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adult cardiomyocyte proliferation

Cheng Sun, Maria I Kontaridis
The heart is one of the first organs to form and function during embryonic development. It is comprised of multiple cell lineages, each integral for proper cardiac development, and include cardiomyocytes, endothelial cells, epicardial cells and neural crest cells. The molecular mechanisms regulating cardiac development and morphogenesis are dependent on signaling crosstalk between multiple lineages through paracrine interactions, cell-ECM interactions, and cell-cell interactions, which together, help facilitate survival, growth, proliferation, differentiation and migration of cardiac tissue...
February 2018: Current Opinion in Physiology
Tamer M A Mohamed, Yen-Sin Ang, Ethan Radzinsky, Ping Zhou, Yu Huang, Arye Elfenbein, Amy Foley, Sergey Magnitsky, Deepak Srivastava
Human diseases are often caused by loss of somatic cells that are incapable of re-entering the cell cycle for regenerative repair. Here, we report a combination of cell-cycle regulators that induce stable cytokinesis in adult post-mitotic cells. We screened cell-cycle regulators expressed in proliferating fetal cardiomyocytes and found that overexpression of cyclin-dependent kinase 1 (CDK1), CDK4, cyclin B1, and cyclin D1 efficiently induced cell division in post-mitotic mouse, rat, and human cardiomyocytes...
February 22, 2018: Cell
Konstantina-Ioanna Sereti, Ngoc B Nguyen, Paniz Kamran, Peng Zhao, Sara Ranjbarvaziri, Shuin Park, Shan Sabri, James L Engel, Kevin Sung, Rajan P Kulkarni, Yichen Ding, Tzung K Hsiai, Kathrin Plath, Jason Ernst, Debashis Sahoo, Hanna K A Mikkola, M Luisa Iruela-Arispe, Reza Ardehali
The cellular mechanisms driving cardiac tissue formation remain poorly understood, largely due to the structural and functional complexity of the heart. It is unclear whether newly generated myocytes originate from cardiac stem/progenitor cells or from pre-existing cardiomyocytes that re-enter the cell cycle. Here, we identify the source of new cardiomyocytes during mouse development and after injury. Our findings suggest that cardiac progenitors maintain proliferative potential and are the main source of cardiomyocytes during development; however, the onset of αMHC expression leads to reduced cycling capacity...
February 21, 2018: Nature Communications
Raphael F P Castellan, Marco Meloni
While a regenerative response is limited in the mammalian adult heart, it has been recently shown that the neonatal mammalian heart possesses a marked but transient capacity for regeneration after cardiac injury, including myocardial infarction. These findings evidence that the mammalian heart still retains a regenerative capacity and highlights the concept that the expression of distinct molecular switches (that activate or inhibit cellular mechanisms regulating tissue development and regeneration) vary during different stages of life, indicating that cardiac regeneration is an age-dependent process...
2018: Frontiers in Cardiovascular Medicine
Wei Huang, Yuliang Feng, Jialiang Liang, Hao Yu, Cheng Wang, Boyu Wang, Mingyang Wang, Lin Jiang, Wei Meng, Wenfeng Cai, Mario Medvedovic, Jenny Chen, Christian Paul, W Sean Davidson, Sakthivel Sadayappan, Peter J Stambrook, Xi-Yong Yu, Yigang Wang
The goal of replenishing the cardiomyocyte (CM) population using regenerative therapies following myocardial infarction (MI) is hampered by the limited regeneration capacity of adult CMs, partially due to their withdrawal from the cell cycle. Here, we show that microRNA-128 (miR-128) is upregulated in CMs during the postnatal switch from proliferation to terminal differentiation. In neonatal mice, cardiac-specific overexpression of miR-128 impairs CM proliferation and cardiac function, while miR-128 deletion extends proliferation of postnatal CMs by enhancing expression of the chromatin modifier SUZ12, which suppresses p27 (cyclin-dependent kinase inhibitor) expression and activates the positive cell cycle regulators Cyclin E and CDK2...
