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https://www.readbyqxmd.com/read/27924974/mir-155-regulates-high-glucose-induced-cardiac-fibrosis-via-the-tgf-%C3%AE-signaling-pathway
#1
Dong Zhang, Yongchun Cui, Bin Li, Xiaokang Luo, Bo Li, Yue Tang
Cardiac fibrosis, as a pathological process, plays an important role in various cardiac diseases. microRNA-155 (miR-155) is one of the most important miRNAs, and previous studies have shown that it is a regulatory factor in various fibrotic diseases. However, the mechanism by which miR-155 affects myocardial fibrosis remains unclear. In this study, we aim to establish the biological function of miR-155 in myocardial fibrosis induced by diabetes in mice. We used normal C57BL/6 wild type (WT) and miR-155 knockout (KO) mice to establish the diabetic model by intraperitoneal injection of streptozotocin, and we utilized echocardiography to evaluate the cardiac function at 30 and 60 days post-modeling...
December 7, 2016: Molecular BioSystems
https://www.readbyqxmd.com/read/27924221/targeting-mll1-h3k4-methyltransferase-activity-to-guide-cardiac-lineage-specific-reprogramming-of-fibroblasts
#2
Liu Liu, Ienglam Lei, Hacer Karatas, Yangbing Li, Li Wang, Leonid Gnatovskiy, Yali Dou, Shaomeng Wang, Li Qian, Zhong Wang
Generation of induced cardiomyocytes (iCMs) directly from fibroblasts offers a great opportunity for cardiac disease modeling and cardiac regeneration. A major challenge of iCM generation is the low conversion rate. To address this issue, we attempted to identify small molecules that could potentiate the reprogramming ability towards cardiac fate by removing inhibitory roadblocks. Using mouse embryonic fibroblasts as the starting cell source, we first screened 47 cardiac development related epigenetic and transcription factors, and identified an unexpected role of H3K4 methyltransferase Mll1 and related factor Men1 in inhibiting iCM reprogramming...
2016: Cell Discovery
https://www.readbyqxmd.com/read/27920122/microrna-33-controls-adaptive-fibrotic-response-in-the-remodeling-heart-by-preserving-lipid-raft-cholesterol
#3
Masataka Nishiga, Takahiro Horie, Yasuhide Kuwabara, Kazuya Nagao, Osamu Baba, Tetsushi Nakao, Tomohiro Nishino, Daihiko Hakuno, Yasuhiro Nakashima, Hitoo Nishi, Fumiko Nakazeki, Yuya Ide, Satoshi Koyama, Masahiro Kimura, Ritsuko Hanada, Tomoyuki Nakamura, Tsukasa Inada, Koji Hasegawa, Simon J Conway, Toru Kita, Takeshi Kimura, Koh Ono
RATIONALE: Heart failure (HF) and atherosclerosis share the underlying mechanisms of chronic inflammation followed by fibrosis. A highly conserved microRNA (miR), miR-33 is considered as a potential therapeutic target for atherosclerosis because it regulates lipid metabolism and inflammation. However, the role of miR-33 in HF remains to be elucidated. OBJECTIVE: To clarify the role of miR-33 involved in HF. METHODS AND RESULTS: We first investigated the expression levels of miR-33a/b in human cardiac tissue samples with dilated cardiomyopathy...
December 5, 2016: Circulation Research
https://www.readbyqxmd.com/read/27918308/cardiac-myofibroblast-engulfment-of-dead-cells-facilitates-recovery-after-myocardial-infarction
#4
Michio Nakaya, Kenji Watari, Mitsuru Tajima, Takeo Nakaya, Shoichi Matsuda, Hiroki Ohara, Hiroaki Nishihara, Hiroshi Yamaguchi, Akiko Hashimoto, Mitsuho Nishida, Akiomi Nagasaka, Yuma Horii, Hiroki Ono, Gentaro Iribe, Ryuji Inoue, Makoto Tsuda, Kazuhide Inoue, Akira Tanaka, Masahiko Kuroda, Shigekazu Nagata, Hitoshi Kurose
Myocardial infarction (MI) results in the generation of dead cells in the infarcted area. These cells are swiftly removed by phagocytes to minimize inflammation and limit expansion of the damaged area. However, the types of cells and molecules responsible for the engulfment of dead cells in the infarcted area remain largely unknown. In this study, we demonstrated that cardiac myofibroblasts, which execute tissue fibrosis by producing extracellular matrix proteins, efficiently engulf dead cells. Furthermore, we identified a population of cardiac myofibroblasts that appears in the heart after MI in humans and mice...
