are precursors of endothelial cells (ECs) that repair the heart through a paracrine mechanism. In the present study, we tested whether EPC-derived exosomes regulate the differentiation of fibroblasts into ECs. We isolated late-stage EPCs from human peripheral blood (PB) and used immunofluorescence and flow cytometry to confirm their identity...
September 18, 2017: DNA and Cell Biology
https://www.readbyqxmd.com/read/28913553/dual-inhibition-of-cathepsin-g-and-chymase-reduces-myocyte-death-and-improves-cardiac-remodeling-after-myocardial-ischemia-reperfusion-injury
#5
Bahman Hooshdaran, Mikhail A Kolpakov, Xinji Guo, Sonni A Miller, Tao Wang, Douglas G Tilley, Khadija Rafiq, Abdelkarim Sabri
Early reperfusion of ischemic cardiac tissue increases inflammatory cell infiltration which contributes to cardiomyocyte death and loss of cardiac function, referred to as ischemia/reperfusion (IR) injury. Neutrophil- and mast cell-derived proteases, cathepsin G (Cat.G) and chymase, are released early after IR, but their function is complicated by potentially redundant actions and targets. This study investigated whether a dual inhibition of Cat.G and chymase influences cardiomyocyte injury and wound healing after experimental IR in mice...
September 14, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28910790/the-cardiovascular-burden-in-end-stage-renal-disease
#6
Mario Cozzolino, Andrea Galassi, Francesca Pivari, Paola Ciceri, Ferruccio Conte
It is well documented that chronic kidney disease patients have an extremely high risk of developing cardiovascular (CV) disease (CVD) compared to the general population. Declining renal function itself represents a continuum of CV risk, and in those individuals who survive to reach end-stage renal disease, the risk of suffering a cardiac event is uncomfortably and unacceptably high. Several pathophysiological pathways have been suggested to account for this, including endothelial dysfunction, dyslipidemia, inflammation, left ventricular hypertrophy, troponins, phosphate, vitamin D, fibroblast growth factor-23, and NT-proBNP...
2017: Contributions to Nephrology
https://www.readbyqxmd.com/read/28910144/ask1-inhibition-halts-disease-progression-in-preclinical-models-of-pulmonary-arterial-hypertension
#7
Grant R Budas, Mario Boehm, Baktybek Kojonazarov, Gayathri Viswanathan, Xia Tian, Swathi Veeroju, Tatyana Novoyatleva, Friedrich Grimminger, Ford Hinojosa-Kirschenbaum, Hossein A Ghofrani, Norbert Weissmann, Werner Seeger, John T Liles, Ralph T Schermuly
RATIONALE Progression of pulmonary arterial hypertension (PAH) is associated with pathologic remodeling of the pulmonary vasculature and the right ventricle (RV). Oxidative stress drives the remodeling process through activation of mitogenactivated protein kinases (MAPKs) which stimulate apoptosis, inflammation and fibrosis. OBJECTIVES We investigated whether pharmacological inhibition of the redoxsensitive apical MAPK Apoptosis Signal-Regulating Kinase 1 (ASK1) can halt the progression of pulmonary vascular and RV remodeling...
September 14, 2017: American Journal of Respiratory and Critical Care Medicine
https://www.readbyqxmd.com/read/28905939/curcumin-administration-suppresses-collagen-synthesis-in-the-hearts-of-rats-with-experimental-diabetes
#8
Shuang Guo, Xiang-Wen Meng, Xiao-Song Yang, Xiu-Fen Liu, Chang-Han Ou-Yang, Chao Liu
Cardiac fibrosis is considered the initial change of diabetic cardiomyopathy (DCM). We have shown that curcumin alleviates collagen deposition in DCM, but the mechanism remains unknown. In this study we sought to investigate the effects of curcumin on cardiac fibrosis in vivo and in vitro and to elucidate the underlying mechanisms. Experimental diabetes was induced in rats by injection of low-dose streptozotocin (STZ) combined with high energy diet. The rats were orally treated with curcumin (300 mg·kg(-1)·d(-1)) for 16 weeks...