February 16, 2018: Nature Communications
Esther Aix, Alex Gallinat, Ignacio Flores
Although recent advances have overturned the old view of the human heart as an inert postmitotic organ, it is clear that the adult heart´s capacity to regenerate after an ischemic episode is very limited. Unlike humans, zebrafish and other lower vertebrates vigorously regenerate damaged myocardium after cardiac injury. Understanding how the zebrafish is able to conserve life-long cardiac regeneration capacity while mammals lose it soon after birth is crucial for the development of new treatments for myocardial infarction...
February 3, 2018: Differentiation; Research in Biological Diversity
Lichan Tao, Yihua Bei, Yongqin Li, Junjie Xiao
Cardiomyocytes loss is a major contributor for many cardiovascular diseases including heart failure and myocardial infarction. Although extremely limited, adult cardiomyocytes are able to proliferate. Understanding the molecular mechanisms controlling cardiomyocytes proliferation is extremely important for enhancing cardiomyocyte proliferation to promote cardiac regeneration and repair. MicroRNAs (miRNAs, miRs) are powerful controllers of many essential biological processes including cell proliferation. Here, we described in detail a protocol for isolation and culture of neonatal rat cardiomyocytes and the determination of miRNAs' effects in proliferation based on two well-established methods including EdU and Ki67 immunofluorescent stainings...
2018: Methods in Molecular Biology
Shuai Nie, Xin Wang, Priyadharshini Sivakumaran, Mark M W Chong, Xin Liu, Tara Karnezis, Nadeeka Bandara, Kaloyan Takov, Cameron J Nowell, Stephen Wilcox, Mitch Shambrook, Andrew F Hill, Nicole C Harris, Andrew E Newcomb, Padraig Strappe, Ramin Shayan, Damián Hernández, Jordan Clarke, Eric Hanssen, Sean M Davidson, Gregory J Dusting, Alice Pébay, Joshua W K Ho, Nicholas Williamson, Shiang Y Lim
The benefits of adult stem cells for repair of the heart have been attributed to the repertoire of salutary paracrine activities they appear to exert. We previously isolated human W8B2+ cardiac stem cells (CSCs) and found they powerfully influence cardiomyocytes and endothelial cells to collectively promote cardiac repair and regeneration. Here, the complexity of the W8B2+ CSC secretomes was characterised and examined in more detail. Using ion exchange chromatography to separate soluble proteins based on their net surface charge, the secreted factors responsible for the pro-survival activity of W8B2+ CSCs were found within the low and medium cation fractions...
January 25, 2018: Scientific Reports
Fan Qiu, Hao Zhang, Yanliang Yuan, Zhiwei Liu, Bing Huang, Haoran Miao, Xiucheng Liu, Qixiang Zhao, Hu Zhang, Hongyan Dong, Zhongming Zhang
AIMS: The activated AMP activated protein kinase (AMPK) serves as a transient protective cardiovascular kinase via preserving adenosine triphosphate (ATP) production under ischemic conditions. However, recent studies reveal that inhibition of AMPK in stroke is neuroprotection. Pigment epithelium derived factor (PEDF) is also known for the protection of ischemic cardiomyocytes. However, the relationship between PEDF and AMPK in cardiomyocytes is poorly understood. METHODS AND RESULTS: Rat neonatal and adult left ventricular cardiomyocytes were isolated and subjected to oxygen-glucose deprivation (OGD)...