December 5, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27918096/back-cover-story-eur-j-immunol-12-16
#5
(no author information available yet)
Our back cover features an H&E stained biopsy section from a patient with eosinophilic myocarditis. Countless heart-infiltrating eosinophils with bright pink granules and bi-lobed nuclei are visible between large, striated cardiomyocytes. In addition, T cells and macrophages are infiltrating the heart. This image relates to the article by Diny et al. (pp. 2749-2760), in which the authors analyze the pathway required for eosinophil trafficking to the heart by examining heart biopsies from myocarditis patients and a murine myocarditis model...
December 2016: European Journal of Immunology
https://www.readbyqxmd.com/read/27917273/involvement-of-microrna-133-and-29-in-cardiac-disturbances-in-diabetic-ovariectomized-rats
#6
Parisa Habibi, Alireza Alihemmati, Mohammadreza Nasirzadeh, Hadi Yousefi, Mohammadrasoul Habibi, Nasser Ahmadiasl
OBJECTIVES: Menopause and diabetes obviously increase the risk of cardiovascular disease in women. The aims of the present study were to evaluate the effects of ovariectomy in type 2 diabetes on the histology and expression of miRNA-29, miRNA-133, IGF-1 and Bcl-2 genes and Bcl-2 protein and caspase 3 activity in the hearts of female rats. MATERIALS AND METHODS: Forty Female Wistar rats were divided into four groups: control, sham, ovariectomized (OVX), and ovariectomized with type 2 diabetes (OVX...
November 2016: Iranian Journal of Basic Medical Sciences
https://www.readbyqxmd.com/read/27916094/-knockdown-of-runx3-inhibits-hypoxia-induced-endothelial-to-mesenchymal-transition-of-human-cardiac-microvascular-endothelial-cells
#7
Yanhua Liu, Bingong Li, Yuqin Wang, Delong Wang, Jin Zou, Xuan Ke, Yanqin Hao
Objective To investigate the effects of Runt-related transcription factor 3 (RUNX3) knockdown on hypoxia-induced endothelial-to-mesenchymal transition (EndoMT) of human cardiac microvascular endothelial cells (HCMECs), and elucidate the underlying molecular mechanism. Methods HCMECs were cultured in hypoxic conditions and infected with RUNX3-RNAi lentivirus to knock-down the expression of RUNX3. Reverse transcription PCR was performed to detect the mRNA expressions of RUNX3 and EndoMT related genes such as CD31, vascular endothelial cadherin (VE-cadherin), α-smooth muscle actin (α-SMA) and fibroblast-specific protein-1 (FSP-1); Western blotting was used to determine the protein expressions of RUNX3, CD31, α-SMA and another molecules involved in EndoMT; and immunofluorescence cytochemistry was applied to observe the colocalization of CD31 and α-SMA...
December 2016: Xi Bao Yu Fen Zi Mian Yi Xue za Zhi, Chinese Journal of Cellular and Molecular Immunology
https://www.readbyqxmd.com/read/27912208/smad-nuclear-interacting-protein-1-acts-as-a-protective-regulator-of-pressure-overload-induced-pathological-cardiac-hypertrophy
#8
Yu-Yan Lu, Da-Chun Xu, Yi-Fan Zhao, Guo-Fu Zhu, Meng-Yun Zhu, Wei-Jing Liu, Xue-Jing Yu, Wei Chen, Zheng Liu, Ya-Wei Xu
BACKGROUND: Smad nuclear interacting protein 1 (SNIP1) plays a critical role in cell proliferation, transformation of embryonic fibroblasts, and immune regulation. However, the role of SNIP1 in cardiac hypertrophy remains unclear. METHODS AND RESULTS: Here we examined the role of SNIP1 in pressure overload-induced cardiac hypertrophy and its mechanisms. Our results demonstrated that SNIP1 expression was downregulated in human dilated cardiomyopathic hearts, aortic banding-induced mice hearts, and angiotensin II-treated cardiomyocytes...
