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Cardiac fibroblast

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https://www.readbyqxmd.com/read/29778534/fibroblast-growth-factor-19-protects-the-heart-from-oxidative-stress-induced-diabetic-cardiomyopathy-via-activation-of-ampk-nrf2-ho-1-pathway
#1
Xin Li, Di Wu, Ye Tian
Diabetes affects cardiac structure and function, where it leads to diabetic cardiomyopathy. Reactive oxygen species (ROS) produced by oxidative stress play an important role in the development of diabetic cardiomyopathy. Fibroblast growth factor (FGF) 19, an enterokine, is synthesized and released into the ileum. In the present study, we revealed that FGF19 induced an antioxidant response through stimulating the expression of nuclear erythroid factor 2 (NE-F2)-related factor 2 (Nrf2) and as well as reducing ROS production through the AMPK signaling pathway...
May 18, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29776409/calcitriol-downregulates-fibroblast-growth-factor-receptor-1-through-histone-deacetylase-activation-in-hl-1-atrial-myocytes
#2
Ting-Wei Lee, Ting-I Lee, Yung-Kuo Lin, Yu-Hsun Kao, Yi-Jen Chen
BACKGROUND: Fibroblast growth factor (FGF)-2 plays a crucial role in the pathophysiology of cardiovascular diseases (CVDs). FGF-2 was reported to induce cardiac hypertrophy through activation of FGF receptor 1 (FGFR1). Multiple laboratory findings indicate that calcitriol may be a potential treatment for CVDs. In this study, we attempted to investigate whether calcitriol regulates FGFR1 expression to modulate the effects of FGF-2 signaling in cardiac myocytes and explored the potential regulatory mechanism...
May 18, 2018: Journal of Biomedical Science
https://www.readbyqxmd.com/read/29775892/microrna-135a-inhibits-cardiac-fibrosis-induced-by-isoproterenol-via-trpm7-channel
#3
Yan Wu, Yonghui Liu, Yitong Pan, Chunxiao Lu, Haonan Xu, Xiaozhi Wang, Tingting Liu, Kai Feng, Yiqun Tang
BACKGROUND: Cardiac fibrosis is a crucial factor of heart failure. It has been reported that several microRNAs (miRNAs, miRs) were involved in cardiac fibrosis, however, the role and possible regulatory mechanism of microRNA-135a (miR-135a) in cardiac fibrosis have not been investigated. Here, we explored the regulation mechanism of miR-135a on cardiac fibrosis. METHODS AND RESULTS: In vitro, cardiac fibroblasts (CFs) from neonatal rats were treated by isoproterenol (ISO) at the final concentration of 10 μM for 24 h and miR-135a expression was decreased obviously...
May 15, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29775649/expression-and-function-of-tlr4-induced-b1r-bradykinin-receptor-on-cardiac-fibroblasts
#4
Claudia Muñoz-Rodríguez, Samuel Fernández, José Miguel Osorio, Francisco Olivares, Renatto Anfossi, Samir Bolivar, Claudio Humeres, Pía Boza, Raúl Vivar, Viviana Pardo-Jimenez, Karen E Hemmings, Neil A Turner, Guillermo Díaz-Araya
Cardiac fibroblasts (CF) are key cells for maintaining extracellular matrix (ECM) protein homeostasis in the heart, and for cardiac repair through CF-to-cardiac myofibroblast (CMF) differentiation. Additionally, CF play an important role in the inflammatory process after cardiac injury, and they express Toll like receptor 4 (TLR4), B1 and B2 bradykinin receptors (B1R and B2R) which are important in the inflammatory response. B1R and B2R are induced by proinflammatory cytokines and their activation by bradykinin (BK: B2R agonist) or des-arg-kallidin (DAKD: B1R agonist), induces NO and PGI2 production which is key for reducing collagen I levels...
May 15, 2018: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29775473/na-k-atpase-signaling-mediates-mir-29b-3p-regulation-and-cardiac-fibrosis-formation-in-mice-with-chronic-kidney-disease
#5
Christopher A Drummond, Xiaoming Fan, Steven T Haller, David J Kennedy, Jiang Liu, Jiang Tian
The Na/K-ATPase is an important membrane ion transporter and a signaling receptor that is essential for maintaining normal cell function. The current study examined the role of Na/K-ATPase signaling in regulating miR-29b-3p, an anti-fibrotic microRNA, in a mouse chronic kidney disease (CKD) model (5/6th partial nephrectomy or PNx). The results showed that CKD induced significant reduction of miR-29b-3p expression in the heart tissue by activation of Src and NFκB signaling in these animals. To demonstrate the role of Na/K-ATPase signaling, we also performed the PNx surgery on Na/K-ATPase α1 heterozygous (α1+/-) mice, which expresses ~40% less Na/K-ATPase α1 compared to their wild type littermates (WT) and exhibits deficiency in Na/K-ATPase signaling...
