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Cardiomyocyte turn over

David A Knowles, Courtney K Burrows, John D Blischak, Kristen M Patterson, Daniel J Serie, Nadine Norton, Carole Ober, Jonathan K Pritchard, Yoav Gilad
Anthracycline-induced cardiotoxicity (ACT) is a key limiting factor in setting optimal chemotherapy regimes, with almost half of patients expected to develop congestive heart failure given high doses. However, the genetic basis of sensitivity to anthracyclines remains unclear. We created a panel of iPSC-derived cardiomyocytes from 45 individuals and performed RNA-seq after 24h exposure to varying doxorubicin dosages. The transcriptomic response is substantial: the majority of genes are differentially expressed and over 6000 genes show evidence of differential splicing, the later driven by reduced splicing fidelity in the presence of doxorubicin...
May 8, 2018: ELife
Shuang Qu, Chunyu Zeng, Wei Eric Wang
It is acknowledged that postnatal mammalian cardiomyocytes (CMs) turn over with a very limited efficacy in both physiological and pathological conditions. Recent studies showed that those newly formed CMs are derived from preexisting CMs. Thus, stimulating CM proliferation becomes a promising strategy for inducing cardiac regeneration. Noncoding RNAs were found differently expressed in CMs with different proliferation potential. Moreover, manipulation of noncoding RNAs, in particular microRNAs, was proved to promote or suppress CM proliferation, indicating that noncoding RNAs are involved in the underlying mechanism of CM proliferation...
2017: Stem Cells International
Ting Wang, Jian Liu, Caitlin McDonald, Katherine Lupino, Xiandun Zhai, Benjamin J Wilkins, Hakon Hakonarson, Liming Pei
The endocrine system is crucial for maintaining whole-body homeostasis. Little is known regarding endocrine hormones secreted by the heart other than atrial/brain natriuretic peptides discovered over 30 years ago. Here, we identify growth differentiation factor 15 (GDF15) as a heart-derived hormone that regulates body growth. We show that pediatric heart disease induces GDF15 synthesis and secretion by cardiomyocytes. Circulating GDF15 in turn acts on the liver to inhibit growth hormone (GH) signaling and body growth...
August 2017: EMBO Molecular Medicine
Sofia-Iris Bibli, Zongmin Zhou, Sven Zukunft, Beate Fisslthaler, Ioanna Andreadou, Csaba Szabo, Peter Brouckaert, Ingrid Fleming, Andreas Papapetropoulos
Aims: Endothelial nitric oxide (NO) synthase (eNOS) is known to play a cardioprotective protective. However, the molecular mechanisms regulating eNOS activity during ischaemia/reperfusion (I/R) injury are incompletely understood. eNOS is a substrate for several kinases that positively or negatively affect its enzymatic activity. Herein, we sought to correlate eNOS phosphorylation status with cardiomyocyte survival and we investigated the contribution of the proline-rich tyrosine kinase 2 (PYK2)/eNOS axis to the regulation of myocardial infarct size in vivo...
July 1, 2017: Cardiovascular Research
Yan-Ting Zhao, Yun-Bo Guo, Lei Gu, Xue-Xin Fan, Hua-Qian Yang, Zheng Chen, Peng Zhou, Qi Yuan, Guang-Ju Ji, Shi-Qiang Wang
Aims: The heart contraction is controlled by the Ca2+-induced Ca2+ release (CICR) between L-type Ca2+ channels and ryanodine receptors (RyRs). The FK506-binding protein FKBP12.6 binds to RyR subunits, but its role in stabilizing RyR function has been debated for long. Recent reports of high-resolution RyR structure show that the HD2 domain that binds to the SPRY2 domain of neighbouring subunit in FKBP-bound RyR1 is detached and invisible in FKBP-null RyR2. The present study was to test the consequence of FKBP12...
March 1, 2017: Cardiovascular Research
Wassim A Basheer, Brett S Harris, Heather L Mentrup, Measho Abreha, Elizabeth L Thames, Jessica B Lea, Deborah A Swing, Neal G Copeland, Nancy A Jenkins, Robert L Price, Lydia E Matesic
Gap junctions (GJ) are intercellular channels composed of connexin subunits that play a critical role in a diverse number of cellular processes in all tissue types. In the heart, GJs mediate electrical coupling between cardiomyocytes and display mislocalization and/or downregulation in cardiac disease (a process known as GJ remodeling), producing an arrhythmogenic substrate. The main constituent of GJs in the ventricular myocardium is Connexin 43 (Cx43), an integral membrane protein that is rapidly turned over and shows decreased expression or function with age...
