ライフサイエンスコーパス: endocardial cushion

1 act myocardium, interventricular septum, and endocardial cushion.

2 esicle, prevertebral bodies (notochord), and endocardial cushion.

3 llular matrix, called cardiac jelly, to form endocardial cushions.

4 delay in the formation of the outflow tract endocardial cushions.

5 lure of fusion" between the atrioventricular endocardial cushions.

6 minantly the product of the atrioventricular endocardial cushions.

7 nchyme that characterizes development of the endocardial cushions.

8 t (OFT) but not atrioventricular canal (AVC) endocardial cushions.

9 s develop from rudimentary structures termed endocardial cushions.

10 n amorphic cellular nodules within their OFT endocardial cushions.

11 of mutant Shp2 (Q79R-Shp2) in the developing endocardial cushions.

12 s of invagination, rather than first forming endocardial cushions.

13 that relies on the successful remodeling of endocardial cushions.

14 ressing GATA4 activity within the developing endocardial cushions.

15 nt embryos are thicker myocardium and larger endocardial cushions.

16 xpressing cells in the cardiac outflow tract endocardial cushions.

17 rder to elucidate its function in developing endocardial cushions.

18 erate the progenitor cells that populate the endocardial cushions.

19 s aberrant Wnt/beta-catenin signaling in the endocardial cushions.

20 sence of hyaluronan (HA), cardiac jelly, and endocardial cushions, a loss of vascular integrity, and

21 nt endocardium was associated with acellular endocardial cushions, absent epithelial-to-mesenchymal t

22 sia of the right ventricle, (3) overabundant endocardial cushions accompanied by ventricular septal d

23 morphogenesis by enhancing apoptosis in the endocardial cushions and (2) promote aortic sac malforma

24 ression of Wnt-9a in ovo results in enlarged endocardial cushions and AV inlet obstruction.

25 of the rock gene were used to treat cultured endocardial cushions and cells.

26 e cardiovascular abnormalities involving the endocardial cushions and myocardium.

27 and Tbx5 are co-expressed in the developing endocardial cushions and myocardium.

28 endoderm, outflow tract and atrioventricular endocardial cushions and post-migratory neural crest der

29 chymal transition that supplies cells to the endocardial cushions and repositions cardiac neural cres

30 ricular septum is equated with fusion of the endocardial cushions and that failure of fusion can expl

31 is essential for proper formation of the AV endocardial cushions and the cardiac outflow tract.

32 P expression is specific for the myocardium; endocardial cushions and valves exhibit only background

33 factor Tbx20 is expressed in the developing endocardial cushions and valves throughout heart develop

34 e specialized cells, unlike that of adjacent endocardial cushions and valves, is not dependent on blo

35 displayed defects in the left ventricle and endocardial cushions, and exhibited dysregulated ventric

36 ural crest, intestine, pancreas, testis, and endocardial cushions, and plays a crucial role in cell p

37 ing, absence of mesenchymal cells within the endocardial cushions, and selective hypoplasia of the RV

38 primary atrial septum, the atrioventricular endocardial cushions, and the cap of mesenchyme on the s

39 Endocardial cushions are critical to maintain unidirecti

40 In Sox9-null mutants, endocardial cushions are markedly hypoplastic.

41 Endocardial cushions are precursors of mature atrioventr

42 Endocardial cushions are the precursors of the cardiac v

43 n the endocardium and its derivatives in the endocardial cushions are unknown.

44 of TGFbeta2, but not TGFbeta3, within mouse endocardial cushions at a time coincident with transform

45 In multiple assays of cells from prefused endocardial cushions, BMP2 is sufficient to activate Sma

46 fail to express ErbB3, which is required for endocardial cushion cell differentiation and proliferati

47 ushion cell proliferation as well as promote endocardial cushion cell migration.

48 Previously, Tbx20 has been implicated in endocardial cushion cell proliferation and differentiati

49 hese studies indicate that Twist1 can induce endocardial cushion cell proliferation as well as promot

50 a2 is expressed and obligatory for mammalian endocardial cushion cell transformation.

51 migration and repressing differentiation in endocardial cushion cells during embryonic development.

52 xperiments were performed in primary chicken endocardial cushion cells in order to elucidate its role

53 esenchymal cell types, the role of Twist1 in endocardial cushion cells is unknown.

