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adult cardiomyocyte proliferation

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https://www.readbyqxmd.com/read/28104772/the-elusive-progenitor-cell-in-cardiac-regeneration-slip-slidin-away
#1
REVIEW
Chen-Leng Cai, Jeffery D Molkentin
The adult human heart is unable to regenerate after various forms of injury, suggesting that this organ lacks a biologically meaningful endogenous stem cell pool. However, injecting the infarcted area of the adult mammalian heart with exogenously prepared progenitor cells of various types has been reported to create new myocardium by the direct conversion of these progenitor cells into cardiomyocytes. These reports remain controversial because follow-up studies from independent laboratories failed to observe such an effect...
January 20, 2017: Circulation Research
https://www.readbyqxmd.com/read/28087623/a-p53-based-genetic-tracing-system-to-follow-postnatal-cardiomyocyte-expansion-in-heart-regeneration
#2
Qi Xiao, Guoxin Zhang, Huijuan Wang, Lai Chen, Shuangshuang Lu, Dejing Pan, Geng Liu, Zhongzhou Yang
For heart regeneration, the proliferative potential of cardiomyocytes in postnatal mice is under intense investigations. However, solely relying on immunostaining of proliferation markers, the long term proliferation dynamics and potential of the cardiomyocytes cannot be readily addressed. Previously, we found that a p53 promoter driving reporter predominantly marked the proliferating lineages in mice. Here, we established a p53 based genetic tracing system to investigate postnatal cardiomyocyte proliferation and heart regeneration...
January 13, 2017: Development
https://www.readbyqxmd.com/read/28077821/ascending-aortic-constriction-promotes-cardiomyocyte-proliferation-in-neonatal-rats
#3
Zhenhua Wang, Sebastian Schmull, Hui Zheng, Jianggui Shan, Rongjiang Zou, Song Xue
Adult heart suffering from increased workload will undergo myocardial hypertrophy, subsequent cardiomyocyte (CM) death, and eventually heart failure. However, the effect of increasing afterload on the neonatal heart remains unknown. We performed ascending aortic constriction (AAC) in neonatal rats 8-12 hours after birth (P0, P indicates postpartum). Seven days after surgery, in vivo heart function was evaluated using cardiac ultrasonography. Haematoxylineosin and Masson staining were used to assess CM diameter and collagen deposition...
January 11, 2017: International Heart Journal
https://www.readbyqxmd.com/read/28063988/engineered-extracellular-microenvironment-with-a-tunable-mechanical-property-for-controlling-cell-behavior-and-cardiomyogenic-fate-of-cardiac-stem-cells
#4
Min-Young Choi, Jong-Tae Kim, Won-Jin Lee, Yunki Lee, Kyung Min Park, Young-Il Yang, Ki Dong Park
: Endogenous cardiac stem cells (CSCs) are known to play a certain role in the myocardial homeostasis of the adult heart. The extracellular matrix (ECM) surrounding CSCs provides mechanical signals to regulate a variety of cell behaviors, yet the impact in the adult heart of these mechanical properties of ECM on CSC renewal and fate decisions is mostly unknown. To elucidate CSC mechanoresponses at the individual cell and myocardial level, we used the sol-to-gel transitional gelatin-poly(ethylene glycol)-tyramine (GPT) hydrogel with a tunable mechanical property to construct a three-dimensional (3D) matrix for culturing native myocardium and CSCs...
January 4, 2017: Acta Biomaterialia
https://www.readbyqxmd.com/read/28018900/redox-regulation-of-heart-regeneration-an-evolutionary-tradeoff
#5
Waleed M Elhelaly, Nicholas T Lam, Mohamed Hamza, Shuda Xia, Hesham A Sadek
Heart failure is a costly and deadly disease, affecting over 23 million patients worldwide, half of which die within 5 years of diagnosis. The pathophysiological basis of heart failure is the inability of the adult heart to regenerate lost or damaged myocardium. Although limited myocyte turnover does occur in the adult heart, it is insufficient for restoration of contractile function (Nadal-Ginard, 2001; Laflamme et al., 2002; Quaini et al., 2002; Hsieh et al., 2007; Bergmann et al., 2009, 2012). In contrast to lower vertebrates (Poss et al...
