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Cardiac fibroblast

Alejandra Garate-Carrillo, Israel Ramirez
Mouse cardiac fibroblasts have been widely used as an in vitro model for studying fundamental biological processes and mechanisms underlying cardiac pathologies, as well as identifying potential therapeutic targets. Cardiac FBs are relatively easy to culture in a dish and can be manipulated using molecular and pharmacological tools. Because FBs rapidly decrease cell cycle division and proliferative rate after birth, they are prone to phenotypic changes and senescence in cell culture soon after a few passages...
2018: Methods in Molecular Biology
Eva Skiöldebrand, Anna Thorfve, Ulrika Björklund, Pegah Johansson, Ruth Wickelgren, Anders Lindahl, Elisabeth Hansson
Chondrocytes are effectively involved in the pathophysiological processes of inflammation in joints. They form cellular processes in the superficial layer of the articular cartilage and form gap junction coupled syncytium to facilitate cell-to-cell communication. However, very little is known about their physiological cellular identity and communication. The aim with the present work is to evaluate the physiological behavior after stimulation with the inflammatory inducers interleukin-1β and lipopolysaccharide...
January 2018: Heliyon
Marcello Ceci, Claudia Carlantoni, Maria Azzurra Missinato, Davide Bonvissuto, Bruna Di Giacomo, Riccardo Contu, Nicla Romano
Zebrafish could be an interesting translational model to understand and improve the post-infarction trial and possible regeneration in humans. The adult zebrafish is able to regenerate efficiently after resecting nearly 20% of the ventricular apex. This process requires the concert activation of the epicardium and endocardium, as well as trans-differentiation of pre-existing cardiomyocytes that together replace the lost tissue. The molecular mechanisms involved in this activation process are not completely clarified...
2018: Cell Death Discovery
Keith G Avin, Julian A Vallejo, Neal X Chen, Kun Wang, Chad D Touchberry, Marco Brotto, Sarah L Dallas, Sharon M Moe, Michael J Wacker
Skeletal muscle dysfunction accompanies the clinical disorders of chronic kidney disease (CKD) and hereditary hypophosphatemic rickets. In both disorders fibroblast growth factor 23 (FGF23), a bone-derived hormone regulating phosphate and vitamin D metabolism, becomes chronically elevated. FGF23 has been shown to play a direct role in cardiac muscle dysfunction; however, it is unknown whether FGF23 signaling can also directly induce skeletal muscle dysfunction. We found expression of potential FGF23 receptors ( Fgfr1-4) and α-Klotho in muscles of two animal models (CD-1 and Cy/+ rat, a naturally occurring rat model of Chronic Kidney Disease-Mineral Bone Disorder) as well as C2 C12 myoblasts and myotubes...
March 20, 2018: American Journal of Physiology. Endocrinology and Metabolism
Ge Li-Sha, Liu Li, Zhou De-Pu, Shi Zhe-Wei, Gu Xiaohong, Chen Guang-Yi, Li Jia, Lin Jia-Feng, Chu Maoping, Li Yue-Chun
This study was designed to explore the effects of ivabradine on cardiomyocyte apoptosis in a murine model of chronic viral myocarditis (CVMC). Mice were inoculated intraperitoneally with Coxsackievirus B3 at days 1, 14, and 28, respectively. On day 42, the mice were gavaged with ivabradine for 30 days until the 72nd day. The heart of infected mice was dilated and a large number of interstitial fibroblasts infiltrated into the myocardium on day 42. Compared with the untreated CVMC mice, mice treated with ivabradine showed a significant reduction in heart rate and less impairment of left ventricular function on day 72...
