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adult cardiomyocyte proliferation

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https://www.readbyqxmd.com/read/28707671/cardiomyocyte-proliferation-remove-brakes-and-push-accelerators
#1
Lingjuan He, Bin Zhou
Adult mammalian hearts cannot repair by themselves after injury due to limited proliferation of cardiomyocytes; removal of cell cycle blocker and/or addition of drugs that boost proliferation of cardiomyocytes provide potential means to cardiac regeneration. Three publications that appeared recently in Nature and Cell Research now provide new hope to the treatment of heart injuries.
July 14, 2017: Cell Research
https://www.readbyqxmd.com/read/28670398/microrna-1825-induces-proliferation-of-adult-cardiomyocytes-and-promotes-cardiac-regeneration-post-ischemic-injury
#2
Raghav Pandey, Sebastian Velasquez, Shazia Durrani, Min Jiang, Michelle Neiman, Jeffrey S Crocker, Joshua B Benoit, Jack Rubinstein, Arghya Paul, Rafeeq Ph Ahmed
In mammals, proliferative capacity of cardiomyocytes is lost soon after birth, while zebrafish and other lower organisms like newts are known to regenerate injured hearts even at an adult age. Here, we show that miR-1825 can induce robust proliferation of adult rat cardiomyocytes and can improve cardiac function in-vivo post myocardial infarction. Rat adult cardiomyocytes transfected with miR-1825 showed a significant increase in DNA synthesis, mitosis, cytokinesis, and an increase in cell number when compared to cel-miR-67 transfected control...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28667270/fam64a-is-a-novel-cell-cycle-promoter-of-hypoxic-fetal-cardiomyocytes-in-mice
#3
Ken Hashimoto, Aya Kodama, Takeshi Honda, Akira Hanashima, Yoshihiro Ujihara, Takashi Murayama, Shin-Ichiro Nishimatsu, Satoshi Mohri
Fetal cardiomyocytes actively proliferate to form the primitive heart in utero in mammals, but they stop dividing shortly after birth. The identification of essential molecules maintaining this active cardiomyocyte proliferation is indispensable for potential adult heart regeneration. A recent study has shown that this proliferation depends on a low fetal oxygen condition before the onset of breathing at birth. We have established an isolation protocol for mouse fetal cardiomyocytes, performed under strict low oxygen conditions to mimic the intrauterine environment, that gives the highest proliferative activities thus far reported...
June 30, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28659827/increased-postnatal-cardiac-hyperplasia-precedes-cardiomyocyte-hypertrophy-in-a-model-of-hypertrophic-cardiomyopathy
#4
Emily T Farrell, Adrian C Grimes, Willem J de Lange, Annie E Armstrong, J Carter Ralphe
Rationale: Hypertrophic cardiomyopathy (HCM) occurs in ~0.5% of the population and is a leading cause of sudden cardiac death (SCD) in young adults. Cardiomyocyte hypertrophy has been the accepted mechanism for cardiac enlargement in HCM, but the early signaling responsible for initiating hypertrophy is poorly understood. Mutations in cardiac myosin binding protein C (MYBPC3) are among the most common HCM-causing mutations. Ablation of Mybpc3 in an HCM mouse model (cMyBP-C(-/-)) rapidly leads to cardiomegaly by postnatal day (PND) 9, though hearts are indistinguishable from wild-type (WT) at birth...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28659386/fate-predetermination-of-cardiac-myocytes-during-zebrafish-heart-regeneration
#5
Isil Tekeli, Anna Garcia-Puig, Mario Notari, Cristina García-Pastor, Isabelle Aujard, Ludovic Jullien, Angel Raya
Adult zebrafish have the remarkable ability to regenerate their heart upon injury, a process that involves limited dedifferentiation and proliferation of spared cardiomyocytes (CMs), and migration of their progeny. During regeneration, proliferating CMs are detected throughout the myocardium, including areas distant to the injury site, but whether all of them are able to contribute to the regenerated tissue remains unknown. Here, we developed a CM-specific, photoinducible genetic labelling system, and show that CMs labelled in embryonic hearts survive and contribute to all three (primordial, trabecular and cortical) layers of the adult zebrafish heart...
