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https://www.readbyqxmd.com/read/28096472/myosin-vi-facilitates-connexin-43-gap-junction-accretion
#1
Bennett Waxse, Prabuddha Sengupta, Geoffrey G Hesketh, Jennifer Lippincott-Schwartz, Folma Buss
In this study, we demonstrate myosin VI enrichment at Cx43 gap junctions in heart tissue, primary cardiomyocytes and cell culture models. The loss of myosin VI via siRNA-mediated knock down or isolation of primary cardiac tissue and fibroblasts from the myosin VI-null mouse results in reduced GJ plaque size with a concomitant reduction in intercellular communication as shown by FRAP and a new method of selective calcein administration. Analysis of the molecular role of myosin VI in Cx43 trafficking indicates that myosin VI is dispensable in the delivery of Cx43 to the cell surface and connexon movement in the plasma membrane...
January 17, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28091697/heat-shock-transcription-factor-1-protects-against-pressure-overload-induced-cardiac-fibrosis-via-smad3
#2
Ning Zhou, Yong Ye, Xingxu Wang, Ben Ma, Jian Wu, Lei Li, Lin Wang, Dao Wen Wang, Yunzeng Zou
: Fibrotic cardiac muscle exhibits high stiffness and low compliance which are major risk factors of heart failure. Although heat shock transcription factor 1 (HSF1) was identified as an intrinsic cardioprotective factor, the role that HSF1 plays in cardiac fibrosis remains unclear. Our study aims to investigate the role of HSF1 in pressure overload-induced cardiac fibrosis and the underlying mechanism. HSF1 phosphorylation was significantly downregulated in transverse aortic constriction (TAC)-treated mouse hearts and mechanically stretched cardiac fibroblasts (cFBs)...
January 13, 2017: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/28087245/the-severe-clinical-phenotype-for-a-heterozygous-fabry-female-patient-correlates-to-the-methylation-of-non-mutated-allele-associated-with-chromosome-10q26-deletion-syndrome
#3
Mohammad Arif Hossain, Hiroko Yanagisawa, Takashi Miyajima, Chen Wu, Ayumi Takamura, Keiko Akiyama, Rina Itagaki, Kaoru Eto, Takeo Iwamoto, Takayuki Yokoi, Kenji Kurosawa, Hironao Numabe, Yoshikatsu Eto
Heterozygous Fabry females usually have an attenuated form of Fabry disease, causing them to be symptomatic; however, in rare cases, they can present with a severe phenotype. In this study, we report on a 37-year-old woman with acroparesthesia, a dysmorphic face, left ventricular hypertrophy, and intellectual disability. Her father had Fabry disease and died due to chronic renal and congestive cardiac failure. Her paternal uncle had chronic renal failure and intellectual disability, and her paternal aunt was affected with congestive cardiac failure...
January 7, 2017: Molecular Genetics and Metabolism
https://www.readbyqxmd.com/read/28079129/circrna_000203-enhances-the-expression-of-fibrosis-associated-genes-by-derepressing-targets-of-mir-26b-5p-col1a2-and-ctgf-in-cardiac-fibroblasts
#4
Chun-Mei Tang, Ming Zhang, Lei Huang, Zhi-Qin Hu, Jie-Ning Zhu, Zhen Xiao, Zhuo Zhang, Qiu-Xiong Lin, Xi-Long Zheng, Min -Yang, Shu-Lin Wu, Jian-Ding Cheng, Zhi-Xin Shan
Circular RNAs (circRNAs) participate in regulating gene expression in diverse biological and pathological processes. The present study aimed to investigate the mechanism underlying the modulation of circRNA_000203 on expressions of fibrosis-associated genes in cardiac fibroblasts. CircRNA_000203 was shown upregulated in the diabetic mouse myocardium and in Ang-II-induced mouse cardiac fibroblasts. Enforced-expression of circRNA_000203 could increase expressions of Col1a2, Col3a1 and α-SMA in mouse cardiac fibroblasts...
January 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28078246/the-effects-of-crocin-insulin-and-their-co-administration-on-the-heart-function-and-pathology-in-streptozotocin-induced-diabetic-rats
#5
Amir Abbas Farshid, Esmaeal Tamaddonfard, Masoumeh Moradi-Arzeloo, Navideh Mirzakhani
OBJECTIVE: Crocin is a saffron constituent with a potent anti-oxidant activity. The present study investigated the effects of crocin and insulin treatments (alone or in combination) on cardiac function and pathology in diabetic rats. MATERIALS AND METHODS: Diabetes was induced by intraperitoneal (i.p.) injection of streptozotocin (STZ, 50 mg/kg). Thereafter, crocin (5, 10 and 20 mg/kg, i.p.), subcutaneous (s.c.) injection of insulin (4 IU/kg) and their combination were administered for eight weeks...