2018: PloS One
https://www.readbyqxmd.com/read/29774121/mir-33-promotes-myocardial-fibrosis-by-inhibiting-mmp16-and-stimulating-p38-mapk-signaling
#6
Zhen Chen, Hua-Sheng Ding, Xin Guo, Jing-Jing Shen, Di Fan, Yan Huang, Cong-Xin Huang
Myocardial fibrosis occurs in the late stages of many cardiovascular diseases, and appears to be stimulated by various microRNAs (miRNAs). We previously found that miR-33 may stimulate cardiac remodeling. Here, we examined the involvement of miR-33 in myocardial fibrosis. Proximal left coronary descending artery occlusion was performed in rat, and antagomiR-33a was injected. Primary cardiac fibroblasts were cultured and transfected with miR-33a mimics and inhibitors. miR-33a levels were increased in the rat after surgery, and collagen deposition and heart fibrosis were observed in vivo ...
April 24, 2018: Oncotarget
https://www.readbyqxmd.com/read/29773058/non-cardiomyocytes-in-heart-regeneration
#7
Jie Feng, Yandong Li, Yu Nie
Heart failure represents a challenging clinical and public health problem and is associated with significant morbidity and mortality. Mechanistically, loss of cardiomyocytes leads to decompensated ventricular remodeling, which eventually progressed to cardiac failure. Regenerative medicine aimed to supplement functional cardiomyocytes is supposedly a promising approach for the effective treatment of heart failure. Over the past decades, investigations on heart regeneration have revealed the regulating networks of cardiomyocyte proliferation...
May 17, 2018: Current Drug Targets
https://www.readbyqxmd.com/read/29772440/inhibition-of-nogo-b-promotes-cardiac-hypertrophy-via-endoplasmic-reticulum-stress
#8
Junli Li, Wenchao Wu, Yanguo Xin, Mingyue Zhao, Xiaojing Liu
AIMS: Nogo-B is a key endoplasmic reticulum (ER) protein that regulates ER stress signaling. However, its role in cardiac hypertrophy remains poorly understood. ER stress is interrelated with autophagy in the process of cardiac hypertrophy. Therefore, we aimed to test the hypothesis that both ER stress and autophagy signaling mediate the function of Nogo-B in cardiac hypertrophy. MAIN METHODS: Rat models of transverse aortic constriction (TAC), neonatal rat cardiomyocytes (NRCMs) stimulated with norepinephrine (Ne) and primary cardiac fibroblasts treated with transforming growth factor β1 (TGF-β1) were used in this study...
May 14, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29770125/fgf23-actions-on-target-tissues-with-and-without-klotho
#9
REVIEW
Beatrice Richter, Christian Faul
Fibroblast growth factor (FGF) 23 is a phosphaturic hormone whose physiologic actions on target tissues are mediated by FGF receptors (FGFR) and klotho, which functions as a co-receptor that increases the binding affinity of FGF23 for FGFRs. By stimulating FGFR/klotho complexes in the kidney and parathyroid gland, FGF23 reduces renal phosphate uptake and secretion of parathyroid hormone, respectively, thereby acting as a key regulator of phosphate metabolism. Recently, it has been shown that FGF23 can also target cell types that lack klotho...
2018: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/29760746/microrna-495-inhibits-the-high-glucose-induced-inflammation-differentiation-and-extracellular-matrix-accumulation-of-cardiac-fibroblasts-through-downregulation-of-nod1
#10
Xiaowei Wang, Haiying Jin, Shifeng Jiang, Yanlan Xu
Background: MicroRNAs (miRNAs) have physiological and pathophysiological functions that are involved in the regulation of cardiac fibrosis. This study aimed to investigate the effects of miR-495 on high glucose-induced cardiac fibrosis in human cardiac fibroblasts (CFs) and to establish the mechanism underlying these effects. Methods: Human CFs were transfected with an miR-495 inhibitor or mimic and incubated with high glucose. The levels of NOD1 and miR-495 were then determined via quantitative RT-PCR...
2018: Cellular & Molecular Biology Letters
https://www.readbyqxmd.com/read/29758552/downregulation-of-s100a4-alleviates-cardiac-fibrosis-via-wnt-%C3%AE-catenin-pathway-in-mice
#11
LiJun Qian, Jian Hong, YanMei Zhang, MengLin Zhu, XinChun Wang, YanJuan Zhang, Ming Chu, Jing Yao, Di Xu
BACKGROUND/AIMS: Cardiac fibrosis is a pathological change leading to cardiac remodeling during the progression of myocardial ischemic diseases, and its therapeutic strategy remains to be explored. S100A4, a calcium-binding protein, participates in fibrotic diseases with an unclear mechanism. This study aimed to investigate the role of S100A4 in cardiac fibrosis. METHODS: Cardiac fibroblasts from neonatal C57BL/6 mouse hearts were isolated and cultured. Myocardial infarction was induced by ligating the left anterior descending coronary artery (LAD)...