September 14, 2017: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/28900153/genetic-ablation-of-fgf23-or-klotho-does-not-modulate-experimental-heart-hypertrophy-induced-by-pressure-overload
#9
Svetlana Slavic, Kristopher Ford, Magalie Modert, Amarela Becirovic, Stephan Handschuh, Andreas Baierl, Nejla Katica, Ute Zeitz, Reinhold G Erben, Olena Andrukhova
Left ventricular hypertrophy (LVH) ultimately leads to heart failure in conditions of increased cardiac pre- or afterload. The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Using transverse aortic constriction (TAC) in gene-targeted mouse models, we examine the role of Fgf23 and Klotho in cardiac hypertrophy and dysfunction induced by pressure overload. TAC profoundly increases serum intact Fgf23 due to increased cardiac and bony Fgf23 transcription and downregulation of Fgf23 cleavage...
September 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28898996/the-expression-of-the-rare-caveolin-3-variant-t78m-alters-cardiac-ion-channels-function-and-membrane-excitability
#10
Giulia Campostrini, Mattia Bonzanni, Alessio Lissoni, Claudia Bazzini, Raffaella Milanesi, Elena Vezzoli, Maura Francolini, Mirko Baruscotti, Annalisa Bucchi, Ilaria Rivolta, Matteo Fantini, Stefano Severi, Riccardo Cappato, Lia Crotti, Peter J Schwartz, Dario DiFrancesco, Andrea Barbuti
Aims: Caveolinopathies are a family of genetic disorders arising from alterations of the caveolin-3 (cav-3) gene. The T78M cav-3 variant has been associated with both skeletal and cardiac muscle pathologies but its functional contribution, especially to cardiac diseases, is still controversial. Here, we evaluated the effect of the T78M cav-3 variant on cardiac ion channel function and membrane excitability. Methods and results: We transfected either the wild type (WT) or T78M cav-3 in caveolin-1 knock-out mouse embryonic fibroblasts and found by immunofluorescence and electron microscopy that both are expressed at the plasma membrane and form caveolae...
August 1, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28895644/relaxin-inhibits-cardiac-fibrosis-in-diabetic-rats-roles-of-protein-kinase-c%C3%AE
#11
Ping Wang, Meng Li, Lei Dong, Hui Chen, Wei Su, Yu-Peng Wang
Relaxin (Rlx) is known to antagonize diabetic cardiac fibrosis. However, its mechanism is poorly understood. Protein kinase Cδ (PKCδ) plays a crucial role in diabetic cardiomyopathy (DCM). This study explored the involvement of PKCδ in Rlx's capacity of suppressing cardiac fibrosis in a rat model of type 2 diabetes mellitus (DM). Type 2 DM of 8-week-old male Sprague-Dawley (SD) rats was induced by a high-fat diet and the injection of streptozocin (STZ, 40 mg/kg). Fourteen-week-old rats with DM and rats in control group which were pre-treated for 1 week with human recombinant relaxin (rhRlx, 30 μg/kg...
September 11, 2017: Experimental and Clinical Endocrinology & Diabetes
https://www.readbyqxmd.com/read/28895502/characterization-of-the-epicardial-adipose-tissue-in-decellularized-human-scaled-whole-hearts-implications-for-the-whole-heart-tissue-engineering
#12
Payam Akhyari, Fabian Oberle, Joern Huelsmann, Hans Heid, Stefan Lehr, Andreas Barbian, Sentaro Nakanishi, Hug Aubin, Alexander Jenke, Artur Lichtenberg
Whole-organ engineering is an innovative field of regenerative medicine with growing translational perspectives. Recent reports suggest the feasibility of decellularization and repopulation of entire human size hearts. However, little is known about the susceptibility of epicardial adipose tissue (EAT) to decellularization. Here, human size hearts of ovine donors were subjected to perfusion-based decellularization using detergent solutions. Upon basic histological evaluation and total DNA measurement myocardial regions prove largely decellularized while EAT demonstrated cellular remnants, further confirmed by transmission electron microscopy...