November 2016: Avicenna Journal of Phytomedicine
https://www.readbyqxmd.com/read/28073835/mechanosensitive-transient-receptor-potential-vanilloid-4-regulates-dermatophagoides-farinae-induced-airway-remodeling-via-2-distinct-pathways-modulating-matrix-synthesis-and-degradation
#6
Farai Gombedza, Vinay Kondeti, Nosayba Al-Azzam, Stephanie Koppes, Ernest Duah, Prachi Patil, Madison Hexter, Daniel Phillips, Charles K Thodeti, Sailaja Paruchuri
Contributions of mechanical signals to airway remodeling during asthma are poorly understood. Transient receptor potential vanilloid 4 (TRPV4), a mechanosensitive ion channel, has been implicated in cardiac and pulmonary fibrosis; however, its role in asthma remains elusive. Employing a Dermatophagoides farinae-induced asthma model, we report here that TRPV4 knockout mice were protected from D. farinae-induced airway remodeling. Furthermore, lung fibroblasts that were isolated from TRPV4 knockout mice showed diminished differentiation potential compared with wild-type mice...
January 10, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28071742/core-transcription-factors-micrornas-and-small-molecules-drive-transdifferentiation-of-human-fibroblasts-towards-the-cardiac-cell-lineage
#7
Nicolas Christoforou, Syandan Chakraborty, Robert D Kirkton, Andrew F Adler, Russell C Addis, Kam W Leong
Transdifferentiation has been described as a novel method for converting human fibroblasts into induced cardiomyocyte-like cells. Such an approach can produce differentiated cells to study physiology or pathophysiology, examine drug interactions or toxicities, and engineer cardiac tissues. Here we describe the transdifferentiation of human dermal fibroblasts towards the cardiac cell lineage via the induced expression of transcription factors GATA4, TBX5, MEF2C, MYOCD, NKX2-5, and delivery of microRNAs miR-1 and miR-133a...
January 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28070494/pure-myopathy-with-enlarged-mitochondria-associated-to-a-new-mutation-in-mtnd2-gene
#8
Alice Zanolini, Ana Potic, Franco Carrara, Eleonora Lamantea, Daria Diodato, Flavia Blasevich, Silvia Marchet, Marina Mora, Francesco Pallotti, Lucia Morandi, Massimo Zeviani, Costanza Lamperti
To date, only few mutations in the mitochondrial DNA (mtDNA)-encoded ND2 subunit of Complex I have been reported, usually presenting a severe phenotype characterized by early onset encephalomyopathy and early death. In this report, we describe a new mutation in the MTND2 gene in a 21-year-old man with a mild myopathic phenotype characterized by exercise intolerance and increased plasma lactate at rest. Electromyography and brain NMR were normal, and no cardiac involvement was present. Muscle biopsy showed a massive presence of ragged red - COX-positive fibres, with enlarged mitochondria containing osmiophilic inclusions...
March 2017: Molecular Genetics and Metabolism Reports
https://www.readbyqxmd.com/read/28069985/high-throughput-imaging-of-cardiac-microtissues-for-the-assessment-of-cardiac-contraction-during-drug-discovery
#9
Amy Pointon, James Pilling, Thierry Dorval, Yinhai Wang, Caroline Archer, Christopher Pollard
Cardiotoxicity is a common cause of attrition in preclinical and clinical drug development. Current in vitro approaches have two main limitations, they either are limited to low throughput methods not amendable to drug discovery or lack the physiological responses to allow an integrated risk assessment. A human 3D cardiac microtissue containing human-induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs), cardiac endothelial cells and cardiac fibroblast were used to assess their suitability to detect drug induced changes in cardiomyocyte contraction...
November 15, 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28069640/sequence-variation-in-ppp1r13l-results-in-a-novel-form-of-cardio-cutaneous-syndrome
#10
Tzipora C Falik-Zaccai, Yiftah Barsheshet, Hanna Mandel, Meital Segev, Avraham Lorber, Shachaf Gelberg, Limor Kalfon, Shani Ben Haroush, Adel Shalata, Liat Gelernter-Yaniv, Sarah Chaim, Dorith Raviv Shay, Morad Khayat, Michal Werbner, Inbar Levi, Yishay Shoval, Galit Tal, Stavit Shalev, Eli Reuveni, Emily Avitan-Hersh, Eugene Vlodavsky, Liat Appl-Sarid, Dorit Goldsher, Reuven Bergman, Zvi Segal, Ora Bitterman-Deutsch, Orly Avni
Dilated cardiomyopathy (DCM) is a life-threatening disorder whose genetic basis is heterogeneous and mostly unknown. Five Arab Christian infants, aged 4-30 months from four families, were diagnosed with DCM associated with mild skin, teeth, and hair abnormalities. All passed away before age 3. A homozygous sequence variation creating a premature stop codon at PPP1R13L encoding the iASPP protein was identified in three infants and in the mother of the other two. Patients' fibroblasts and PPP1R13L-knocked down human fibroblasts presented higher expression levels of pro-inflammatory cytokine genes in response to lipopolysaccharide, as well as Ppp1r13l-knocked down murine cardiomyocytes and hearts of Ppp1r13l-deficient mice...