2016: Frontiers in Cell and Developmental Biology
https://www.readbyqxmd.com/read/27941320/necroptosis-induced-by-ad-hgf-activates-endogenous-c-kit-cardiac-stem-cells-and-promotes-cardiomyocyte-proliferation-and-angiogenesis-in-the-infarcted-aged-heart
#6
Jiabao Liu, Peng Wu, Hao Wang, Yunle Wang, Yingqiang Du, Weili Cheng, Zhihui Xu, Ningtian Zhou, Liansheng Wang, Zhijian Yang
BACKGROUND/AIMS: The discovery of c-kit+ cardiac stem cells (CSCs) provided us with new therapeutic targets to repair the damaged heart. However, the precise mechanisms regulating CSC proliferation and differentiation in the aged heart remained elusive. Necroptosis, a type of regulated cell death, has recently been shown to occur following myocardial infarction (MI); however, its effect on c-kit+ CSCs remains unknown. We investigated the effects of hepatocyte growth factor (HGF) and necroptosis on the proliferation and differentiation of endogenous c-kit+ CSCs in aged rat hearts following MI...
2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27929112/chromatin-remodelling-factor-brg1-regulates-myocardial-proliferation-and-regeneration-in-zebrafish
#7
Chenglu Xiao, Lu Gao, Yu Hou, Congfei Xu, Nannan Chang, Fang Wang, Keping Hu, Aibin He, Ying Luo, Jun Wang, Jinrong Peng, Fuchou Tang, Xiaojun Zhu, Jing-Wei Xiong
The zebrafish possesses a remarkable capacity of adult heart regeneration, but the underlying mechanisms are not well understood. Here we report that chromatin remodelling factor Brg1 is essential for adult heart regeneration. Brg1 mRNA and protein are induced during heart regeneration. Transgenic over-expression of dominant-negative Xenopus Brg1 inhibits the formation of BrdU(+)/Mef2C(+) and Tg(gata4:EGFP) cardiomyocytes, leading to severe cardiac fibrosis and compromised myocardial regeneration. RNA-seq and RNAscope analyses reveal that inhibition of Brg1 increases the expression of cyclin-dependent kinase inhibitors such as cdkn1a and cdkn1c in the myocardium after ventricular resection; and accordingly, myocardial-specific expression of dn-xBrg1 blunts myocardial proliferation and regeneration...
December 8, 2016: Nature Communications
https://www.readbyqxmd.com/read/27882462/proliferative-potential-of-cardiomyocytes-in-hypertrophic-cardiomyopathy-correlation-with-myocardial-remodeling
#8
T V Sukhacheva, Yu A Chudinovskikh, M V Eremeeva, R A Serov, L A Bockeria
Proliferating Ki-67(+) cardiomyocytes were detected in the interventricular septum myocardium of adult patients with hypertrophic cardiomyopathy. In the same patients, the severity of hypertrophy and the degree of cardiomyocyte differentiation were assessed by the content of myofibrils, ultrastructural morphology, and the pattern of connexin 43-containing gap junction distribution. Adult Ki-67(+) cardiomyocytes containing sarcomeric α-actin (sarc α-act(+)) in the sarcoplasm (diameter 23.9±6.9 μ) were detected in the myocardium of patients with hypertrophic cardiomyopathy; their relative content varied from 2 to 3084 cells per 1 million cardiomyocytes...
November 2016: Bulletin of Experimental Biology and Medicine
https://www.readbyqxmd.com/read/27875683/redox-paradox-can-hypoxia-heal-ischemic-hearts
#9
Nuno Guimarães-Camboa, Sylvia M Evans
Adult cardiomyocytes are largely thought to lack proliferative and therefore regenerative potential. Reporting in Nature, Nakada et al. (2016) find that a hypoxic regime reduces mitochondrial metabolism and promotes proliferation in adult mouse cardiomyocytes, resulting in increased regeneration following myocardial infarction. These findings suggest the potential to transform post-MI care.
November 21, 2016: Developmental Cell
https://www.readbyqxmd.com/read/27872447/evolving-approaches-to-heart-regeneration-by-therapeutic-stimulation-of-resident-cardiomyocyte-cell-cycle
#10
Raife Dilek Turan, Galip Servet Aslan, Doğacan Yücel, Remziye Döğer, Fatih Kocabaş
Heart has long been considered a terminally differentiated organ. Recent studies, however, have suggested that there is a modest degree of cardiomyocyte (CM) turnover in adult mammalian heart, albeit not sufficient for replacement of lost CMs following cardiac injuries. Cardiac regeneration studies in various model organisms including zebrafish, newt, and more recently in neonatal mouse, have demonstrated that CM dedifferentiation and concomitant proliferation play important roles in replacement of lost CMs and restoration of cardiac contractility...