January 17, 2018: International Journal of Cardiology
Niranjana Natarajan, Yamen Abbas, Donald M Bryant, Juan Manuel Gonzalez-Rosa, Michka Sharpe, Aysu Uygur, Lucas H Cocco-Delgado, Nhi Ngoc Ho, Norma P Gerard, Craig J Gerard, Calum A Macrae, Caroline E Burns, C Geoffrey Burns, Jessica L Whited, Richard T Lee
Background -Defining conserved molecular pathways in animal models of successful cardiac regeneration could yield insight into why adult mammals have inadequate cardiac regeneration after injury. Insight into the transcriptomic landscape of early cardiac regeneration from model organisms will shed light on evolutionarily conserved pathways in successful cardiac regeneration. Methods -Here we describe a cross-species transcriptomic screen in three model organisms for cardiac regeneration -axolotl, neonatal mice and zebrafish...
January 18, 2018: Circulation
Min Yee, Ethan David Cohen, William Domm, George A Porter, Andrew N McDavid, Michael A O'Reilly
Supplemental oxygen given to preterm infants has been associated with permanently altering postnatal lung development. Now that these individuals are reaching adulthood, there is growing concern that early-life oxygen exposure may also promote cardiovascular disease through poorly understood mechanisms. We previously reported that adult mice exposed to 100% oxygen between postnatal days 0-4 develop pulmonary hypertension defined pathologically by capillary rarefaction, dilation of arterioles and veins, cardiac failure, and a reduced lifespan...
January 18, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
Zhidan Chen, Yang Li, Ying Wang, Juying Qian, Hong Ma, Xiang Wang, Guoliang Jiang, Ming Liu, Yanpeng An, Leilei Ma, Le Kang, Jianguo Jia, Chunjie Yang, Guoping Zhang, Ying Chen, Wei Gao, Mingqiang Fu, Zheyong Huang, Huiru Tang, Yichun Zhu, Junbo Ge, Hui Gong, Yunzeng Zou
Low density lipoprotein receptor-related protein 6 (LRP6), a wnt co-receptor, regulates multiple functions in various organs. However, the roles of LRP6 in the adult heart are not well understood. Methods: We observed LRP6 expression in heart with end-stage dilated cardiomyopathy (DCM) by western blot. Tamoxifen-inducible cardiac-specific LRP6 knockout mouse was constructed. Hemodynamic and echocardiographic analyses were performed to these mice. Results: Cardiac LRP6 expression was dramatically decreased in patients with end-stage dilated cardiomyopathy (DCM) compared to control group...
2018: Theranostics
Ingrid Fomison-Nurse, Eugene Eng Leng Saw, Sophie Gandhi, Pujika Emani Munasinghe, Isabelle Van Hout, Michael J A Williams, Ivor Galvin, Richard Bunton, Philip Davis, Vicky Cameron, Rajesh Katare
Increased apoptosis and premature cellular ageing of the diabetic heart underpin the development of diabetic heart disease. The molecular mechanisms underlying these pathologies are still unclear. Here we determined the role of pro-senescence microRNA (miR)-34a in accelerating the ageing of the diabetic heart. RT-PCR analysis showed a significant increase in the level of circulating miR-34a from early stages in asymptomatic type-2 diabetic individuals compared to non-diabetic controls. We also observed significant upregulation of miR-34a in the type-2 human diabetic heart suggesting circulating miR-34a may be cardiac in origin...
January 4, 2018: Cell Death and Differentiation
L M Reyes, A Shah, A Quon, J S Morton, S T Davidge
Exposure to prenatal hypoxia in rats leads to intrauterine growth restriction (IUGR), decreases fetal cardiomyocyte proliferation and increases the risk to develop cardiovascular diseases (CVD) later in life. The tumor necrosis factor-related weak inducer of apoptosis (TWEAK) induces cardiomyocyte proliferation through activation of the fibroblast growth factor-inducible molecule 14 (Fn-14) receptor. The TWEAK/Fn-14 pathway becomes quiescent shortly after birth, however, it becomes upregulated with CVD; suggesting that it could be a link between the increased susceptibility to CVD in pregnancies complicated by hypoxia/IUGR...