54 t provide a suitable migratory substrate for endocardial cushion cells unless MMP-2 and MT-MMP are ac

55 nt resulted in increased Tbx20 expression in endocardial cushion cells, and loss of Tbx20 led to incr

56 ibited with Tbx20-specific siRNA in cultured endocardial cushion cells.

57 sly reported associations: phenylephrine and endocardial cushion defect (odds ratio = 8.0; 95% confid

58 interval): cyanotic CHD (6.44, 3.95-10.50), endocardial cushion defects (5.47, 2.89-10.36), and left

59 Endocardial cushion defects were found in 3 out of 39 he

60 truncus arteriosus, transposition complexes, endocardial cushion defects, and univentricular hearts.

61 eptal defects, and left-sided malformations (endocardial cushion defects, hypoplastic left heart, and

62 uble-outlet right ventricle (DORV), TOF, and endocardial cushion defects.

63 cteristic heart valve lesions resulting from endocardial cushion defects.

64 cardiovascular lineages and is required for endocardial cushion development and embryonic viability,

65 elates second heart field, neural crest, and endocardial cushion development and suggests that pertur

66 ination of the diverse signals that regulate endocardial cushion development and valve elongation.

67 A collagen gel assay, long used to examine endocardial cushion development in avian models, is now

68 this defect, we examined the later steps in endocardial cushion development including mesenchymal ce

69 trioventricular septal defects have abnormal endocardial cushion development with the delayed appeara

70 by beta-catenin has been implicated in early endocardial cushion development, but its roles in later

71 ole Rho GTPase-associated kinases (ROCKs) in endocardial cushion development.

72 cession of molecular steps in the pathway of endocardial cushion development.

73 al cell differentiation and migration during endocardial cushion development.

74 cts on GATA4/SMAD4 interactions required for endocardial cushion development.

75 y disrupting a signaling cascade involved in endocardial cushion development.

76 hion cells in order to elucidate its role in endocardial cushion development.

77 EKK3 as a critical signaling molecule during endocardial cushion development.

78 l appropriately, suggesting a defect late in endocardial cushion development.

79 e effects of wild-type Shp2 and Q79R-Shp2 on endocardial cushion development.

80 iginate from errors in atrioventricular (AV) endocardial cushion development.

81 in, mouse embryo hearts develop overabundant endocardial cushions due to hyperproliferation and lack

82 f the rock1 and rock2 genes was found in the endocardial cushions during development.

83 n mesenchymal valve precursor populations in endocardial cushions during embryonic development.

84 (AV) septal defects resulting from aberrant endocardial cushion (EC) formation are observed at incre

85 d regurgitation in a dilated heart and lacks endocardial cushion (EC) formation.

86 Cardiac valves originate from endocardial cushions (EC) formed by endothelial-to-mesen

87 abutting myocardium and endocardium to form endocardial cushions (EC) in a process known as epitheli

88 es develop from undifferentiated mesenchymal endocardial cushions (EC), and activated interstitial ce

89 ctures derived from mesenchymal cells of the endocardial cushions (ECs) are composed of highly organi

90 proceeds through coordinated steps by which endocardial cushions (ECs) form thin, elongated and stra

91 During valvulogenesis, globular endocardial cushions elongate and remodel into highly or

92 KK3 integrates signaling cascades activating endocardial cushion EMT.

93 cies variations for avian and mouse cultured endocardial cushion explants.

94 in protein, which marks mesenchymal cells in endocardial cushions following epithelial-mesenchymal tr

95 -mesenchymal transition in explant assays of endocardial cushions following Notch inhibition within s

96 opportunity to identify a gene required for endocardial cushion formation and for specification or m

97 valuate the molecular requirements of normal endocardial cushion formation and the segmental interact

98 tation, cardiac myocyte differentiation, and endocardial cushion formation are preprogrammed in the p

99 itical non-redundant role in early phases of endocardial cushion formation during cardiac morphogenes

100 3 in vessel remodeling, vessel integrity and endocardial cushion formation during the development of

101 ayed defects in atrioventricular canal (AVC) endocardial cushion formation in the heart.

102 secting regulatory pathways are required for endocardial cushion formation, valve progenitor cell pro

103 cardial projections accompanied by defective endocardial cushion formation.

104 heart is consistent with a role for Slug in endocardial cushion formation.

105 endothelial-to-mesenchymal transition during endocardial cushion formation.