May 7, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29754768/mutations-in-ppcs-encoding-phosphopantothenoylcystein-synthetase-cause-autosomal-recessive-dilated-cardiomyopathy
#12
Arcangela Iuso, Marit Wiersma, Hans-Joachim Schüller, Ben Pode-Shakked, Dina Marek-Yagel, Mathias Grigat, Thomas Schwarzmayr, Riccardo Berutti, Bader Alhaddad, Bart Kanon, Nicola A Grzeschik, Jürgen G Okun, Zeev Perles, Yishay Salem, Ortal Barel, Amir Vardi, Marina Rubinshtein, Tal Tirosh, Gal Dubnov-Raz, Ana C Messias, Caterina Terrile, Iris Barshack, Alex Volkov, Camilla Avivi, Eran Eyal, Elisa Mastantuono, Muhamad Kumbar, Shachar Abudi, Matthias Braunisch, Tim M Strom, Thomas Meitinger, Georg F Hoffmann, Holger Prokisch, Tobias B Haack, Bianca J J M Brundel, Dorothea Haas, Ody C M Sibon, Yair Anikster
Coenzyme A (CoA) is an essential metabolic cofactor used by around 4% of cellular enzymes. Its role is to carry and transfer acetyl and acyl groups to other molecules. Cells can synthesize CoA de novo from vitamin B5 (pantothenate) through five consecutive enzymatic steps. Phosphopantothenoylcystein synthetase (PPCS) catalyzes the second step of the pathway during which phosphopantothenate reacts with ATP and cysteine to form phosphopantothenoylcystein. Inborn errors of CoA biosynthesis have been implicated in neurodegeneration with brain iron accumulation (NBIA), a group of rare neurological disorders characterized by accumulation of iron in the basal ganglia and progressive neurodegeneration...
May 3, 2018: American Journal of Human Genetics
https://www.readbyqxmd.com/read/29753686/pharmacological-inhibition-of-the-mitochondrial-nadph-oxidase-4-pkc%C3%AE-gal-3-pathway-reduces-left-ventricular-fibrosis-following-myocardial-infarction
#13
Maria Del Carmen Asensio-Lopez, Antonio Lax Perez, Maria Josefa Fernandez Del Palacio, Yassine Sassi, Roger J Hajjar, Domingo A Pascual-Figal
Although the initial reparative fibrosis after myocardial infarction (MI) is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental. Although metformin prevents adverse cardiac remodeling, as well as provides glycemic control, the underlying mechanisms remain poorly documented. This study describes the effect of mitochondrial NADPH oxidase 4 (mitoNox) and protein kinase C-alpha (PKCα) on the cardiac fibrosis and galectin 3 (Gal-3) expression...
April 23, 2018: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/29751971/cardiac-hypertrophy-elevates-serum-levels-of-fibroblast-growth-factor-23
#14
Isao Matsui, Tatsufumi Oka, Yasuo Kusunoki, Daisuke Mori, Nobuhiro Hashimoto, Ayumi Matsumoto, Karin Shimada, Satoshi Yamaguchi, Keiichi Kubota, Sayoko Yonemoto, Tomoaki Higo, Yusuke Sakaguchi, Yoshitsugu Takabatake, Takayuki Hamano, Yoshitaka Isaka
Several experimental studies have shown that fibroblast growth factor 23 (FGF23) induces left ventricular hypertrophy (LVH). However, the opposite directional relationship, namely a potential effect of LVH on FGF23, remains uncertain. Here we evaluated the effects of LVH on FGF23 using cardiomyocyte-specific calcineurin A transgenic mice. At six weeks, these mice showed severe LVH, with elevated levels of serum intact FGF23. FGF23 levels were elevated in cardiomyocytes, but not osteocytes, of the transgenic animals...
May 8, 2018: Kidney International
https://www.readbyqxmd.com/read/29750994/regulation-of-cardiac-fibroblast-mmp2-gene-expression-by-scleraxis
#15
Raghu S Nagalingam, Hamza A Safi, Danah S Al-Hattab, Rushita A Bagchi, Natalie M Landry, Ian M C Dixon, Jeffrey T Wigle, Michael P Czubryt
Remodeling of the cardiac extracellular matrix is responsible for a number of the detrimental effects on heart function that arise secondary to hypertension, diabetes and myocardial infarction. This remodeling consists both of an increase in new matrix protein synthesis, and an increase in the expression of matrix metalloproteinases (MMPs) that degrade existing matrix structures. Previous studies utilizing knockout mice have demonstrated clearly that MMP2 plays a pathogenic role during matrix remodeling, thus it is important to understand the mechanisms that regulate MMP2 gene expression...
