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https://www.readbyqxmd.com/read/29352247/high-content-analysis-identifies-unique-morphological-features-of-reprogrammed-cardiomyocytes
#1
Matthew D Sutcliffe, Philip M Tan, Antonio Fernandez-Perez, Young-Jae Nam, Nikhil V Munshi, Jeffrey J Saucerman
Direct reprogramming of fibroblasts into cardiomyocytes is a promising approach for cardiac regeneration but still faces challenges in efficiently generating mature cardiomyocytes. Systematic optimization of reprogramming protocols requires scalable, objective methods to assess cellular phenotype beyond what is captured by transcriptional signatures alone. To address this question, we automatically segmented reprogrammed cardiomyocytes from immunofluorescence images and analyzed cell morphology. We also introduce a method to quantify sarcomere structure using Haralick texture features, called SarcOmere Texture Analysis (SOTA)...
January 19, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29349588/amphiregulin-enhances-cardiac-fibrosis-and-aggravates-cardiac-dysfunction-in-mice-with-experimental-myocardial-infarction-partly-through-activating-egfr-dependent-pathway
#2
Liang Liu, Xian Jin, Cui-Fen Hu, Ya-Ping Zhang, Zhong'e Zhou, Rong Li, Cheng-Xing Shen
Cardiac fibrosis (CF), a main process of ventricular remodeling after myocardial infarction (MI), plays a crucial role in the pathogenesis of heart failure (HF) post-MI. It is known that amphiregulin (AR) is involved in fibrosis of several organs. However, the expression of AR and its role post-MI are yet to be determined. This study aimed to investigate the impact of AR on CF post-MI and related mechanisms. Significantly upregulated AR expression was evidenced in the infarct border zone of MI mice in vivo and the AR secretion was enhanced in macrophages, but not in cardiac fibroblasts...
January 18, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29348253/multifunctional-role-of-chymase-in-acute-and-chronic-tissue-injury-and-remodeling
#3
REVIEW
Louis J Dell'Italia, James F Collawn, Carlos M Ferrario
Chymase is the most efficient Ang II (angiotensin II)-forming enzyme in the human body and has been implicated in a wide variety of human diseases that also implicate its many other protease actions. Largely thought to be the product of mast cells, the identification of other cellular sources including cardiac fibroblasts and vascular endothelial cells demonstrates a more widely dispersed production and distribution system in various tissues. Furthermore, newly emerging evidence for its intracellular presence in cardiomyocytes and smooth muscle cells opens an entirely new compartment of chymase-mediated actions that were previously thought to be limited to the extracellular space...
January 19, 2018: Circulation Research
https://www.readbyqxmd.com/read/29348198/interleukin-10-stiffens-the-heart
#4
Daniela Cihakova
Cardiac-resident macrophages are a diverse population of cells that have a critical role in the pathogenesis of heart failure. A new understanding of communication between macrophages and cardiac fibroblasts could lead to novel therapeutic strategies for heart failure with preserved ejection function.
January 18, 2018: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29344085/synthesis-secretion-function-metabolism-and-application-of-natriuretic-peptides-in-heart-failure
#5
REVIEW
Shihui Fu, Ping Ping, Fengqi Wang, Leiming Luo
As a family of hormones with pleiotropic effects, natriuretic peptide (NP) system includes atrial NP (ANP), B-type NP (BNP), C-type NP (CNP), dendroaspis NP and urodilatin, with NP receptor-A (guanylate cyclase-A), NP receptor-B (guanylate cyclase-B) and NP receptor-C (clearance receptor). These peptides are genetically distinct, but structurally and functionally related for regulating circulatory homeostasis in vertebrates. In humans, ANP and BNP are encoded by NP precursor A (NPPA) and NPPB genes on chromosome 1, whereas CNP is encoded by NPPC on chromosome 2...
2018: Journal of Biological Engineering
https://www.readbyqxmd.com/read/29339450/cardiac-macrophages-promote-diastolic-dysfunction
#6
Maarten Hulsmans, Hendrik B Sager, Jason D Roh, María Valero-Muñoz, Nicholas E Houstis, Yoshiko Iwamoto, Yuan Sun, Richard M Wilson, Gregory Wojtkiewicz, Benoit Tricot, Michael T Osborne, Judy Hung, Claudio Vinegoni, Kamila Naxerova, David E Sosnovik, Michael R Zile, Amy D Bradshaw, Ronglih Liao, Ahmed Tawakol, Ralph Weissleder, Anthony Rosenzweig, Filip K Swirski, Flora Sam, Matthias Nahrendorf
Macrophages populate the healthy myocardium and, depending on their phenotype, may contribute to tissue homeostasis or disease. Their origin and role in diastolic dysfunction, a hallmark of cardiac aging and heart failure with preserved ejection fraction, remain unclear. Here we show that cardiac macrophages expand in humans and mice with diastolic dysfunction, which in mice was induced by either hypertension or advanced age. A higher murine myocardial macrophage density results from monocyte recruitment and increased hematopoiesis in bone marrow and spleen...
