Desmin stimulates differentiation of cardiomyocytes and up-regulation of brachyury and nkx2.5

Hofner, Manuela; Höllrigl, Alexandra; Puz, Sonja; Stary, Martina; Weitzer, Georg

doi:10.1111/j.1432-0436.2007.00162.x

Cited by 24 publications

(41 citation statements)

References 42 publications

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“…Viability of presumptive pre‐myocardial mesoderm was reduced, number and size of cardiomyocyte clusters were drastically reduced in EBs and contraction of cardiomyocytes was reduced and often arrhythmic. Expression of mesodermal transcription factor genes brachyury and goosecoid were significantly attenuated, suggesting that desmin S6,7,8A affects already cardioblasts, as has been observed for a mutant desmin lacking the amino‐terminal domain (Höllrigl et al, 2002) and for overexpressed desmin (Hofner et al, 2007). Consequently, expression of early myocardial transcription factor genes nkx2.5 and mef2c were also delayed and remained low throughout differentiation of cardiomyocytes, suggesting that desmin S6,7,8A affects to some extent the expression of mesodermal transcription factors and to a significantly increased degree the expression of cardiac‐specific transcription factor genes nkx2.5 and mef2c .…”

Section: Discussionmentioning

confidence: 60%

“…Thus cell death caused by desmin S6,7,8A already starts during early steps of cardiomyocyte differentiation, consequently causing a reduction of cardiomyogenesis in EBs. The delay of cardiomyogenesis in des +/S6,7,8A EBs, however, also suggests a subtle involvement of desmin in regulatory mechanisms important for the commitment and differentiation of cardiomyocytes as has been demonstrated by overexpression of desmin in pre‐cardiac mesoderm (Hofner et al, 2007).…”

Section: Resultsmentioning

confidence: 91%

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Differentiation of cardiomyocytes requires functional serine residues within the amino-terminal domain of desmin

et al. 2007

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Section: Discussionmentioning

confidence: 60%

Section: Resultsmentioning

confidence: 91%

Differentiation of cardiomyocytes requires functional serine residues within the amino-terminal domain of desmin

et al. 2007

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“…video 2), and contracted rhythmically for another 30 days. In sharp contrast, cardiomyogenesis in ESC-derived EBs began on day 7.5 8 10 h [Hofner et al, 2007] in 86 8 6% of EBs and rhythmical contraction lasted only for 18 8 44 days. Likewise, SMC development in CBs required more time than in EBs ( fig.…”

Section: Aggregation Of Cvpc Facilitates Efficient and Reproducible Dmentioning

confidence: 89%

Embryonic Stem Cells Facilitate the Isolation of Persistent Clonal Cardiovascular Progenitor Cell Lines and Leukemia Inhibitor Factor Maintains Their Self-Renewal and Myocardial Differentiation Potential in vitro

Hoebaus

Heher

Gottschamel

et al. 2013

Cells Tissues Organs

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Compelling evidence for the existence of somatic stem cells in the heart of different mammalian species has been provided by numerous groups; however, so far it has not been possible to maintain these cells as self-renewing and phenotypically stable clonal cell lines in vitro. Thus, we sought to identify a surrogate stem cell niche for the isolation and persistent maintenance of stable clonal cardiovascular progenitor cell lines, enabling us to study the mechanism of self-renewal and differentiation in these cells. Using postnatal murine hearts with a selectable marker as the stem cell source and embryonic stem cells and leukemia inhibitory factor (LIF)-secreting fibroblasts as a surrogate niche, we succeeded in the isolation of stable clonal cardiovascular progenitor cell lines. These cell lines self-renew in an LIF-dependent manner. They express both stemness transcription factors Oct4, Sox2, and Nanog and early myocardial transcription factors Nkx2.5, GATA4, and Isl-1 at the same time. Upon LIF deprivation, they exclusively differentiate to functional cardiomyocytes and endothelial and smooth muscle cells, suggesting that these cells are mesodermal intermediates already committed to the cardiogenic lineage. Cardiovascular progenitor cell lines can be maintained for at least 149 passages over 7 years without phenotypic changes, in the presence of LIF-secreting fibroblasts. Isolation of wild-type cardiovascular progenitor cell lines from adolescent and old mice has finally demonstrated the general feasibility of this strategy for the isolation of phenotypically stable somatic stem cell lines.

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“…Inhibition of desmin expression hinders myoblast differentiation [44••, 45], while its amino-terminal mutations interfere with cardiogenesis [46]. Desmin can enhance the expression of myogenic and cardiogenic regulators [44••–48] while its own expression is controlled by them in return [49, 50]. The underlying mechanism by which a cytoskeletal protein, like desmin, could confer regulation of transcription factor steady state levels can only be speculated at this point.…”

Section: Mechanisms Of Desmin Related Disease Developmentmentioning

confidence: 99%

Desmin related disease: a matter of cell survival failure

Capetanaki

Papathanasiou

Diokmetzidou

et al. 2015

Current Opinion in Cell Biology

116

126

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Maintenance of the highly organized striated muscle tissue requires a cell-wide dynamic network that through interactions with all vital cell structures, provides an effective mechanochemical integrator of morphology and function, absolutely necessary for intra- and intercellular coordination of all muscle functions. A good candidate for such a system is the desmin intermediate filament cytoskeletal network. Human desmin mutations and post-translational modifications cause disturbance of this network, thus leading to loss of function of both desmin and its binding partners, as well as potential toxic effects of the formed aggregates. Both loss of normal function and gain of toxic function are linked to mitochondrial defects, cardiomyocyte death, muscle degeneration and development of skeletal myopathy and cardiomyopathy.

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Desmin stimulates differentiation of cardiomyocytes and up-regulation of brachyury and nkx2.5

Cited by 24 publications

References 42 publications

Differentiation of cardiomyocytes requires functional serine residues within the amino-terminal domain of desmin

Differentiation of cardiomyocytes requires functional serine residues within the amino-terminal domain of desmin

Embryonic Stem Cells Facilitate the Isolation of Persistent Clonal Cardiovascular Progenitor Cell Lines and Leukemia Inhibitor Factor Maintains Their Self-Renewal and Myocardial Differentiation Potential in vitro

Desmin related disease: a matter of cell survival failure

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