November 2016: Anatolian Journal of Cardiology
https://www.readbyqxmd.com/read/27832814/obesity-induced-cardiac-lipid-accumulation-in-adult-mice-is-modulated-by-g-protein-coupled-receptor-kinase-2-levels
#11
Elisa Lucas, Rocio Vila-Bedmar, Alba C Arcones, Marta Cruces-Sande, Victoria Cachofeiro, Federico Mayor, Cristina Murga
BACKGROUND: The leading cause of death among the obese population is heart failure and stroke prompted by structural and functional changes in the heart. The molecular mechanisms that underlie obesity-related cardiac remodeling are complex, and include hemodynamic and metabolic alterations that ultimately affect the functionality of the myocardium. G protein-coupled receptor kinase 2 (GRK2) is an ubiquitous kinase able to desensitize the active form of several G protein-coupled receptors (GPCR) and is known to play an important role in cardiac GPCR modulation...
November 10, 2016: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/27812722/cardiomyocyte-proliferation-in-zebrafish-and-mammals-lessons-for-human-disease
#12
REVIEW
Gianfranco Matrone, Carl S Tucker, Martin A Denvir
Cardiomyocytes proliferate profusely during early development and for a brief period after birth in mammals. Within a month after birth, this proliferative capability is dramatically reduced in mammals unlike lower vertebrates where it persists into adult life. The zebrafish, for example, retains the ability to regenerate the apex of the heart following resection by a mechanism predominantly driven by cardiomyocyte proliferation. Differences in proliferative capacity of cardiomyocytes in adulthood between mammals and lower vertebrates are closely liked to ontogenetic or phylogenetic factors...
November 3, 2016: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/27799944/repair-injured-heart-by-regulating-cardiac-regenerative-signals
#13
REVIEW
Wen-Feng Cai, Guan-Sheng Liu, Lei Wang, Christian Paul, Zhi-Li Wen, Yigang Wang
Cardiac regeneration is a homeostatic cardiogenic process by which the sections of malfunctioning adult cardiovascular tissues are repaired and renewed employing a combination of both cardiomyogenesis and angiogenesis. Unfortunately, while high-quality regeneration can be performed in amphibians and zebrafish hearts, mammalian hearts do not respond in kind. Indeed, a long-term loss of proliferative capacity in mammalian adult cardiomyocytes in combination with dysregulated induction of tissue fibrosis impairs mammalian endogenous heart regenerative capacity, leading to deleterious cardiac remodeling at the end stage of heart failure...
2016: Stem Cells International
https://www.readbyqxmd.com/read/27798600/hypoxia-induces-heart-regeneration-in-adult-mice
#14
Yuji Nakada, Diana C Canseco, SuWannee Thet, Salim Abdisalaam, Aroumougame Asaithamby, Celio X Santos, Ajay M Shah, Hua Zhang, James E Faber, Michael T Kinter, Luke I Szweda, Chao Xing, Zeping Hu, Ralph J Deberardinis, Gabriele Schiattarella, Joseph A Hill, Orhan Oz, Zhigang Lu, Cheng Cheng Zhang, Wataru Kimura, Hesham A Sadek
The adult mammalian heart is incapable of regeneration following cardiomyocyte loss, which underpins the lasting and severe effects of cardiomyopathy. Recently, it has become clear that the mammalian heart is not a post-mitotic organ. For example, the neonatal heart is capable of regenerating lost myocardium, and the adult heart is capable of modest self-renewal. In both of these scenarios, cardiomyocyte renewal occurs via the proliferation of pre-existing cardiomyocytes, and is regulated by aerobic-respiration-mediated oxidative DNA damage...
January 12, 2017: Nature
https://www.readbyqxmd.com/read/27752085/myc-overexpression-enhances-of-epicardial-contribution-to-the-developing-heart-and-promotes-extensive-expansion-of-the-cardiomyocyte-population
#15
Cristina Villa Del Campo, Ghislaine Lioux, Rita Carmona, Rocío Sierra, Ramón Muñoz-Chápuli, Cristina Clavería, Miguel Torres
Myc is an essential regulator of cell growth and proliferation. Myc overexpression promotes the homeostatic expansion of cardiomyocyte populations by cell competition, however whether this applies to other cardiac lineages remains unknown. The epicardium contributes signals and cells to the developing and adult injured heart and exploring strategies for modulating its activity is of great interest. Using inducible genetic mosaics, we overexpressed Myc in the epicardium and determined the differential expansion of Myc-overexpressing cells with respect to their wild type counterparts...