November 2015: Journal of Molecular and Cellular Cardiology
Zhi-Qiang Luo, Xing-Hai Hao, Jin-Hua Li, Jiang Dai, Ke-Ye Liu, Yong-Qiang Lai
OBJECTIVE: This study demonstrated left atrial endocardial dysfunction and platelet activation in patients with atrial fibrillation and mitral stenosis. METHODS: Study included 80 patients with mitral stenosis and atrial fibrillation (40 each with and without left atrial thrombosis), 15 healthy volunteers, and 10 left atrial appendage (LAA) specimens from donor hearts. Blood samples were collected through peripheral vein and left atrium, with peripheral blood samples of volunteers as controls...
November 2014: Journal of Thoracic and Cardiovascular Surgery
Ada Popolo, Silvana Morello, Rosalinda Sorrentino, Aldo Pinto
Connexin 43 (Cx43) is the major protein of cardiac ventricular gap junctions and is crucial to cell-cell communication and cardiac function. Several authors report that adrenergic stimulation affects Cx43 expression via protein kinase A (PKA) and MAPK-regulated pathways. Adenosine has been shown to exert direct antiadrenergic effects on the heart, protecting it from toxic effects of overstimulation. The aim of our study was to understand the involvement of Cx43 in the anti-adrenergic effect of adenosine on cardiomyocytes...
September 5, 2013: European Journal of Pharmacology
Nils Hersch, Benjamin Wolters, Georg Dreissen, Ronald Springer, Norbert Kirchgeßner, Rudolf Merkel, Bernd Hoffmann
Cardiomyocytes are responsible for the permanent blood flow by coordinated heart contractions. This vital function is accomplished over a long period of time with almost the same performance, although heart properties, as its elasticity, change drastically upon aging or as a result of diseases like myocardial infarction. In this paper we have analyzed late rat embryonic heart muscle cells' morphology, sarcomere/costamere formation and force generation patterns on substrates of various elasticities ranging from ∼1 to 500 kPa, which covers physiological and pathological heart stiffnesses...
March 15, 2013: Biology Open
Frédéric Bouchard, Joanne Paquin
All-trans-retinoic acid (atRA) is an essential signaling molecule in embryonic development. It regulates cell differentiation by activating nuclear retinoic acid receptors (RAR) and retinoid-X receptors (RXR), which both control gene expression. In addition, atRA could act in the cytoplasm by modulating the activity of mitogen-activated protein kinases (MAPK) ERK and p38, which also have a role in cell differentiation. AtRA can induce the differentiation of P19 embryonic carcinoma stem cells into adipocytes, cardiomyocytes, and skeletal muscle cells, concurrently, in the same culture...
July 15, 2013: Stem Cells and Development
Wei Pan, Yun Zhong, Chuanfang Cheng, Benrong Liu, Li Wang, Aiqun Li, Longgen Xiong, Shiming Liu
Dysregulated autophagy may lead to the development of disease. Role of autophagy and the diagnostic potential of microRNAs that regulate the autophagy in cardiac hypertrophy have not been evaluated. A rat model of cardiac hypertrophy was established using transverse abdominal aortic constriction (operation group). Cardiomyocyte autophagy was enhanced in rats from the operation group, compared with those in the sham operation group. Moreover, the operation group showed up-regulation of beclin-1 (an autophagy-related gene), and down-regulation of miR-30 in cardiac tissue...
2013: PloS One
Debapriya Dutta, Riccardo Calvani, Roberto Bernabei, Christiaan Leeuwenburgh, Emanuele Marzetti
The prevalence of cardiovascular disease increases with advancing age. Although long-term exposure to cardiovascular risk factors plays a major role in the etiopathogenesis of cardiovascular disease, intrinsic cardiac aging enhances the susceptibility to developing heart pathologies in late life. The progressive decline of cardiomyocyte mitochondrial function is considered a major mechanism underlying heart senescence. Damaged mitochondria not only produce less ATP but also generate increased amounts of reactive oxygen species and display a greater propensity to trigger apoptosis...
April 13, 2012: Circulation Research
Paras Kumar Mishra, Vishalakshi Chavali, Naira Metreveli, Suresh C Tyagi
The contribution of extracellular matrix (ECM) to stem cell survival and differentiation is unequivocal, and matrix metalloproteinase-9 (MMP9) induces ECM turn over; however, the role of MMP9 in the survival and differentiation of cardiac stem cells is unclear. We hypothesize that ablation of MMP9 enhances the survival and differentiation of cardiac stem cells into cardiomyocytes in diabetics. To test our hypothesis, Ins2(+/-) Akita, C57 BL/6J, and double knock out (DKO: Ins2(+/-)/MMP9(-/-)) mice were used...
