2021
DOI: 10.1038/s41598-021-00996-y
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Desmoglein 2 regulates cardiogenesis by restricting hematopoiesis in the developing murine heart

Abstract: Cardiac morphogenesis relies on intricate intercellular signaling. Altered signaling impacts cardiac function and is detrimental to embryonic survival. Here we report an unexpected regulatory role of the desmosomal cell adhesion molecule desmoglein 2 (Dsg2) on murine heart development. A large percentage of Dsg2-mutant embryos develop pericardial hemorrhage. Lethal myocardial rupture is occasionally observed, which is not associated with loss of cardiomyocyte contact but with expansion of abnormal, non-myocyte… Show more

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Cited by 6 publications
(7 citation statements)
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“…Despite the inability to document a rupture in Pkp2 or Jup mutants, accumulating blood in the pericardial cavity was interpreted as leakage of blood due to weak cardiomyocyte junctions [17,74]. Our detailed histological assessment of embryonic hearts with Dsg2 mutation suggests that rupture is not the cause of pericardial blood cell accumulation in most instances [72]. The analyses revealed that desmosome deficiency does not result in myocyte rupture or leakiness but that the accumulating blood in the pericardial cavity is caused by differentiation of endocardial/epicardial cells into hematopoietic Runx1 + cells, which excessively proliferate and subsequently transmigrate into the pericardial cavity [72].…”
Section: The Impact Of Desmosomal Proteins On Cardiac Morphogenesismentioning
confidence: 76%
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“…Despite the inability to document a rupture in Pkp2 or Jup mutants, accumulating blood in the pericardial cavity was interpreted as leakage of blood due to weak cardiomyocyte junctions [17,74]. Our detailed histological assessment of embryonic hearts with Dsg2 mutation suggests that rupture is not the cause of pericardial blood cell accumulation in most instances [72]. The analyses revealed that desmosome deficiency does not result in myocyte rupture or leakiness but that the accumulating blood in the pericardial cavity is caused by differentiation of endocardial/epicardial cells into hematopoietic Runx1 + cells, which excessively proliferate and subsequently transmigrate into the pericardial cavity [72].…”
Section: The Impact Of Desmosomal Proteins On Cardiac Morphogenesismentioning
confidence: 76%
“…Our detailed histological assessment of embryonic hearts with Dsg2 mutation suggests that rupture is not the cause of pericardial blood cell accumulation in most instances [72]. The analyses revealed that desmosome deficiency does not result in myocyte rupture or leakiness but that the accumulating blood in the pericardial cavity is caused by differentiation of endocardial/epicardial cells into hematopoietic Runx1 + cells, which excessively proliferate and subsequently transmigrate into the pericardial cavity [72]. Interestingly, the loss of cuboidal endothelial cell morphology and reduction of cell junctions between endocardial cells have also been observed in zebrafish treated with Jup morpholinos [73].…”
Section: The Impact Of Desmosomal Proteins On Cardiac Morphogenesismentioning
confidence: 91%
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“…The latter forms a complex scaffold for organelles and myofibrils [ 73 , 74 , 75 ]. The recently observed considerably altered desmin organization in Dsg2 mutants during embryonic cardiogenesis with detrimental consequences on cardiac differentiation and function underscores the importance of an intact desmin network for cellular integrity [ 76 ]. It is therefore safe to assume that disturbances of the three dimensional desmin network in the Dsg2 -mutant hearts also interfere with proper postnatal myocardial maturation [ 74 ].…”
Section: Discussionmentioning
confidence: 99%