January 16, 2018: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29339198/cd90-cardiac-fibroblasts-reduce-fibrosis-of-acute-myocardial-injury-in-rats
#7
Yuqiao Chang, Cixia Li, Yangyang Jia, Peng Chen, Yonglong Guo, Airong Li, Zhikun Guo
OBJECTIVE: To explore the differentiation tendency of CD90+ cardiac fibroblast (CFs) into cardiomyogenic cells in vitro and repair functions in acute myocardial infarction rats. METHODS: CD90+ subpopulation was sorted from rat CFs by flow cytometry. 10 μmoL/L of 5-Azacytosine (5-aza) was used to induce differentiation of CFs into cardiomyogenic cells. An acute myocardial infarction model was prepared by ligation of the rat left anterior descending coronary artery...
January 12, 2018: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/29337052/sweet-yet-underappreciated-proteoglycans-and-extracellular-matrix-remodeling-in-heart-disease
#8
REVIEW
Geir Christensen, Kate M Herum, Ida G Lunde
Extracellular matrix remodeling is extensive in several heart diseases and hampers cardiac filling, often leading to heart failure. Proteoglycans have over the last two decades emerged as molecules with important roles in matrix remodeling and fibrosis in the heart. Here we discuss and review current literature on proteoglycans that have been studied in cardiac remodeling. The small leucine rich proteoglycans (SLRPs) are located within the extracellular matrix and are organizers of the matrix structure. Membrane-bound proteoglycans, such as syndecans and glypicans, act as receptors and direct cardiac fibroblast signaling...
January 11, 2018: Matrix Biology: Journal of the International Society for Matrix Biology
https://www.readbyqxmd.com/read/29331689/baicalin-inhibits-pressure-overload-induced-cardiac-fibrosis-through-regulating-ampk-tgf-%C3%AE-smads-signaling-pathway
#9
Yichuan Xiao, Jiantao Ye, Ying Zhou, Junjun Huang, Xiawen Liu, Biyun Huang, Liu Zhu, Bo Wu, Genshui Zhang, Yi Cai
AMP-activated protein kinase (AMPK) is a central regulator of multiple metabolic pathways. It has been shown that activation of AMPK could inhibit fibroblast proliferation and extracellular matrix (ECM) accumulation, thereby suppressing cardiac fibrosis. Baicalin, the major component found in skullcap, possesses multiple protective effects on the cardiovascular system. However, little is known about the effect of baicalin on cardiac fibrosis and the molecular mechanism by which baicalin exerts its anti-fibrotic effects has not been investigated...
January 10, 2018: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/29325796/lcz696-sacubitril-valsartan-an-angiotensin-receptor-neprilysin-inhibitor-attenuates-cardiac-hypertrophy-fibrosis-and-vasculopathy-in-a-rat-model-of-chronic-kidney-disease
#10
Yasunori Suematsu, Wanghui Jing, Ane Nunes, Moti L Kashyap, Mahyar Khazaeli, Nosratola D Vaziri, Hamid Moradi
BACKGROUND: Chronic kidney disease (CKD) is associated with cardiac hypertrophy, fibrosis and increased risk of cardiovascular mortality. LCZ696 (Sacubitril/valsartan) is a promising agent which has shown significant potential in treatment of heart failure. We hypothesized that LCZ696 is more effective than valsartan alone in treatment of cardiovascular abnormalities associated with experimental CKD. METHODS AND RESULTS: Male Sprague Dawley rats underwent 5/6 nephrectomy and were subsequently randomized to no treatment (CKD), 30 mg/kg valsartan (VAL), or 60 mg/kg LCZ696 (LCZ)...
January 8, 2018: Journal of Cardiac Failure
https://www.readbyqxmd.com/read/29322373/epac-is-required-for-exogenous-and-endogenous-stimulation-of-adenosine-a2b-receptor-for-inhibition-of-angiotensin-ii-induced-collagen-synthesis-and-myofibroblast-differentiation
#11
Sarawuth Phosri, Kwanchai Bunrukchai, Warisara Parichatikanond, Vilasinee H Sato, Supachoke Mangmool
Angiotensin II (Ang II) plays an important role on the pathogenesis of cardiac fibrosis. Prolong and overstimulation of angiotensin II type 1 receptor with Ang II-induced collagen synthesis and myofibroblast differentiation in cardiac fibroblasts, leading to cardiac fibrosis. Although adenosine and its analogues are known to have cardioprotective effects, the mechanistic by which adenosine A2 receptors (A2Rs) inhibit Ang II-induced cardiac fibrosis is not clearly understood. In the present study, we examined the effects of exogenous adenosine and endogenous adenosine on Ang II-induced collagen and myofibroblast differentiation determined by α-smooth muscle action (α-SMA) overexpression and their underlying signal transduction...