May 8, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29748594/reassessing-endothelial-to-mesenchymal-transition-in-cardiovascular-diseases
#16
REVIEW
Yan Li, Kathy O Lui, Bin Zhou
Endothelial cells and mesenchymal cells are two different cell types with distinct morphologies, phenotypes, functions, and gene profiles. Accumulating evidence, notably from lineage-tracing studies, indicates that the two cell types convert into each other during cardiovascular development and pathogenesis. During heart development, endothelial cells transdifferentiate into mesenchymal cells in the endocardial cushion through endothelial-to-mesenchymal transition (EndoMT), a process that is critical for the formation of cardiac valves...
May 10, 2018: Nature Reviews. Cardiology
https://www.readbyqxmd.com/read/29743891/a-loss-of-function-screen-of-epigenetic-modifiers-and-splicing-factors-during-early-stage-of-cardiac-reprogramming
#17
Yang Zhou, Sahar Alimohamadi, Li Wang, Ziqing Liu, Joseph B Wall, Chaoying Yin, Jiandong Liu, Li Qian
Direct reprogramming of cardiac fibroblasts (CFs) to induced cardiomyocytes (iCMs) is a newly emerged promising approach for cardiac regeneration, disease modeling, and drug discovery. However, its potential has been drastically limited due to the low reprogramming efficiency and largely unknown underlying molecular mechanisms. We have previously screened and identified epigenetic factors related to histone modification during iCM reprogramming. Here, we used shRNAs targeting an additional battery of epigenetic factors involved in chromatin remodeling and RNA splicing factors to further identify inhibitors and facilitators of direct cardiac reprogramming...
2018: Stem Cells International
https://www.readbyqxmd.com/read/29735591/the-alchemist-s-nightmare-might-mesenchymal-stem-cells-that-are-recruited-to-repair-the-injured-heart-be-transformed-into-fibroblasts-rather-than-cardiomyocytes
#18
REVIEW
Milton Packer
The injection of mesenchymal stem cells into the injured myocardium to induce cardiac regeneration has yielded disappointing results, conceivably because cells with cardioreparative potential must be supplied for long periods of time to produce a salutary effect. Accordingly, investigators have devised ways of directing such cells to the heart on an ongoing basis: by enhancing the action of endogenous peptides that function as cardiac homing signals (eg, stromal cell-derived factor-1). Stromal cell-derived factor-1 is released during acute cardiac injury and heart failure, but it has a short half-life because of degradation by dipeptidyl peptidase-4...
May 8, 2018: Circulation
https://www.readbyqxmd.com/read/29735309/the-elevation-of-circulating-fibroblast-growth-factor-23-without-kidney-disease-does-not-increase-cardiovascular-disease-risk
#19
Eva-Maria Pastor-Arroyo, Nicole Gehring, Christiane Krudewig, Sarah Costantino, Carla Bettoni, Thomas Knöpfel, Sibylle Sabrautzki, Bettina Lorenz-Depiereux, Johanne Pastor, Tim M Strom, Martin Hrabě de Angelis, Giovanni G Camici, Francesco Paneni, Carsten A Wagner, Isabel Rubio-Aliaga
High circulating fibroblast growth factor 23 (FGF23) levels are probably a major risk factor for cardiovascular disease in chronic kidney disease. FGF23 interacts with the receptor FGFR4 in cardiomyocytes inducing left ventricular hypertrophy. Moreover, in the liver FGF23 via FGFR4 increases the risk of inflammation which is also found in chronic kidney disease. In contrast, X-linked hypophosphatemia is characterized by high FGF23 circulating levels due to loss of function mutations of the phosphate-regulating gene with homologies to an endopeptidase on the X chromosome (PHEX), but is not characterized by high cardiovascular morbidity...
May 5, 2018: Kidney International
https://www.readbyqxmd.com/read/29734659/s-phase-synchronization-facilitates-the-early-progression-of-induced-cardiomyocyte-reprogramming-through-enhanced-cell-cycle-exit
#20
Emre Bektik, Adrienne Dennis, Gary Pawlowski, Chen Zhou, Danielle Maleski, Satoru Takahashi, Kenneth R Laurita, Isabelle Deschênes, Ji-Dong Fu
Direct reprogramming of fibroblasts into induced cardiomyocytes (iCMs) holds a great promise for regenerative medicine and has been studied in several major directions. However, cell-cycle regulation, a fundamental biological process, has not been investigated during iCM-reprogramming. Here, our time-lapse imaging on iCMs, reprogrammed by Gata4, Mef2c, and Tbx5 (GMT) monocistronic retroviruses, revealed that iCM-reprogramming was majorly initiated at late-G1- or S-phase and nearly half of GMT-reprogrammed iCMs divided soon after reprogramming...
May 4, 2018: International Journal of Molecular Sciences
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