October 18, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27695872/understanding-cardiomyocyte-proliferation-an-insight-into-cell-cycle-activity
#16
Murugavel Ponnusamy, Pei-Feng Li, Kun Wang
Cardiomyocyte proliferation and regeneration are key to the functional recovery of myocardial tissue from injury. In the recent years, studies on cardiomyocyte proliferation overturned the traditional belief that adult cardiomyocytes permanently withdraw from the cell cycle activity. Hence, targeting cardiomyocyte proliferation is one of the potential therapeutic strategies for myocardial regeneration and repair. To achieve this, a deep understanding of the fundamental mechanisms involved in cardiomyocyte cell cycle as well as differences between neonatal and adult cardiomyocytes' cell cycle activity is required...
September 30, 2016: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/27694478/role-of-fen1-s187-phosphorylation-in-counteracting-oxygen-induced-stress-and-regulating-postnatal-heart-development
#17
Lina Zhou, Huifang Dai, Jian Wu, Mian Zhou, Hua Yuan, Juan Du, Lu Yang, Xiwei Wu, Hong Xu, Yuejin Hua, Jian Xu, Li Zheng, Binghui Shen
Flap endonuclease 1 (FEN1) phosphorylation is proposed to regulate the action of FEN1 in DNA repair as well as Okazaki fragment maturation. However, the biologic significance of FEN1 phosphorylation in response to DNA damage remains unknown. Here, we report an in vivo role for FEN1 phosphorylation, using a mouse line carrying S187A FEN1, which abolishes FEN1 phosphorylation. Although S187A mouse embryonic fibroblast cells showed normal proliferation under low oxygen levels (2%), the mutant cells accumulated oxidative DNA damage, activated DNA damage checkpoints, and showed G1-phase arrest at atmospheric oxygen levels (21%)...
January 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27689781/poly-3-hydroxyoctanoate-a-promising-new-material-for-cardiac-tissue-engineering
#18
Andrea V Bagdadi, Maryam Safari, Prachi Dubey, Pooja Basnett, Panagiotis Sofokleous, Eleanor Humphrey, Ian Locke, Mohan Edirisinghe, Cesare Terracciano, Aldo R Boccaccini, Jonathan C Knowles, Sian E Harding, Ipsita Roy
Cardiac tissue engineering (CTE) is currently a prime focus of research due to an enormous clinical need. In this work, a novel functional material, Poly(3-hydroxyoctanoate), P(3HO), a medium chain length polyhydroxyalkanoate (PHA), produced using bacterial fermentation, was studied as a new potential material for CTE. Engineered constructs with improved mechanical properties, crucial for supporting the organ during new tissue regeneration, and enhanced surface topography, to allow efficient cell adhesion and proliferation, were fabricated...
September 30, 2016: Journal of Tissue Engineering and Regenerative Medicine
https://www.readbyqxmd.com/read/27622691/single-cell-transcriptome-and-epigenomic-reprogramming-of-cardiomyocyte-derived-cardiac-progenitor-cells
#19
COMMENT
Xin Chen, Tushar Chakravarty, Yiqiang Zhang, Xiaojin Li, Jiang F Zhong, Charles Wang
The molecular basis underlying the dedifferentiation of mammalian adult cardiomyocytes (ACMs) into myocyte-derived cardiac progenitor cells (mCPCs) during cardiac tissue regeneration is poorly understood. We present data integrating single-cell transcriptome and whole-genome DNA methylome analyses of mouse mCPCs to understand the epigenomic reprogramming governing their intrinsic cellular plasticity. Compared to parental cardiomyocytes, mCPCs display epigenomic reprogramming with many differentially-methylated regions, both hypermethylated and hypomethylated, across the entire genome...
September 13, 2016: Scientific Data
https://www.readbyqxmd.com/read/27599529/heart-development-diseases-and-regeneration%C3%A3-new-approaches-from-innervation-fibroblasts-and-reprogramming
#20
Masaki Ieda
It is well known that cardiac function is tightly controlled by neural activity; however, the molecular mechanism of cardiac innervation during development and the relationship with heart disease remain undetermined. My work has revealed the molecular networks that govern cardiac innervation and its critical roles in heart diseases such as silent myocardial ischemia and arrhythmias. Cardiomyocytes proliferate during embryonic development, but lose their proliferative capacity after birth. Cardiac fibroblasts are a major source of cells during fibrosis and induce cardiac hypertrophy after myocardial injury in the adult heart...
September 23, 2016: Circulation Journal: Official Journal of the Japanese Circulation Society
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