Regulation of proliferation of the fetal myocardium

Armstrong, Margaret T.; Lee, David Y.; Armstrong, Peter B.

doi:10.1002/1097-0177(2000)9999:9999<::aid-dvdy1049>3.3.co;2-s

Cited by 47 publications

(28 citation statements)

References 67 publications

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“…These receptors activate proliferation via an intracellular phosphorylation cascade that generally includes ERK (mitogenactivated protein kinase; MAPK) and other components that regulate cell cycle progression. In cell culture, both IGFs stimulate the proliferation of primary fetal cardiomyocytes (Liu et al, 1996;Hertig et al, 1999), as do many other mitogens (Armstrong et al, 2000). In mouse embryos, treatment with exogenous IGF induces cardiomyocyte proliferation (Fraidenraich et al, 2004), and excess IGF2 caused by absence of the clearance receptor IGF2R leads to ventricular hyperplasia (Lau et al, 1994;Wang et al, 1994;Eggenschwiler et al, 1997).…”

Section: Introductionsupporting

confidence: 88%

IGF signaling directs ventricular cardiomyocyte proliferation during embryonic heart development

et al. 2011

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SUMMARYSecreted factors from the epicardium are believed to be important in directing heart ventricular cardiomyocyte proliferation and morphogenesis, although the specific factors involved have not been identified or characterized adequately. We found that IGF2 is the most prominent mitogen made by primary mouse embryonic epicardial cells and by a newly derived immortalized mouse embryonic epicardial cell line called MEC1. In vivo, Igf2 is expressed in the embryonic mouse epicardium during midgestation heart development. Using a whole embryo culture assay in the presence of inhibitors, we confirmed that IGF signaling is required to activate the ERK proliferation pathway in the developing heart, and that the epicardium is required for this response. Global disruption of the Igf2 gene, or conditional disruption of the two IGF receptor genes Igf1r and Insr together in the myocardium, each resulted in a significant decrease in ventricular wall proliferation and in ventricular wall hypoplasia. Ventricular cardiomyocyte proliferation in mutant embryos was restored to normal at E14.5, concurrent with the establishment of coronary circulation. Our results define IGF2 as a previously unexplored epicardial mitogen that is required for normal ventricular chamber development.

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Section: Introductionsupporting

confidence: 88%

IGF signaling directs ventricular cardiomyocyte proliferation during embryonic heart development

et al. 2011

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“…There are obvious differences in cellular shape and in the surrounding of the cells, but there are also differences in cellular processes, such as responsiveness to growth factors (Armstrong et al, 2000) and in myofibrillogenesis . Therefore, we wanted to find out whether the disassembly of myofibrils with the delay between different parts of the sarcomere could also be observed in cardiomyocytes in situ.…”

Section: Myofibrillar Disassembly In Cultured Cardiomyocytes During Cmentioning

confidence: 63%

Sequential myofibrillar breakdown accompanies mitotic division of mammalian cardiomyocytes

Ahuja¹,

Perriard²,

Perriard³

et al. 2004

Journal of Cell Science

146

123

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The contractile tissue of the heart is composed of individual cardiomyocytes. During mammalian embryonic development, heart growth is achieved by cell division while at the same time the heart is already exerting its essential pumping activity. There is still some debate whether the proliferative activity is carried out by a less differentiated, stem cell-like type of cardiomyocytes or whether embryonic cardiomyocytes are able to perform both of these completely different dynamic tasks, contraction and cell division. Our analysis of triple-stained specimen of cultured embryonic cardiomyocytes and of whole mount preparations of embryonic mouse hearts by confocal microscopy revealed that differentiated cardiomyocytes are indeed able to proliferate. However, to go through cell division, a disassembly of the contractile elements, the myofibrils, has to take place. This disassembly occurs in two steps with Z-disk and thin (actin)-filament-associated proteins getting disassembled before disassembly of the M-bands and the thick (myosin) filaments happens. After cytokinesis reassembly of the myofibrillar proteins to their mature cross-striated pattern can be seen. Another interesting observation was that the cell-cell contacts remain seemingly intact during division, probably reflecting the requirement of intact integration sites of the individual cells in the contractile tissue. Our results suggest that embryonic cardiomyocytes have developed an interesting strategy to deal with their major cytoskeletal elements, the myofibrils, during mitosis. The complex disassembly-reassembly process might also provide a mechanistic explanation, why cardiomyocytes cede to divide postnatally.

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“…Indeed, high levels of IGF-IR mRNA were found in S. aurata heart (SJ Chan, personal communication). Finally, several studies in mammals and chickens have shown the importance of IGF-II for myocardial proliferation during fetal life or preservation of myocardial structure postinfarct (Armstrong et al 2000, Kotlyar et al 2001. It is worth noting that IGF-II immunoreactivity in skeletal and heart muscle, shown in this study, matches our results with respect to the cellular localization of myostatin in fish (Radaelli et al 2003b), which is known as a negative regulator of muscle growth in mammals.…”

Section: Discussionmentioning

confidence: 93%

Expression and cellular localization of insulin-like growth factor-II protein and mRNA in Sparus aurata during development

Radaelli¹,

Patruno²,

Maccatrozzo³

et al. 2003

Journal of Endocrinology

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The spatial localization of IGF-II protein and mRNA was investigated during larval and postlarval developmental stages of the gilthead sea bream (Sparus aurata) by immunohistochemistry and in situ hybridization, using specific antisera and riboprobes. Steady-state levels of IGF-II mRNA in larvae were determined by Northern blot analysis and were found to be increased. Immunoreactivity towards IGF-II was found in larval skin, muscle, gills, gut, olfactory epithelium and kidney. After metamorphosis, the strongest immunoreactivity was found in red skeletal muscle. Positive reaction with IGF-II antibodies was also found in the olfactory epithelium and in the epithelia of pharynx, oesophagus, stomach and kidney. In the adult, the most intense signal was observed in the red and pink musculature and in heart musculature. Immunostaining was also found in saccus vasculosus, thymus, spleen and ovary. IGF-II mRNA was detected by in situ hybridization in the brain, olfactory epithelium, eye, pharynx, skeletal musculature and liver. The spatial distribution of IGF-II shown in this study is consistent with previous findings on the cellular localization of IGF type 1 receptor in the sea bream and supports a role for IGF-II during development and growth of sea bream. Furthermore, these results suggest that IGF-II acts in an autocrine/paracrine manner.

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Regulation of proliferation of the fetal myocardium

Cited by 47 publications

References 67 publications

IGF signaling directs ventricular cardiomyocyte proliferation during embryonic heart development

IGF signaling directs ventricular cardiomyocyte proliferation during embryonic heart development

Sequential myofibrillar breakdown accompanies mitotic division of mammalian cardiomyocytes

Expression and cellular localization of insulin-like growth factor-II protein and mRNA in Sparus aurata during development

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