September 12, 2017: Tissue Engineering. Part A
https://www.readbyqxmd.com/read/28895052/the-effects-of-periostin-in-a-rat-model-of-isoproterenol-mediated-cardiotoxicity
#13
Mahmut Sözmen, Alparslan K Devrim, Yonca B Kabak, Tuba Devrim, Mert Sudagidan
Periostin is an extracellular matrix protein from fasciclin family, and it plays an important role in the cell adhesion, migration, and growth of the organism. Periostin prevents apoptosis while stimulating cardiomyocytes. The present study was designed to investigate cardioprotective effects of the recombinant murine periostin peptide administration in a rat model of isoproterenol (ISO)-induced myocardial injury. The experiment was performed on 84 adult male Sprague Dawley rats in 4 groups (n = 21): control group (1), periostin-treated group (2), ISO-treated group (3), and ISO + periostin-treated group (4)...
September 11, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28891814/fibroblast-specific-tgf-%C3%AE-smad2-3-signaling-underlies-cardiac-fibrosis
#14
Hadi Khalil, Onur Kanisicak, Vikram Prasad, Robert N Correll, Xing Fu, Tobias Schips, Ronald J Vagnozzi, Ruijie Liu, Thanh Huynh, Se-Jin Lee, Jason Karch, Jeffery D Molkentin
The master cytokine TGF-β mediates tissue fibrosis associated with inflammation and tissue injury. TGF-β induces fibroblast activation and differentiation into myofibroblasts that secrete extracellular matrix proteins. Canonical TGF-β signaling mobilizes Smad2 and Smad3 transcription factors that control fibrosis by promoting gene expression. However, the importance of TGF-β-Smad2/3 signaling in fibroblast-mediated cardiac fibrosis has not been directly evaluated in vivo. Here, we examined pressure overload-induced cardiac fibrosis in fibroblast- and myofibroblast-specific inducible Cre-expressing mouse lines with selective deletion of the TGF-β receptors Tgfbr1/2, Smad2, or Smad3...
September 11, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28888004/cardiomyocyte-coculture-on-layered-fibrous-scaffolds-assembled-from-micropatterned-electrospun-mats
#15
Yaowen Liu, Guisen Xu, Jiaojun Wei, Qiang Wu, Xiaohong Li
Challenges remain in engineering cardiac tissues with functional and morphological properties similar to those of native myocardium. In the current study, micropatterned fibrous mats are obtained by deposition of electrospun fibers on lithographic collectors to reproduce the anisotropic structure of myocardium, and carbon nanotubes are included in fibers to provide conductivities at the same level of cardiac muscles. The patterned mats are assembled layer-by-layer into patterned scaffolds for coculture of primary cardiomyocytes (CMs) with cardiac fibroblasts (CFs) and endothelial cells (ECs)...
December 1, 2017: Materials Science & Engineering. C, Materials for Biological Applications
https://www.readbyqxmd.com/read/28886967/class-i-hdacs-control-a-jip1-dependent-pathway-for-kinesin-microtubule-binding-in-cardiomyocytes
#16
Weston W Blakeslee, Ying-Hsi Lin, Matthew S Stratton, Philip D Tatman, Tianjing Hu, Bradley S Ferguson, Timothy A McKinsey
Class I histone deacetylase (HDAC) inhibitors block hypertrophy and fibrosis of the heart by suppressing pathological signaling and gene expression programs in cardiac myocytes and fibroblasts. The impact of HDAC inhibition in unstressed cardiac cells remains poorly understood. Here, we demonstrate that treatment of cultured cardiomyocytes with small molecule HDAC inhibitors leads to dramatic induction of c-Jun amino-terminal kinase (JNK)-interacting protein-1 (JIP1) mRNA and protein expression. In contrast to prior findings, elevated levels of endogenous JIP1 in cardiomyocytes failed to significantly alter JNK signaling or cardiomyocyte hypertrophy...