June 2017: Open Biology
https://www.readbyqxmd.com/read/28655642/the-use-and-abuse-of-cre-lox-recombination-to-identify-adult-cardiomyocyte-renewal-rate-and-origin
#6
REVIEW
Iolanda Aquila, Fabiola Marino, Eleonora Cianflone, Pina Marotta, Michele Torella, Vincenzo Mollace, Ciro Indolfi, Bernardo Nadal-Ginard, Daniele Torella
The adult mammalian heart, including the human, is unable to regenerate segmental losses after myocardial infarction. This evidence has been widely and repeatedly used up-to-today to suggest that the myocardium, contrary to most adult tissues, lacks an endogenous stem cell population or more specifically a bona-fide cardiomyocyte-generating progenitor cell of biological significance. In the last 15 years, however, the field has slowly evolved from the dogma that no new cardiomyocytes were produced from shortly after birth to the present consensus that new cardiomyocytes are formed throughout lifespan...
June 24, 2017: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/28642276/dedifferentiation-proliferation-and-redifferentiation-of-adult-mammalian-cardiomyocytes-after-ischemic-injury
#7
Wei Eric Wang, Liangpeng Li, Xuewei Xia, Wenbin Fu, Qiao Liao, Cong Lan, Dezhong Yang, Hongmei Chen, Rongchuan Yue, Cindy S Zeng, Lin Zhou, Bin Zhou, Dayue D Duan, Xiongwen Chen, Steven R Houser, Chunyu Zeng
Background -Adult mammalian hearts have a limited ability to generate new cardiomyocytes. Proliferation of existing adult cardiomyocytes (ACM) is a potential source of new cardiomyocytes. Understanding the fundamental biology of ACM proliferation could be of great clinical significance for treating myocardial infarction (MI). We aim to understand the process and regulation of ACM proliferation and its role in new cardiomyocyte formation of post-MI mouse hearts. Methods -β-actin-GFP transgenic mice and fate-mapping Myh6-MerCreMer-tdTomato/lacZ mice were used to trace the fate of ACMs...
June 22, 2017: Circulation
https://www.readbyqxmd.com/read/28638481/neonatal-heart-enriched-mir-708-promotes-proliferation-and-stress-resistance-of-cardiomyocytes-in-rodents
#8
Shengqiong Deng, Qian Zhao, Lixiao Zhen, Chuyi Zhang, Cuicui Liu, Guangxue Wang, Lin Zhang, Luer Bao, Ying Lu, Lingyu Meng, Jinhui Lü, Ping Yu, Xin Lin, Yuzhen Zhang, Yi-Han Chen, Huimin Fan, William C Cho, Zhongmin Liu, Zuoren Yu
Adult heart has limited potential for regeneration after pathological injury due to the limited cell proliferation of cardiomyocytes and the quiescent status of progenitor cells. As such, induction of cell-cycle reentry of cardiomyocytes is one of the key strategies for regeneration of damaged heart. In this study, a subset of miRNAs including miR-708 were identified to be much more abundant in the embryonic and neonatal cardiomyocytes than that in adult rodents. Overexpression of miR-708 promoted cellular proliferation of H9C2 cells or primary cardiomyocytes from neonatal rats or mice in vitro...
2017: Theranostics
https://www.readbyqxmd.com/read/28629520/the-erythropoietin-system-protects-the-heart-upon-injury-by-cardiac-progenitor-cell-activation
#9
Maria P Zafeiriou
Erythropoietin (EPO) is a growth hormone, widely known for its role in erythropoiesis. The broad expression of erythropoietin receptor (EPOR) in adult organs suggested that EPO may also affect other cells besides late erythroid progenitors. In the embryonic heart, EPOR is expressed in all cells including the immature proliferating cardiomyocytes. In contrast to the embryonic heart in adulthood, EPOR expression is decreased and mainly detected in immature proliferating cells (i.e., resident cardiac progenitor cells) rather than in terminally differentiated cells (i...
2017: Vitamins and Hormones
https://www.readbyqxmd.com/read/28621328/live-cell-screening-platform-identifies-ppar%C3%AE-as-a-regulator-of-cardiomyocyte-proliferation-and-cardiac-repair
#10
Ajit Magadum, Yishu Ding, Lan He, Teayoun Kim, Mohankrishna Dalvoy Vasudevarao, Qinqiang Long, Kevin Yang, Nadeera Wickramasinghe, Harsha V Renikunta, Nicole Dubois, Gilbert Weidinger, Qinglin Yang, Felix B Engel
Zebrafish can efficiently regenerate their heart through cardiomyocyte proliferation. In contrast, mammalian cardiomyocytes stop proliferating shortly after birth, limiting the regenerative capacity of the postnatal mammalian heart. Therefore, if the endogenous potential of postnatal cardiomyocyte proliferation could be enhanced, it could offer a promising future therapy for heart failure patients. Here, we set out to systematically identify small molecules triggering postnatal cardiomyocyte proliferation. By screening chemical compound libraries utilizing a Fucci-based system for assessing cell cycle stages, we identified carbacyclin as an inducer of postnatal cardiomyocyte proliferation...