106 Developmental abnormalities in endocardial cushions frequently contribute to congenital

107 dextrodorsal outflow ridge and the superior endocardial cushion, fusion with the inferior margins of

108 protein at comparable levels did not enhance endocardial cushion growth or alter the morphology of th

109 Their endocardial cushions have increased Erk activation, but

110 heart tube fails to develop normally and the endocardial cushions in both the conus and the atriovent

111 We have previously shown that the endocardial cushions in FOG-2 deficient mice are hyperpl

112 The dramatic enlargement of the endocardial cushions in the absence of Hhex is due to de

113 The formation of endocardial cushions in the atrioventricular (AV) canal

114 ation (EMT) occurs during the development of endocardial cushions in the atrioventricular (AV) canal

115 rmation occurs during the development of the endocardial cushions in the atrioventricular (AV) canal

116 f the single heart tube fail to form and the endocardial cushions in the atrioventricular and conus/t

117 mutant embryos showed significantly enlarged endocardial cushions in the atrioventricular canal and i

118 throughout the fibrous cardiac skeleton and endocardial cushions in the developing heart but is abse

119 Development of the endocardial cushions in the heart involves cell migratio

120 NFATc1 is necessary for remodeling endocardial cushions into mature heart valve leaflets an

121 lopment of the cardiac atrioventricular (AV) endocardial cushions is essential for proper ventricular

122 Fusion of the sternum and endocardial cushions is impaired in the mutant mice asso

123 teoglycan-rich extracellular matrix (ECM) of endocardial cushions is replaced by a specialized and st

124 ch Tbx20 regulates the Wnt pathway to direct endocardial cushion maturation and valve elongation, and

125 evidence for Wnt signaling as a regulator of endocardial cushion maturation as well as valve leaflet

126 nt for myocardial segmental regulation of AV endocardial cushion mesenchymal cell formation in mice.

127 ively affect RV development or generation of endocardial cushion mesenchyme but did result in marked

128 mouse heart, ECE-2 mRNA is expressed in the endocardial cushion mesenchyme from embyronic day (E) 12

129 ute at least in part to the formation of the endocardial cushion mesenchyme.

130 ments for TGFbeta2 and TGFbeta3 during mouse endocardial cushion morphogenesis.

131 ar septal defects can result from incomplete endocardial cushion morphogenesis.

132 an is particularly strongly expressed in the endocardial cushions of the atrioventricular and outflow

133 ) and the secreted Wnt antagonist Frzb in AV endocardial cushions of the developing chicken heart.

134 ly expressed in myocardial cells, and not in endocardial cushion or outflow tract tissues.

135 d dominant negative MEK-1 prevented enhanced endocardial cushion outgrowth, whereas expression of con

136 Deletion of ERK1 completely rescued the endocardial cushion phenotype, whereas ERK2 protein redu

137 Formation of endocardial cushions, primordia of valves and septa, is

138 to the proximal aspects of the outflow tract endocardial cushions, resulting in the failure of membra

139 hereas ERK2 protein reduction did not affect endocardial cushion size.

140 Cardiac valves arise from endocardial cushions, specialized regions of the develop

141 ic forces, but the interrelationship between endocardial cushion structure and the mechanics of atrio

142 highly expressed in the conotruncus and the endocardial cushion, structures that give rise to the af

143 quired for the successful development of the endocardial cushion swellings and the embryonic heart se

144 hat neural crest contribution to the outflow endocardial cushions (the precursors of the semilunar va

145 al, and thus play a key role in formation of endocardial cushions, the detailed signaling mechanisms

146 ellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the hear

147 These cardiac structures arise from the endocardial cushions through dynamic interactions betwee

148 embryonic day 12.5, when fusion between the endocardial cushion tissue and the atrial and ventricula

149 rimarily in the myocardium, endocardium, and endocardial cushion tissue.

150 ur-chambered organ requires the formation of endocardial cushion tissue.

151 ell proliferation and differentiation in the endocardial cushion tissue.

152 l cells into the extracellular matrix of the endocardial cushion tissues.

153 We found no difference in the ability of the endocardial cushions to undergo myocardialization or in

154 te a function for Smad6 in the regulation of endocardial cushion transformation.

155 Atrioventricular and outflow tract endocardial cushions were excised from chick embryos, in

156 enchymal transition within the outflow tract endocardial cushions were observed.

157 ells undergoes EMT to form the mesenchyme of endocardial cushions, which function as primordia for de

158 sequent malalignment of the atrioventricular endocardial cushions with the proximal outflow cushions.

159 These structures arise from the endocardial cushions within the atrioventricular canal (