September 5, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28883544/global-fibroblast-activation-throughout-the-left-ventricle-but-localized-fibrosis-after-myocardial-infarction
#17
Chandan K Nagaraju, Eef Dries, Natasa Popovic, Abhishek A Singh, Peter Haemers, H Llewelyn Roderick, Piet Claus, Karin R Sipido, Ronald B Driesen
Fibroblast (Fb) differentiation and interstitial fibrosis contribute to cardiac remodeling and loss of function after myocardial infarction (MI). We investigated regional presence and regulation of fibrosis in a pig MI model. In vivo analysis of regional function and perfusion defined three regions: the scar, the myocardium adjacent to the scar (MIadjacent, reduced function, reduced perfusion reserve), and the remote myocardium (MIremote, minimal functional deficit, maintained perfusion). Interstitial and perivascular fibrosis, and increase of collagen type I, was only observed in the MIadjacent...
September 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28882883/cytoprotective-activated-protein-c-averts-nlrp3-inflammasome-induced-ischemia-reperfusion-injury-via-mtorc1-inhibition
#18
Sumra Nazir, Ihsan Gadi, Moh'd Mohanad Al-Dabet, Ahmed Elwakiel, Shrey Kohli, Sanchita Ghosh, Jayakumar Manoharan, Satish Ranjan, Fabian Bock, Ruediger C Braun-Dullaeus, Charles T Esmon, Tobias B Huber, Eric Camerer, Chris Dockendorff, John H Griffin, Berend Isermann, Khurrum Shahzad
Cytoprotection by activated protein C (aPC) following ischemia-reperfusion injury (IRI) is associated with apoptosis inhibition. However, IRI is hallmarked by inflammation and hence conceptually cell-death forms disjunct from immunologically silent apoptosis are more likely to be relevant. As pyroptosis, cell death resulting from inflammasome activation, is typically observed in IRI we speculated that aPC ameliorates IRI by inhibiting inflammasome activation. Here we analyzed the impact of aPC on inflammasome activity in myocardial and renal IRI...
September 7, 2017: Blood
https://www.readbyqxmd.com/read/28877982/non-canonical-regulation-of-insulin-mediated-erk-activation-by-phosphoinositide-3-kinase-%C3%AE
#19
Maradumane L Mohan, Arunachal Chatterjee, Swetha Ganapathy, Sromona Mukherjee, Sowmya Srikanthan, George P Jolly, Rohit S Anand, Sathyamangla V Naga Prasad
Classically Class IB Phosphoinositide 3-kinase (PI3Kγ) plays a role in ERK activation following G-protein coupled receptor (GPCR) activation. Knock-down of PI3Kγ unsuspectingly resulted in loss of ERK activation to receptor tyrosine kinase-agonists like epidermal growth factor or insulin. Mouse embryonic fibroblasts (MEFs) or primary adult cardiac fibroblasts isolated from PI3Kγ knock-out mice (PI3KγKO) showed loss in insulin-stimulated ERK activation. However, expression of kinase-dead PI3Kγ resulted in rescue of insulin-stimulated ERK activation...
September 6, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/28869726/-direct-reprogramming-from-fibroblasts-into-cardiamyocytes
#20
Zhengyan Xu, Ying Li
Cardiac regenerative therapy has attracted much attention as a novel approach for heart diseases. Direct reprogramming of fibroblasts into cardiomyocytes without going through a pluripotent stem cell stage would provide a promising source of cells for cell transplantation in future. This review summarizes the research methods and problems of direct reprogramming of fibroblasts into cardiomyocytes in vitro and in vivo, and forecasts the future development of this new strategy.
July 25, 2017: Sheng Wu Gong Cheng Xue Bao, Chinese Journal of Biotechnology
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