June 16, 2017: Cell Research
https://www.readbyqxmd.com/read/28617969/conditionally-targeted-deletion-of-psen1-leads-to-diastolic-heart-dysfunction
#11
Xiao-Wei Song, Qing-Ning Yuan, Ying Tang, Mi Cao, Ya-Feng Shen, Zhen-Yu Zeng, Chang-Hai Lei, SongHua Li, Xian-Xian Zhao, Yong-Ji Yang
Recently, PSEN1 has been reported to have mutations in dilated cardiomyopathy pedigrees. However, the function and mechanism of PSEN1 in cardiomyopathy remains unresolved. Here, we established 4 types of genetically modified mice to determine the function of PSEN1 in cardiac development and pathology. PSEN1 null mutation resulted in perinatal death, retardation of heart growth, ventricular dilatation, septum defects, and valvular thickening. PSEN1 knockout in adults led to decreased muscle fibers, widened sarcomere Z lines and reduced lengths of sarcomeres in cardiomyocytes...
June 15, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28581498/dystrophin-glycoprotein-complex-sequesters-yap-to-inhibit-cardiomyocyte-proliferation
#12
Yuka Morikawa, Todd Heallen, John Leach, Yang Xiao, James F Martin
The regenerative capacity of the adult mammalian heart is limited, because of the reduced ability of cardiomyocytes to progress through mitosis. Endogenous cardiomyocytes have regenerative capacity at birth but this capacity is lost postnatally, with subsequent organ growth occurring through cardiomyocyte hypertrophy. The Hippo pathway, a conserved kinase cascade, inhibits cardiomyocyte proliferation in the developing heart to control heart size and prevents regeneration in the adult heart. The dystrophin-glycoprotein complex (DGC), a multicomponent transmembrane complex linking the actin cytoskeleton to extracellular matrix, is essential for cardiomyocyte homeostasis...
July 13, 2017: Nature
https://www.readbyqxmd.com/read/28581497/the-extracellular-matrix-protein-agrin-promotes-heart-regeneration-in-mice
#13
Elad Bassat, Yara Eid Mutlak, Alex Genzelinakh, Ilya Y Shadrin, Kfir Baruch Umansky, Oren Yifa, David Kain, Dana Rajchman, John Leach, Daria Riabov Bassat, Yael Udi, Rachel Sarig, Irit Sagi, James F Martin, Nenad Bursac, Shenhav Cohen, Eldad Tzahor
The adult mammalian heart is non-regenerative owing to the post-mitotic nature of cardiomyocytes. The neonatal mouse heart can regenerate, but only during the first week of life. Here we show that changes in the composition of the extracellular matrix during this week can affect cardiomyocyte growth and differentiation in mice. We identify agrin, a component of neonatal extracellular matrix, as required for the full regenerative capacity of neonatal mouse hearts. In vitro, recombinant agrin promotes the division of cardiomyocytes that are derived from mouse and human induced pluripotent stem cells through a mechanism that involves the disassembly of the dystrophin-glycoprotein complex, and Yap- and ERK-mediated signalling...
July 13, 2017: Nature
https://www.readbyqxmd.com/read/28578380/the-zebrafish-ventricle-a-hub-of-cardiac-endothelial-cells-for-in-vitro-cell-behavior-studies
#14
Chinmoy Patra, Zacharias Kontarakis, Harmandeep Kaur, Amey Rayrikar, Debanjan Mukherjee, Didier Y R Stainier
Despite our increasing understanding of zebrafish heart development and regeneration, there is limited information about the distribution of endothelial cells (ECs) in the adult zebrafish heart. Here, we investigate and compare the distribution of cardiac ECs (cECs) in adult mouse and zebrafish ventricles. Surprisingly, we find that (i) active coronary vessel growth is present in adult zebrafish, (ii) ~37 and ~39% of cells in the zebrafish heart are ECs and cardiomyocytes, respectively, a composition similar to that seen in mouse...