January 10, 2018: Purinergic Signalling
https://www.readbyqxmd.com/read/29321306/digitoxin-suppresses-human-cytomegalovirus-replication-via-na-k-atpase-%C3%AE-1-subunit-dependent-ampk-and-autophagy-activation
#12
Rupkatha Mukhopadhyay, Rajkumar Venkatadri, Jenny Katsnelson, Ravit Arav-Boger
Host-directed therapeutics for human cytomegalovirus (HCMV) requires elucidation of cellular mechanisms that inhibit HCMV. We report on a novel pathway used by cardiac glycosides to inhibit HCMV replication: induction of AMPK activity and autophagy flux through the Na+, K+/ATPase α1 subunit. Our data illustrate an intricate balance between autophagy regulators AMPK, mTOR and ULK1 during infection and treatment with the cardiac glycoside, digitoxin. Both infection and digitoxin induced AMPK phosphorylation, but ULK1 was differentially phosphorylated at unique sites leading to opposing effects on autophagy...
January 10, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29316264/heme-oxygenase-1-affects-generation-and-spontaneous-cardiac-differentiation-of-induced-pluripotent-stem-cells
#13
Jacek Stepniewski, Tomasz Pacholczak, Aniela Skrzypczyk, Maciej Ciesla, Agata Szade, Krzysztof Szade, Romain Bidanel, Agnieszka Langrzyk, Radoslaw Grochowski, Felix Vandermeeren, Neli Kachamakova-Trojanowska, Mateusz Jez, Grazyna Drabik, Mahito Nakanishi, Alicja Jozkowicz, Jozef Dulak
Cellular stress can influence efficiency of iPSCs generation and their differentiation. However, the role of intracellular cytoprotective factors in these processes is still not well known. Therefore, we investigated the effect of HO-1 (Hmox1) or Nrf2 (Nfe2l2), two major cytoprotective genes. Hmox1-/- fibroblasts demonstrated decreased reprogramming efficiency in comparison to Hmox1+/+ cells. Reversely, pharmacological enhancement of HO-1 resulted in higher number of iPSCs colonies. Importantly, elevated level of both p53 and p53-regulated miR-34a and 14-3-3σ was observed in HO-1-deficient fibroblasts whereas downregulation of p53 in these cells markedly increased their reprogramming efficiency...
January 9, 2018: IUBMB Life
https://www.readbyqxmd.com/read/29315687/patterning-of-the-hepato-pancreatobiliary-boundary-by-bmp-reveals-heterogeneity-within-the-murine-liver-bud
#14
Amrita Palaria, Jesse R Angelo, Taylor Guertin, Jesse Mager, Kimberly D Tremblay
During development, the endoderm initiates organ-restricted gene expression patterns in a spatiotemporally controlled manner. This process, termed induction, requires signals from adjacent mesodermal derivatives. Fibroblast Growth Factor (FGF) and Bone Morphogenetic Protein (BMP) emanating from the cardiac mesoderm and the septum transversum mesenchyme (STM), respectively, are believed to be simultaneously and uniformly required to directly induce hepatic gene expression from the murine endoderm. Using small molecule inhibitors of BMP signals during liver bud induction in the developing mouse embryo, we find that BMP signaling is not uniformly required to induce hepatic gene expression...
January 5, 2018: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/29314607/h3-relaxin-inhibits-the-collagen-synthesis-via-ros-and-p2x7r-mediated-nlrp3-inflammasome-activation-in-cardiac-fibroblasts-under-high-glucose
#15
Xiaohui Zhang, Yu Fu, Hui Li, Li Shen, Qing Chang, Liya Pan, Siting Hong, Xinhua Yin
Excessive production of reactive oxygen species (ROS) and P2X7R activation induced by high glucose increases NLRP3 inflammasome activation, which contributes to the pathogenesis of diabetic cardiomyopathy. Although H3 relaxin has been shown to inhibit cardiac fibrosis induced by isoproterenol, the mechanism has not been well studied. Here, we demonstrated that high glucose (HG) induced the collagen synthesis by activation of the NLRP3 inflammasome, leading to caspase-1 activation, interleukin-1β (IL-1β) and IL-18 secretion in neonatal rat cardiac fibroblasts...