January 9, 2017: EMBO Molecular Medicine
https://www.readbyqxmd.com/read/28065931/intermedin-1-53-inhibits-myocardial-fibrosis-in-rats-by-down-regulating-transforming-growth-factor-%C3%AE
#11
Jian Fang, Jiangwei Luan, Gaohong Zhu, Chang Qi, Zhiyong Yang, Sheng Zhao, Bin Li, Xinzhong Zhang, Naipeng Guo, Xiaodong Li, Dandan Wang
BACKGROUND Myocardial fibrosis is the result of persistent anoxia and ischemic myocardial fibers caused by coronary atherosclerotic stenosis, which lead to heart failure, threatening the patient's life. This study aimed to explore the regulatory role of intermedin 1-53 (IMD1-53) in cardiac fibrosis using neonatal rat cardiac fibroblasts and a myocardial infarction (MI) rat model both in vitro and in vivo. MATERIAL AND METHODS The Western blot method was used to detect the protein expression of collagen I and collagen III in myocardial fibroblasts...
January 9, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28062938/mineral-metabolism-and-cardiovascular-disease-in-ckd
#12
REVIEW
Hideki Fujii, Nobuhiko Joki
The mineral bone disorder of CKD, called Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD), has a major role in the etiology and progression of cardiovascular disease in CKD patients. Since the main emphasis in CKD-MBD is on three categories (bone abnormalities, laboratory abnormalities, and vascular calcifications), we have routinely accepted ectopic cardiovascular calcifications as a central risk factor in the pathophysiology of CKD-MBD for cardiac events. However, recent compelling evidence suggests that some CKD-MBD-specific factors other than vascular calcification might contribute to the onset of cardiovascular disease...
January 6, 2017: Clinical and Experimental Nephrology
https://www.readbyqxmd.com/read/28057794/purinergic-signaling-in-the-cardiovascular-system
#13
REVIEW
Geoffrey Burnstock
There is nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory-motor nerves, as well as in intracardiac neurons. Centers in the brain control heart activities and vagal cardiovascular reflexes involve purines. Adenine nucleotides and nucleosides act on purinoceptors on cardiomyocytes, AV and SA nodes, cardiac fibroblasts, and coronary blood vessels. Vascular tone is controlled by a dual mechanism. ATP, released from perivascular sympathetic nerves, causes vasoconstriction largely via P2X1 receptors...
January 6, 2017: Circulation Research
https://www.readbyqxmd.com/read/28055991/role-of-mir-24-furin-and-transforming-growth-factor-%C3%AE-1-signal-pathway-in-fibrosis-after-cardiac-infarction
#14
Zhufeng Chen, Sumei Lu, Miao Xu, Peng Liu, Rui Ren, Wanshan Ma
BACKGROUND Cardiac fibrosis after primary infarction is a type of pathological phenomena as shown by increased collagen in myocardial cells. Transforming growth factor (TGF)-β1 is a critical factor participating in myocardial fibrosis. A previous study has shown the inhibitory role on TGF-β1 by microRNA-24 (miR-24) via targeting Furin. This study thus investigated the role of miR-24 and Furin/TGF-β1 in rat myocardial fibrosis. MATERIAL AND METHODS A total of 40 adult SD rats (both males and females) were prepared for myocardial infarction model by ligating the descending branch of left coronary artery after anesthesia...
January 5, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28052262/neil3-dependent-regulation-of-cardiac-fibroblast-proliferation-prevents-myocardial-rupture
#15
Maria B Olsen, Gunn A Hildrestrand, Katja Scheffler, Leif Erik Vinge, Katrine Alfsnes, Vuk Palibrk, Junbai Wang, Christine G Neurauter, Luisa Luna, Jostein Johansen, Jonas D S Øgaard, Ingrid K Ohm, Geir Slupphaug, Anna Kuśnierczyk, Arnt E Fiane, Sverre-Henning Brorson, Lili Zhang, Lars Gullestad, William E Louch, Per Ole Iversen, Ingunn Østlie, Arne Klungland, Geir Christensen, Ivar Sjaastad, Pål Sætrom, Arne Yndestad, Pål Aukrust, Magnar Bjørås, Alexandra V Finsen
Myocardial infarction (MI) triggers a reparative response involving fibroblast proliferation and differentiation driving extracellular matrix modulation necessary to form a stabilizing scar. Recently, it was shown that a genetic variant of the base excision repair enzyme NEIL3 was associated with increased risk of MI in humans. Here, we report elevated myocardial NEIL3 expression in heart failure patients and marked myocardial upregulation of Neil3 after MI in mice, especially in a fibroblast-enriched cell fraction...