March 2012: Canadian Journal of Physiology and Pharmacology
Yo Tanaka, Hiroto Akaike, Yasuhiko Sugii, Takehiko Kitamori
We established a confluent cardiomyocyte culture method using an 800-µm diameter cylindrical microchannel in this report. This was realized by introducing cardiomyocytes 2 times before and after turning over a microchip. The optimum condition was starting the flowing medium 2.0 h after seeding and flowing the medium at 1.0 µL/min. By applying this technology to a cardiomyocyte-based spherical heart pump device, one may develop self-fluid regulated devices that could be applied for implantable or circulation analysis device on a chip...
2011: Analytical Sciences: the International Journal of the Japan Society for Analytical Chemistry
Mounia Boulberdaa, Kyoji Urayama, Canan G Nebigil
Prokineticins (PK1 and PK2) are peptide hormones that exert their biological activity via two common G-protein-coupled receptors: prokineticin receptor (PKR) 1 and 2. Their physiology was originally explored mostly in the context of angiogenic actions in the reproductive tract and gut motility. Since autocrine and paracrine loops have been established between PK2 and PKR1 in the heart, in this review we focus on the PK2/PKR1 signalling in the functions of the heart and kidney. PKR1 signalling is required for cardiomyocyte survival and angiogenesis...
November 1, 2011: Cardiovascular Research
Myriam Iglewski, Joseph A Hill, Sergio Lavandero, Beverly A Rothermel
Sustained hypertension promotes structural, functional and metabolic remodeling of cardiomyocyte mitochondria. As long-lived, postmitotic cells, cardiomyocytes turn over mitochondria continuously to compensate for changes in energy demands and to remove damaged organelles. This process involves fusion and fission of existing mitochondria to generate new organelles and separate old ones for degradation via autophagy. Autophagy is a lysosome-dependent proteolytic pathway capable of processing cellular components, including organelles and protein aggregates...
December 2010: Current Hypertension Reports
O J Kemi, U Wisløff
One of the main outcomes of aerobic endurance exercise training is the improved maximal oxygen uptake, and this is pivotal to the improved work capacity that follows the exercise training. Improved maximal oxygen uptake in turn is at least partly achieved because exercise training increases the ability of the myocardium to produce a greater cardiac output. In healthy subjects, this has been demonstrated repeatedly over many decades. It has recently emerged that this scenario may also be true under conditions of an initial myocardial dysfunction...
August 2010: Acta Physiologica
Silvia Pérez López, Jesús Otero Hernández, Natalia Vázquez Moreno, Dolores Escudero Augusto, Francisco Alvarez Menéndez, Aurora Astudillo González
BACKGROUND: Brain death (BD) causes hemodynamic and neuroendocrine alterations including a catecholamine surge, which in turn causes histologic lesions in cardiac muscle such as contraction bands, focal mononuclear cell infiltrates and cardiomyocyte necrosis. These changes are likely to compromise heart function and could therefore also affect the graft response after heart transplantation. This study was designed to examine the catecholamine surge, the catecholamine release pattern and the histologic lesions traditionally described as characteristic of BD in hearts procured from BD donors...
August 2009: Journal of Heart and Lung Transplantation
Bernard Abrenica, Mohamed AlShaaban, Michael P Czubryt
Pathologic cardiac hypertrophy imposes a significant clinical burden on patients, yet the precise intracellular mechanisms responsible for its induction are only partially understood. We examined a potential role for AKAP121 to regulate cardiomyocyte hypertrophy, since recent reports have implicated other AKAPs in this process. We report here that knockdown of AKAP121 expression in isolated neonatal rat cardiomyocytes results in pronounced cellular hypertrophy. Loss of AKAP121 expression is associated with dephosphorylation and nuclear localization of NFATc3, a downstream effector of the hypertrophic phosphatase calcineurin...
May 2009: Journal of Molecular and Cellular Cardiology
Olaf Bergmann, Ratan D Bhardwaj, Samuel Bernard, Sofia Zdunek, Fanie Barnabé-Heider, Stuart Walsh, Joel Zupicich, Kanar Alkass, Bruce A Buchholz, Henrik Druid, Stefan Jovinge, Jonas Frisén
It has been difficult to establish whether we are limited to the heart muscle cells we are born with or if cardiomyocytes are generated also later in life. We have taken advantage of the integration of carbon-14, generated by nuclear bomb tests during the Cold War, into DNA to establish the age of cardiomyocytes in humans. We report that cardiomyocytes renew, with a gradual decrease from 1% turning over annually at the age of 25 to 0.45% at the age of 75. Fewer than 50% of cardiomyocytes are exchanged during a normal life span...
April 3, 2009: Science
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