January 5, 2018: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29305939/ablation-of-interleukin-17-alleviated-cardiac-interstitial-fibrosis-and-improved-cardiac-function-via-inhibiting-long-non-coding-rna-ak081284-in-diabetic-mice
#16
Yang Zhang, Yi-Yuan Zhang, Ting-Ting Li, Jin Wang, Yuan Jiang, Yue Zhao, Xue-Xin Jin, Gen-Long Xue, Ying Yang, Xiao-Fang Zhang, Yang-Yang Sun, Zhi-Ren Zhang, Xu Gao, Zhi-Min Du, Yan-Jie Lu, Bao-Feng Yang, Zhen-Wei Pan
Interleukin 17 (IL-17) plays an important role in the pathogenesis of cardiac interstitial fibrosis. In this study, we explored the role of interleukin-17 in the development of diabetic cardiomyopathy and the underlying mechanisms. The level of IL-17 increased in both the serum and cardiac tissue of diabetic mice. Knockout of IL-17 improved cardiac function of diabetic mice induced by streptozotocin (STZ), and significantly alleviated interstitial fibrosis as manifested by reduced collagen mRNA expression and collagen deposition evaluated by Masson's staining...
January 3, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29302675/copper-induced-reduction-in-myocardial-fibrosis-is-associated-with-increased-matrix-metalloproteins-in-a-rat-model-of-cardiac-hypertrophy
#17
Yinjie Liu, Ying Xiao, Jiaming Liu, Li Feng, Y James Kang
Trientine (TETA), a copper (Cu) chelator, is capable of replenishing Cu in the heart, and Cu repletion reduces cardiac fibrosis in a rodent model of cardiac hypertrophy. This study was undertaken to explore possible mechanisms by which Cu repletion diminishes cardiac fibrosis. Adult male Sprague-Dawley rats were subjected to ascending aortic constriction to induce cardiac hypertrophy. Four months after the operation, cardiac hypertrophy along with fibrosis was fully developed. TETA treatment was then followed at a dose of 21...
January 5, 2018: Metallomics: Integrated Biometal Science
https://www.readbyqxmd.com/read/29301848/physiologic-pathologic-and-therapeutic-paracrine-modulation-of-cardiac-excitation-contraction-coupling
#18
REVIEW
Joshua Mayourian, Delaine K Ceholski, David M Gonzalez, Timothy J Cashman, Susmita Sahoo, Roger J Hajjar, Kevin D Costa
Cardiac excitation-contraction coupling (ECC) is the orchestrated process of initial myocyte electrical excitation, which leads to calcium entry, intracellular trafficking, and subsequent sarcomere shortening and myofibrillar contraction. Neurohumoral β-adrenergic signaling is a well-established mediator of ECC; other signaling mechanisms, such as paracrine signaling, have also demonstrated significant impact on ECC but are less well understood. For example, resident heart endothelial cells are well-known physiological paracrine modulators of cardiac myocyte ECC mainly via NO and endothelin-1...
January 5, 2018: Circulation Research
https://www.readbyqxmd.com/read/29288823/high-resolution-3d-microscopy-study-of-cardiomyocytes-on-polymer-scaffold-nanofibers-reveals-formation-of-unusual-sheathed-structure
#19
Victor Balashov, Anton Efimov, Olga Agapova, Alexander Pogorelov, Igor Agapov, Konstantin Agladze
Building functional and robust scaffolds for engineered biological tissue requires a nanoscale mechanistic understanding of how cells use the scaffold for their growth and development. A vast majority of the scaffolds used for cardiac tissue engineering are based on polymer materials, the matrices of nanofibers. Attempts to load the polymer fibers of the scaffold with additional sophisticated features, such as electrical conductivity and controlled release of the growth factors or other biologically active molecules, as well as trying to match the mechanical features of the scaffold to those of the extracellular matrix, cannot be efficient without a detailed knowledge of how the cells are attached and strategically positioned with respect to the scaffold nanofibers at micro and nanolevel...
December 27, 2017: Acta Biomaterialia
https://www.readbyqxmd.com/read/29287092/connective-tissue-growth-factor-dependent-collagen-gene-expression-induced-by-mas-agonist-ar234960-in-human-cardiac-fibroblasts
#20
Arunachal Chatterjee, John Barnard, Christine Moravec, Russell Desnoyer, Kalyan Tirupula, Sadashiva S Karnik
Perspectives on whether the functions of MAS, a G protein-coupled receptor, are beneficial or deleterious in the heart remain controversial. MAS gene knockout reduces coronary vasodilatation leading to ischemic injury. G protein signaling activated by MAS has been implicated in progression of adaptive cardiac hypertrophy to heart failure and fibrosis. In the present study, we observed increased expression of MAS, connective tissue growth factor (CTGF) and collagen genes in failing (HF) human heart samples when compared to non-failing (NF)...
2017: PloS One
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