December 18, 2017: Journal of Developmental Origins of Health and Disease
Tien-Jui Tsang, Ying-Chang Hsueh, Erika I Wei, David J Lundy, Bill Cheng, You-Tzung Chen, Shoei-Shen Wang, Patrick C H Hsieh
Rationale: Reducing cardiomyocyte death and enhancing their proliferation after myocardial infarction is perhaps the single largest challenge for cardiac tissue regeneration. Survivin (SVV) is the smallest member of the inhibitor of apoptosis (IAP) family but plays two important roles; inhibiting caspase-9 activation in the intrinsic apoptosis pathway, and regulating microtubule dynamics and chromosome segregation during cell division. Genetic depletion of cardiac SVV leads to incomplete cardiomyocyte division and abnormal heart development...
2017: Theranostics
Suphansa Sawamiphak, Zacharias Kontarakis, Alessandro Filosa, Sven Reischauer, Didier Y R Stainier
Cells can sacrifice their individuality by fusing, but the prevalence and significance of this process are poorly understood. To approach these questions, here we generate transgenic reporter lines in zebrafish to label and specifically ablate fused cells. In addition to skeletal muscle cells, the reporters label cardiomyocytes starting at an early developmental stage. Genetic mosaics generated by cell transplantation show cardiomyocytes expressing both donor- and host-derived transgenes, confirming the occurrence of fusion in larval hearts...
November 15, 2017: Nature Communications
H R Ahmad, Satwat Hashmi
The stem cells keep us young by endogenously repairing us upon need. They do so bysmartly one step forward towards differentiation while another step backward to nurturethe undifferentiated stem cells. They are building blocks for every organ witha differential rate of repair of worn out tissues. Since stem cells can be cultured with a normal karyo type, they could be the ideal source for heart repair after myocardial infarction. As opposed to lower vertebrates and neonatal mice, cardiac regeneration in adult mammalian heart seems to be difficult to assess with a solid evidence of cytokinesis...
July 2017: Pakistan Journal of Medical Sciences Quarterly
Paula A da Costa Martins
Reporting in Nature Genetics, Patterson et al. (2017) show that adult mammalian hearts possess an innate capacity to regenerate, which depends on a small population of mononuclear diploid cardiomyocytes. These cells undergo karyokinesis and cytokinesis, raising the possibility that endogenous cardiac muscle cells can be stimulated to proliferate for myocardial repair.
October 5, 2017: Cell Stem Cell
John P Leach, Todd Heallen, Min Zhang, Mahdis Rahmani, Yuka Morikawa, Matthew C Hill, Ana Segura, James T Willerson, James F Martin
Mammalian organs vary widely in regenerative capacity. Poorly regenerative organs, such as the heart are particularly vulnerable to organ failure. Once established, heart failure commonly results in mortality. The Hippo pathway, a kinase cascade that prevents adult cardiomyocyte proliferation and regeneration, is upregulated in human heart failure. Here we show that deletion of the Hippo pathway component Salvador (Salv) in mouse hearts with established ischaemic heart failure after myocardial infarction induces a reparative genetic program with increased scar border vascularity, reduced fibrosis, and recovery of pumping function compared with controls...
October 12, 2017: Nature
Mohammed Arif, Raghav Pandey, Perwez Alam, Shujia Jiang, Sakthivel Sadayappan, Arghya Paul, Rafeeq P H Ahmed
An innovative approach for cardiac regeneration following injury is to induce endogenous cardiomyocyte (CM) cell cycle re-entry. In the present study, CMs from adult rat hearts were isolated and transfected with cel-miR-67 (control) and rno-miR-210. A significant increase in CM proliferation and mono-nucleation were observed in miR-210 group, in addition to a reduction in CM size, multi-nucleation, and cell death. When compared to control, β-catenin and Bcl-2 were upregulated while APC (adenomatous polyposis coli), p16, and caspase-3 were downregulated in miR-210 group...
December 2017: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
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