October 26, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27910042/direct-cardiac-reprogramming-as-a-novel-therapeutic-strategy-for-treatment-of-myocardial-infarction
#9
Hong Ma, Li Wang, Jiandong Liu, Li Qian
Direct reprogramming of fibroblasts into induced cardiomyocytes (iCMs) holds great promise as a novel therapy for the treatment of heart failure, a common and morbid disease that is usually caused by irreversible loss of functional cardiomyocytes (CMs). Recently, we and others showed that in a murine model of acute myocardial infarction, delivery of three transcription factors, Gata4, Mef2c, and Tbx5 converted endogenous cardiac fibroblasts into functional iCMs. These iCMs integrated electrically and mechanically with surrounding myocardium, resulting in a reduction in scar size and an improvement in heart function...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27904680/enhancement-of-early-cardiac-differentiation-of-dedifferentiated-fat-cells-by-dimethyloxalylglycine-via-notch-signaling-pathway
#10
Fuhai Li, Zongzhuang Li, Zhi Jiang, Ye Tian, Zhi Wang, Wei Yi, Chenyun Zhang
Background: Hypoxia has been reported to possess the ability to induce mature lipid-filled adipocytes to differentiate into fibroblast-like multipotent dedifferentiated fat (DFAT) cells and stem cells such as iPSCs (interstitial pluripotent stem cells) and ESCs (embryonic stem cells) and then to differentiate into cardiomyocytes. However, the effect of hypoxia on cardiac differentiation of DFAT cells and its underlying molecular mechanism remains to be investigated. Objective: To investigate the role of hypoxia in early cardiac differentiation of DFAT cells and the underlying molecular mechanism...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27890729/maturation-of-human-embryonic-stem-cell-derived-cardiomyocytes-hesc-cms-in-3d-collagen-matrix-effects-of-niche-cell-supplementation-and-mechanical-stimulation
#11
W Zhang, C W Kong, M H Tong, W H Chooi, N Huang, R A Li, B P Chan
: Cardiomyocytes derived from human embryonic stem cells (hESC-CMs) are regarded as a promising source for regenerative medicine, drug testing and disease modeling. Nevertheless, cardiomyocytes are immature in terms of their contractile structure, metabolism and electrophysiological properties. Here, we fabricate cardiac muscle strips by encapsulating hESC-CMs in collagen-based biomaterials. Supplementation of niche cells at 3% to the number of hESC-CMs enhance the maturation of the hESC-CMs in 3D tissue matrix...
November 24, 2016: Acta Biomaterialia
https://www.readbyqxmd.com/read/27889772/sonodynamic-therapy-inhibits-fibrogenesis-in-rat-cardiac-fibroblasts-induced-by-tgf-%C3%AE-1
#12
Yuanyuan Guo, Zengxiang Dong, Yuanqi Shi, Wei Wang, Lu Wang, Jing Sun, Xin Sun, Zhen Tian, Jianting Yao, Zhitao Li, Jiali Cheng, Ye Tian
BACKGROUND/AIMS: Sonodynamic therapy (SDT) is a localized ultrasound-activated therapy for atherosclerosis when combined with a sonosensitizer, 5-aminolevulinic acid (ALA), but whether it can prevent cardiac fibrosis has not been studied. In the present study, we evaluated the effects SDT on fibrogenesis in rat cardiac fibroblasts. METHODS: The primary cardiac fibroblasts were isolated from rats, and induced to fibrogenesis with TGF-β1. With this in vitro model, we tested the preventive effects of SDT on fibrogenesis and further the underlying mechanism...