2018: Frontiers in Pharmacology
J Montag, B Petersen, A K Flögel, E Becker, A Lucas-Hahn, G J Cost, C Mühlfeld, T Kraft, H Niemann, B Brenner
Familial Hypertrophic Cardiomyopathy (HCM) is the most common inherited cardiac disease. About 30% of the patients are heterozygous for mutations in the MYH7 gene encoding the ß-myosin heavy chain (MyHC). Hallmarks of HCM are cardiomyocyte disarray and hypertrophy of the left ventricle, the symptoms range from slight arrhythmias to sudden cardiac death or heart failure. To gain insight into the underlying mechanisms of the diseases' etiology we aimed to generate genome edited pigs with an HCM-mutation. We used TALEN-mediated genome editing and successfully introduced the HCM-point mutation R723G into the MYH7 gene of porcine fibroblasts and subsequently cloned pigs that were heterozygous for the HCM-mutation R723G...
March 19, 2018: Scientific Reports
Nikolaos G Frangogiannis
Inflammation plays a crucial role in cardiac repair, but may also extend ischemic injury and contribute to post-infarction remodeling. This review manuscript discusses recent advances in our understanding of the cell biology of the post-infarction inflammatory response. Recently published studies demonstrated that the functional repertoire of inflammatory and reparative cells may extend beyond the roles suggested by traditional teachings. Neutrophils may play an important role in cardiac repair by driving macrophages toward a reparative phenotype...
February 2018: Current Opinion in Physiology
Zhiwei Wang, Jie Zhang, Guangpu Fan, Hui Zhao, Xu Wang, Jing Zhang, Peide Zhang, Wei Wang
We developed a new method, SUT (Scheme Update on tissue Transparency), to view cardiac microstructures and unveil the molecular changes underlying cardiac diseases. SUT is an effective method to clear whole-hearts from different species. Over the course of 4 - 6 days we obtained transparent whole-layer left ventricular tissues from mice with only an approximate 1% protein loss. In addition, EAL (Electrophoretic Antibody Labeling) was used to achieve fast antibody labeling by electric force, which significantly reduced antibody incubation time from days to hours...
February 1, 2018: Biomedical Optics Express
Ayako Uchinaka, Maho Yoshida, Kiyoka Tanaka, Yoshinosuke Hamada, Seiji Mori, Yoshitaka Maeno, Shigeru Miyagawa, Yoshiki Sawa, Kohzo Nagata, Hirofumi Yamamoto, Naomasa Kawaguchi
OBJECTIVE: Left ventricular (LV) remodeling alters the contractile and relaxation properties and induces myocardial stiffness. As LV remodeling progresses, the amount of collagen type III (Col3) is gradually decreased, being replaced by collagen type I (Col1). We evaluated whether Col3 overexpression improved cardiac function and remodeling in a rat with ischemic cardiomyopathy (ICM). We also investigated the functional motif and mechanism of thrombin-cleaved N-terminal osteopontin (N-OPN) on cardiac remodeling...
February 21, 2018: Journal of Thoracic and Cardiovascular Surgery
Chengliang Zhang, Yanfeng Zhang, Hong Zhu, Jiajia Hu, Zhongshang Xie
Cardiac fibrosis is associated with diverse heart diseases. In response to different pathological irritants, cardiac fibroblasts may be induced to proliferate and differentiate into cardiac myofibroblasts, thus contributing to cardiac fibrosis. TGF-β signaling is implicated in the development of heart failure through the induction of cardiac fibrosis. C-Ski, an inhibitory regulator of TGF-β signaling, has been reported to suppress TGF-β1-induced human cardiac fibroblasts' proliferation and ECM protein increase; however, the underlying molecular mechanism needs further investigation...
March 15, 2018: Cellular Signalling
Shinako Masuda, Katsuhisa Matsuura, Tatsuya Shimizu
Fibroblasts not only play key roles under physiological and pathological conditions in various tissues and organs including the heart but also are indispensable for fabricating bioengineered cardiac tissues and their functions through cell-cell interactions. Because tissue functions and cells surrounding fibroblasts in vivo are different among tissues, the properties of fibroblasts might be different according to their tissue origin. Understanding the molecular mechanisms of fibroblasts may lead to fabrication of bioengineered tissues close to biological tissues...