June 2, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28523343/hh-signaling-in-regeneration-of-the-ischemic-heart
#15
REVIEW
Marina Dunaeva, Johannes Waltenberger
Myocardial infarction (MI) is caused by the occlusion of a coronary artery due to underlying atherosclerosis complicated by localized thrombosis. The blockage of blood flow leads to cardiomyocyte (CM) death in the infarcted area. Adult mammalian cardiomyocytes have little capacity to proliferate in response to injury; however, some pathways active during embryogenesis and silent during adult life are recruited in response to tissue injury. One such example is hedgehog (Hh) signaling. Hh is involved in the embryonic development of the heart and coronary vascular system...
May 18, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28469272/adult-murine-cardiomyocytes-exhibit-regenerative-activity-with-cell-cycle-reentry-through-stat3-in-the-healing-process-of-myocarditis
#16
Akimitsu Miyawaki, Masanori Obana, Yusuke Mitsuhara, Aya Orimoto, Yusuke Nakayasu, Tomomi Yamashita, So-Ichiro Fukada, Makiko Maeda, Hiroyuki Nakayama, Yasushi Fujio
Mammalian cardiomyocytes substantially lose proliferative capacity immediately after birth, limiting adult heart regeneration after injury. However, clinical myocarditis appears to be self-limiting with tissue-reparative properties. Here, we investigated the molecular mechanisms underlying the recovery from myocarditis with regard to cardiomyocyte proliferation using an experimental autoimmune myocarditis (EAM) model. Three weeks after EAM induction (EAM3w), cardiac tissue displayed infiltration of inflammatory cells with cardiomyocyte apoptosis...
May 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28464412/heart-specific-expression-of-laminopathic-mutations-in-transgenic-zebrafish
#17
Ajay D Verma, Veena K Parnaik
Lamins are key determinants of nuclear organization and function in the metazoan nucleus. Mutations in human lamin A cause a spectrum of genetic diseases that affect cardiac muscle and skeletal muscle as well as other tissues. A few laminopathies have been modeled using the mouse. As zebrafish is a well established model for the study of cardiac development and disease, we have investigated the effects of heart-specific lamin A mutations in transgenic zebrafish. We have developed transgenic lines of zebrafish expressing conserved lamin A mutations that cause cardiac dysfunction in humans...
May 2, 2017: Cell Biology International
https://www.readbyqxmd.com/read/28459713/cardiac-outcomes-after-perinatal-sertraline-exposure-in-mice
#18
Sarah E Haskell, Cecilia Lo, Mitchell E Kent, Timothy M Eggleston, Kenneth A Volk, Benjamin E Reinking, Robert D Roghair
Selective serotonin reuptake inhibitors are prescribed to 6-10% of pregnant women in the United States. Using an intrauterine plus neonatal exposure model to represent exposure throughout human pregnancy, we hypothesized sertraline exposure would impact intracardiac serotonin signaling and lead to small left heart syndrome in the absence of maternal psychopathology. C57BL/6 adult female mice received sertraline (5 mg/kg/d IP) or saline throughout pregnancy to time of delivery. Pups maintained exposure on postnatal days 1-14 to encompass the developmental window analogous to human gestation...
April 25, 2017: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/28455218/age-dependent-functional-crosstalk-between-cardiac-fibroblasts-and-cardiomyocytes-in-a-3d-engineered-cardiac-tissue
#19
Yanzhen Li, Huda Asfour, Nenad Bursac
Complex heterocellular interactions between cardiomyocytes and fibroblasts in the heart involve their bidirectional signaling via cell-cell contacts, paracrine factors, and extracellular matrix (ECM). These interactions vary with heart development and pathology leading to changes in cardiac structure and function. Whether cardiac fibroblasts of different ages interact differentially with cardiomyocytes to distinctly impact their function remains unknown. Here, we explored the direct structural and functional effects of fetal and adult cardiac fibroblasts on cardiomyocytes using a tissue-engineered 3D co-culture system...
June 2017: Acta Biomaterialia
https://www.readbyqxmd.com/read/28378126/global-transcriptomic-analysis-of-induced-cardiomyocytes-predicts-novel-regulators-for-direct-cardiac-reprogramming
#20
Mahmood Talkhabi, Seyed Morteza Razavi, Ali Salari
Heart diseases are the most significant cause of morbidity and mortality in the world. De novo generated cardiomyocytes (CMs) are a great cellular source for cell-based therapy and other potential applications. Direct cardiac reprogramming is the newest method to produce CMs, known as induced cardiomyocytes (iCMs). During a direct cardiac reprogramming, also known as transdifferentiation, non-cardiac differentiated adult cells are reprogrammed to cardiac identity by forced expression of cardiac-specific transcription factors (TFs) or microRNAs...
June 2017: Journal of Cell Communication and Signaling
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