November 25, 2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27876880/overexpression-of-serpine2-protease-nexin-1-contribute-to-pathological-cardiac-fibrosis-via-increasing-collagen-deposition
#13
Xuelian Li, Dandan Zhao, Zhenfeng Guo, Tianshi Li, Muge Qili, Bozhi Xu, Ming Qian, Haihai Liang, Xiaoqiang E, Samuel Chege Gitau, Lu Wang, Longtao Huangfu, Qiuxia Wu, Chaoqian Xu, Hongli Shan
Although increases in cardiovascular load (pressure overload) are known to elicit ventricular remodeling including cardiomyocyte hypertrophy and interstitial fibrosis, the molecular mechanisms of pressure overload or AngII -induced cardiac interstitial fibrosis remain elusive. In this study, serpinE2/protease nexin-1 was over-expressed in a cardiac fibrosis model induced by pressure-overloaded via transverse aortic constriction (TAC) in mouse. Knockdown of serpinE2 attenuates cardiac fibrosis in a mouse model of TAC...
November 23, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27875248/vildagliptin-and-caloric-restriction-for-cardioprotection-in-pre-diabetic-rats
#14
Pongpan Tanajak, Hiranya Pintana, Natthaphat Siri-Angkul, Juthamas Khamseekaew, Nattayaporn Apaijai, Siriporn C Chattipakorn, Nipon Chattipakorn
Long-term high-fat diet (HFD) consumption causes cardiac dysfunction. Although calorie restriction (CR) has been shown to be useful in obesity, we hypothesized that combined CR with dipeptidyl peptidase-4 (DPP-4) inhibitor provides greater efficacy than monotherapy in attenuating cardiac dysfunction and metabolic impairment in HFD-induced obese-insulin resistant rats. Thirty male Wistar rats were divided into 2 groups to be fed on either a normal diet (ND, n = 6) or a HFD (n = 24) for 12 weeks. Then, HFD rats were divided into 4 subgroups (n = 6/subgroup) to receive just the vehicle, CR diet (60% of mean energy intake and changed to ND), vildagliptin (3 mg/kg/day) or combined CR and vildagliptin for 4 weeks...
February 2017: Journal of Endocrinology
https://www.readbyqxmd.com/read/27875022/a-comparison-of-left-and-right-atrial-fibroblasts-reveals-different-collagen-production-activity-and-stress-induced-mitogen-activated-protein-kinase-signaling-in-rats
#15
Cheng-Chih Chung, Yu-Hsun Kao, Chih-Jung Yao, Yung-Kuo Lin, Yi-Jen Chen
AIM: Atrial fibrosis plays a pivotal role in the pathophysiology of heart failure (HF). The left atrium (LA) experiences greater fibrosis than the right atrium (RA) during HF. It is not clear whether LA cardiac fibroblasts contain distinctive activities that predispose LA to fibrosis. METHODS: LA and RA fibrosis were evaluated in healthy and isoproterenol induced HF Sprague-Dawley rats. Rat LA and RA primary isolated fibroblasts were subjected to proliferation assay, oxidative stress assay, cell migration analysis, collagen measurement, cytokine array and western blot...
November 22, 2016: Acta Physiologica
https://www.readbyqxmd.com/read/27870967/osthole-inhibits-the-expressions-of-collagen-i-and-iii-through-smad-signaling-pathway-after-treatment-with-tgf-%C3%AE-1-in-mouse-cardiac-fibroblasts
#16
Jin-Cheng Liu, Feng Wang, Mei-Lin Xie, Zong-Qi Cheng, Qiong Qin, Lin Chen, Rong Chen
BACKGROUND: Osthole, a natural coumarin and bioactive compound isolated from the fruit of Cnidium monnieri (L.) Cusson, was reported to prevent isoprenaline-induced myocardial fibrosis in mice by inhibiting the transforming growth factor-β1 (TGF-β1) expression, but the underlying mechanism is still unclear. The aim of this study is to illuminate whether the mechanism of osthole inhibiting collagen I and III expressions is associated with Smad signaling pathway in mouse cardiac fibroblasts (CFs) treated with TGF-β1...