March 2, 2018: Biomaterials
Ibrahim El-Battrawy, Zhihan Zhao, Huan Lan, Xin Li, Gökhan Yücel, Siegfried Lang, Katherine Sattler, Jan-Dierk Schünemann, Wolfram-Hubertus Zimmermann, Lukas Cyganek, Jochen Utikal, Thomas Wieland, Karen Bieback, Ralf Bauer, Antonius Ratte, Regina Pribe-Wolferts, Kleopatra Rapti, Daniel Nowak, Janina Wittig, Dierk Thomas, Patrick Most, Hugo A Katus, Ursula Ravens, Constanze Schmidt, Martin Borggrefe, Xiao-Bo Zhou, Oliver J Müller, Ibrahim Akin
BACKGROUND: Limb-Girdle muscular dystrophies (LGMD) are a heritable group of genetically determined disorders with a primary involvement of the pelvic or shoulder girdle musculature with partially cardiac manifestation, such as dilated cardiomyopathy (DCM) and life-threatening tachyarrhythmia. We report here that human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes from a patient with LGMD2I and DCM associated with recurrent ventricular tachycardia displayed ion channel dysfunction and abnormality of calcium homeostasis...
March 2018: Circ Genom Precis Med
Jaime Ibarrola, Rafael Sádaba, Amaia Garcia-Peña, Vanessa Arrieta, Ernesto Martinez-Martinez, Virginia Alvarez, Amaya Fernández-Celis, Alicia Gainza, Enrique Santamaría, Joaquin Fernández-Irigoyen, Victoria Cachofeiro, Renaud Fay, Patrick Rossignol, Natalia López-Andrés
AIMS: Galectin-3 (Gal-3), a β-galactoside-binding lectin involved in cardiac inflammation and fibrosis, could regulate oxidative stress, although the mechanisms have not been elucidated. We herein investigated the changes in oxidative stress-related mediators induced by Gal-3 in human cardiac fibroblasts and in pathological animal and human models of cardiac diseases. RESULTS: Using quantitative proteomics and immunodetection approaches, we have identified that Gal-3 down-regulated fumarate hydratase (FH) in human cardiac fibroblasts...
May 1, 2018: International Journal of Cardiology
Robert D Johnson, Patrizia Camelliti
The heart is a complex organ composed of multiple cell types, including cardiomyocytes and different non-myocyte populations, all working closely together to determine the hearts properties and maintain normal cardiac function. Connexins are abundantly expressed proteins that form plasma membrane hemichannels and gap junctions between cells. Gap junctions are intracellular channels that allow for communication between cells, and in the heart they play a crucial role in cardiac conduction by coupling adjacent cardiomyocytes...
March 15, 2018: International Journal of Molecular Sciences
Irene Salamon, Gloria Saccani Jotti, Gianluigi Condorelli
PURPOSE OF REVIEW: In this review, we summarize new knowledge on long noncoding RNAs (lncRNAs) linked to cardiovascular disease, in particular to heart failure. RECENT FINDINGS: LncRNAs are dysregulated in specific developmental and pathological conditions and regulate critical responses to stress. LncRNAs are being recognized as molecules regulating myocardial remodeling during disease, participating for instance in the regulation of cardiomyocyte hypertrophy and function and fibroblast proliferation...
March 14, 2018: Current Opinion in Cardiology
Zhen-Guo Ma, Xin Zhang, Yu-Pei Yuan, Ya-Ge Jin, Ning Li, Chun-Yan Kong, Peng Song, Qi-Zhu Tang
T cell infiltration and the subsequently increased intracardial chronic inflammation play crucial roles in the development of cardiac hypertrophy and heart failure. A77 1726, the active metabolite of leflunomide, has been reported to have powerful anti-inflammatory and T cells-inhibiting properties. However, the effect of A77 1726 on cardiac hypertrophy remains completely unknown. Herein, we found that A77 1726 treatment attenuated pressure overload or angiotensin II-induced cardiac hypertrophy in vivo, as well as agonist-induced hypertrophic response of cardiomyocytes in vitro...