January 3, 2017: Cell Reports
https://www.readbyqxmd.com/read/28043025/nf-%C3%AE%C2%BAb-activation-is-cell-type-specific-in-the-heart
#16
Efraín E Rivera-Serrano, Barbara Sherry
Viral myocarditis is common and can progress to cardiac failure. Cardiac cell pro-inflammatory responses are critical for viral clearance, however sustained inflammatory responses contribute to cardiac damage. The transcription factor NF-κB regulates expression of many pro-inflammatory cytokines, but basal and induced activation of NF-κB in different cardiac cell types have not been compared. Here, we used primary cultures of cardiac myocytes and cardiac fibroblasts to identify cardiac cell type-specific events...
December 30, 2016: Virology
https://www.readbyqxmd.com/read/28039944/hydrochlorothiazide-modulates-ischemic-heart-failure-induced-cardiac-remodeling-via-inhibiting-angiotensin-ii-type-1-receptor-pathway-in-rats
#17
Jinghong Luo, Xuanlan Chen, Chufan Luo, Guihua Lu, Longyun Peng, Xiuren Gao, Zhiyi Zuo
AIMS: Our previous study indicates that hydrochlorothiazide inhibits transforming growth factor (TGF)-β/Smad signaling pathway, improves cardiac function and reduces fibrosis. We determined whether these effects were common among the diuretics and whether angiotensin II receptor type 1 (AT1) signaling pathway played a role in these effects. METHODS: Heart failure was produced by ligating the left anterior descending coronary artery in adult male Sprague-Dawley rats...
December 31, 2016: Cardiovascular Therapeutics
https://www.readbyqxmd.com/read/28031326/myocyte-derived-hsp90-modulates-collagen-upregulation-via-biphasic-activation-of-stat-3-in-fibroblasts-during-cardiac-hypertrophy
#18
Ritwik Datta, Trisha Bansal, Santanu Rana, Kaberi Datta, Ratul Datta Chaudhuri, Mamta Chawla-Sarkar, Sagartirtha Sarkar
Signal transducer and activator of transcription-3 (STAT-3) mediated signalling in relation to upregulated collagen expression in fibroblasts is well defined during cardiac hypertrophy. Recent findings from our laboratory have identified Heat shock protein 90 (Hsp90) as a critical modulator of fibrotic signalling in cardiac fibroblasts in this disease milieu. The present study was therefore intended to analyze the role of Hsp90 in the STAT-3 mediated collagen upregulation process. Our data revealed a significant difference between in vivo and in vitro results pointing to a possible involvement of myocyte-fibroblast crosstalk in this process...
December 28, 2016: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28031118/-isolation-purification-and-primary-culture-of-adult-mouse-cardiac-fibroblasts
#19
Rujun Li, Kaizheng Gong, Zhengang Zhang
Objective To establish a method for primary culture of adult mouse cardiac fibroblasts. Methods Myocardial tissues from adult mice were digested with 1 g/L trypsin and 0.8 g/L collagenase IV by oscillating water bath for a short time repeatedly. Cardiac fibroblasts and myocardial cells were isolated with differential adhesion method. Immunofluorescence staining was used to assess the purity of cardiac fibroblasts. The cell morphology was observed under an inverted phase contrast microscope. The proliferation of cardiac fibroblasts was analyzed by growth curve and CCK-8 assay...
January 2017: Xi Bao Yu Fen Zi Mian Yi Xue za Zhi, Chinese Journal of Cellular and Molecular Immunology
https://www.readbyqxmd.com/read/28025989/microrna-142-3p-inhibits-hypoxia-reoxygenation%C3%A2-induced-apoptosis-and-fibrosis-of-cardiomyocytes-by-targeting-high-mobility-group-box%C3%A2-1
#20
Yi Wang, Min Ouyang, Qiong Wang, Zaijin Jian
Myocardial ischemia/reperfusion (I/R) injury may cause the apoptosis of cardiomyocytes as well as cardiac fibrosis, which is characterized as the transdifferentiation of fibroblasts to myofibroblasts and collagen deposition. MicroRNAs (miRNAs or miRs) have been demonstrated to be involved in myocardial I/R injury. However, the underlying molecular mechanism remains largely unclear. In the present study, mouse cardiomyocyte M6200 cells were treated with hypoxia/reoxygenation (H/R). Our data indicated that H/R treatment led to cell apoptosis, the increased expression of fibrosis‑related proteins, namely collagen I, II, III, and fibronectin, as well as the downregulation of miR-142-3p in M6200 cells...
November 2016: International Journal of Molecular Medicine
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