November 10, 2016: International Journal of Cardiology
https://www.readbyqxmd.com/read/27867037/cardiac-fibroblasts-adopt-osteogenic-fates-and-can-be-targeted-to-attenuate-pathological-heart-calcification
#17
Indulekha C L Pillai, Shen Li, Milagros Romay, Larry Lam, Yan Lu, Jie Huang, Nathaniel Dillard, Marketa Zemanova, Liudmilla Rubbi, Yibin Wang, Jason Lee, Ming Xia, Owen Liang, Ya-Hong Xie, Matteo Pellegrini, Aldons J Lusis, Arjun Deb
Mammalian tissues calcify with age and injury. Analogous to bone formation, osteogenic cells are thought to be recruited to the affected tissue and induce mineralization. In the heart, calcification of cardiac muscle leads to conduction system disturbances and is one of the most common pathologies underlying heart blocks. However the cell identity and mechanisms contributing to pathological heart muscle calcification remain unknown. Using lineage tracing, murine models of heart calcification and in vivo transplantation assays, we show that cardiac fibroblasts (CFs) adopt an osteoblast cell-like fate and contribute directly to heart muscle calcification...
November 15, 2016: Cell Stem Cell
https://www.readbyqxmd.com/read/27863907/evidence-of-epigenetic-tags-in-cardiac-fibrosis
#18
REVIEW
Vincenzo Grimaldi, Maria Rosaria De Pascale, Alberto Zullo, Andrea Soricelli, Teresa Infante, Francesco Paolo Mancini, Claudio Napoli
In cardiac fibrosis, following an injury or a stress, non-functional fibrotic tissue substitutes normal myocardium, thus leading to progressive heart failure. Activated fibroblasts are principal determinants of cardiac fibrosis by producing excessive fibrotic extracellular matrix and causing hypertrophy of cardiomyocytes. Epigenetic changes, such as DNA methylation, histone modifications, and miRNAs have been involved in these mechanisms. Therefore, there is a strong interest in reverting such epigenetic transformations in order to arrest myocardial fibrotic degeneration...
November 15, 2016: Journal of Cardiology
https://www.readbyqxmd.com/read/27862165/grk2-%C3%AE-arrestin-mediates-arginine-vasopressin-induced-cardiac-fibroblast-proliferation
#19
Yunxuan Chen, Feifei Xu, Lingling Zhang, Xiaojun Wang, Yifan Wang, AnthonyYiu-Ho Woo, Weizhong Zhu
Cardiac fibrosis is a pathological feature commonly foundinheartsexposed to hemodynamic orneurohormonal stress. Elevated levels of arginine vasopressin (AVP) are closely associated with the progression ofheart failure and could be an underlyingcauseof cardiac fibrosis. The aim of this study is to characterize the effect of AVP on neonatal rat cardiac fibroblasts (NRCFs) and to illustrate itssignallingmechanism. The proliferative effect of AVP was assessed by methylthiazolyldiphenyl-tetrazoliumassay and 5-bromo-2'-deoxyuridine (BrdU) incorporation assay, and the amounts of cellular signallingproteins α-smooth muscle actin(α-SMA),matrix metalloproteinase (MMP) 2, MMP9, and phosphorylated ERK1/2 were determined by Western blotting...
November 14, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/27854328/parenchymal-and-stromal-cells-contribute-to-pro-inflammatory-myocardial-environment-at-early-stages-of-diabetes-protective-role-of-resveratrol
#20
Monia Savi, Leonardo Bocchi, Roberto Sala, Caterina Frati, Costanza Lagrasta, Denise Madeddu, Angela Falco, Serena Pollino, Letizia Bresciani, Michele Miragoli, Massimiliano Zaniboni, Federico Quaini, Daniele Del Rio, Donatella Stilli
Background: Little information is currently available concerning the relative contribution of cardiac parenchymal and stromal cells in the activation of the pro-inflammatory signal cascade, at the initial stages of diabetes. Similarly, the effects of early resveratrol (RSV) treatment on the negative impact of diabetes on the different myocardial cell compartments remain to be defined. Methods: In vitro challenge of neonatal cardiomyocytes and fibroblasts to high glucose and in vivo/ex vivo experiments on a rat model of Streptozotocin-induced diabetes were used to specifically address these issues...
November 16, 2016: Nutrients
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