March 14, 2018: Clinical Science (1979-)
Ying-Chun Shih, Chao-Ling Chen, Yan Zhang, Rebecca L Mellor, Evelyn M Kanter, Yun Fang, Hua-Chi Wang, Chen-Ting Hung, Jing-Yi Nong, Hui-Ju Chen, Tzu-Han Lee, Yi-Shuan Tseng, Chiung-Nien Chen, Chau-Chung Wu, Shuei-Liong Lin, Kathryn A Yamada, Jeanne M Nerbonne, Kai-Chien Yang
<u>Rationale:</u> Cardiac fibrosis plays a critical role in the pathogenesis of heart failure (HF). Excessive accumulation of extracellular matrix (ECM) resulting from cardiac fibrosis impairs cardiac contractile function and increases arrhythmogenicity. Current treatment options for cardiac fibrosis, however, are limited and there is a clear need to identify novel mediators of cardiac fibrosis to facilitate the development of better therapeutics. Exploiting co-expression gene network analysis on RNA sequencing data from failing human heart, we identified thioredoxin domain containing 5 (TXNDC5), a cardiac fibroblast (CF)-enriched endoplasmic reticulum (ER) protein, as a potential novel mediator of cardiac fibrosis and we completed experiments to test this hypothesis directly...
March 13, 2018: Circulation Research
Hyemi Bae, Jeongyoon Choi, Young-Won Kim, Donghee Lee, Jung-Ha Kim, Jae-Hong Ko, Hyoweon Bang, Taeho Kim, Inja Lim
This study investigated the expression of voltage-gated K⁺ (KV ) channels in human cardiac fibroblasts (HCFs), and the effect of nitric oxide (NO) on the KV currents, and the underlying phosphorylation mechanisms. In reverse transcription polymerase chain reaction, two types of KV channels were detected in HCFs: delayed rectifier K⁺ channel and transient outward K⁺ channel. In whole-cell patch-clamp technique, delayed rectifier K⁺ current (IK ) exhibited fast activation and slow inactivation, while transient outward K⁺ current (Ito ) showed fast activation and inactivation kinetics...
March 12, 2018: International Journal of Molecular Sciences
Jonathan James Weldrick, Mohammad Abdul-Ghani, Lynn A Megeney, Patrick G Burgon
The capacity to isolate and study single cardiomyocytes has dramatically enhanced our understanding of the fundamental mechanisms of the heart. Currently, two primary methods for the isolation of cardiomyocytes are employed; i) The neonatal isolation protocol and, ii) the Langendorff isolation method. A major limiting feature of both procedures is the inability to isolate cardiomyocytes between 3 days and 3 weeks post-birth. Herein we report the establishment and validation of a new method for the rapid and efficient isolation of mouse cardiomyocytes, regardless of age...
March 13, 2018: Canadian Journal of Physiology and Pharmacology
Juan Xu, Haiqing Wu, Songwen Chen, Baozhen Qi, Genqing Zhou, Lidong Cai, Liqun Zhao, Yong Wei, Shaowen Liu
Atrial fibrosis serves as an important contributor to atrial fibrillation (AF). Recent data have suggested that microRNA-30c (miR-30c) is involved in fibrotic remodelling and cancer development, but the specific role of miR-30c in atrial fibrosis remains unclear. The purpose of this study was to investigate the role of miR-30c in atrial fibrosis and its underlying mechanisms through in vivo and in vitro experiments. Our results indicate that miR-30c is significantly down-regulated in the rat abdominal aortic constriction (AAC) model and in the cellular model of fibrosis induced by transforming growth factor-β1 (TGF-β1)...
March 13, 2018: Journal of Cellular and Molecular Medicine
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