ライフサイエンスコーパス: cardiocyte

1 as c-jun, that regulate growth of the adult cardiocyte.

2 in a computational model of the ventricular cardiocyte.

3 rea was greater in hypertrophied than normal cardiocytes.

4 es given above for pressure-hypertrophied RV cardiocytes.

5 46 +/- 1.32 dyne/cm2 in the hypertrophied RV cardiocytes.

6 87.85 +/- 6.95 poise in the hypertrophied RV cardiocytes.

7 art failure is due to ongoing loss of viable cardiocytes.

8 se metabolism in isolated skeletal muscle or cardiocytes.

9 lt cardiocytes nor at 100 nmol/L in neonatal cardiocytes.

10 sion pathways can be differentiated in adult cardiocytes.

11 ctile behavior was maintained in transfected cardiocytes.

12 sion pathways can be differentiated in adult cardiocytes.

13 fos expression was Ang II dependent in adult cardiocytes.

14 by inhibiting its expression in ventricular cardiocytes.

15 anine incorporation into protein in neonatal cardiocytes.

16 evel transcriptional activity in primary rat cardiocytes.

17 Ang II treatment of either adult or neonatal cardiocytes.

18 60-dependent impaired clearance of apoptotic cardiocytes.

19 ylation site found by mimicking it in normal cardiocytes.

20 Ro60 on the surface of apoptotic human fetal cardiocytes.

21 of betaGal mRNA in quiescent and contracting cardiocytes.

22 y regulate translational efficiency in adult cardiocytes.

23 poptotic, but not proliferating, human fetal cardiocytes.

24 y canine kidney cells (MDCK) and primary rat cardiocytes.

25 educed eIF4E promoter activity by 66+/-4% in cardiocytes.

26 matrix (ECM) and hypertrophic growth of the cardiocytes.

27 stently observed on early and late apoptotic cardiocytes.

28 pitated from apoptotic, but not nonapoptotic cardiocytes.

29 nits in model systems, which may differ from cardiocytes.

30 e normalizes contractility in these isolated cardiocytes.

31 1) is the principal Ca2+ efflux mechanism in cardiocytes.

32 cytes could damage surrounding healthy fetal cardiocytes.

33 other cardiocytes connected to an individual cardiocyte (4.60 +/- 0.10 [mean +/- SE] was significantl

34 p70(S6K), and (iv) similar changes in adult cardiocytes after treatment with 12-O-tetradecanoylphorb

35 e fetal factors, protein/RNA on an apoptotic cardiocyte and infiltrating macrophages.

36 natants generated from cocultures of healthy cardiocytes and apo-CHB-IgG cardiocytes compared with he

37 ernatants derived from cocultures of healthy cardiocytes and apo-CHB-IgG cardiocytes promoted Smad2 p

38 Supernatants from cocultures of healthy cardiocytes and apoptotic cardiocytes bound by IgG from

39 po-CHB-IgG cardiocytes compared with healthy cardiocytes and apoptotic cardiocytes preincubated with

40 with supernatants from cocultures of healthy cardiocytes and apoptotic cardiocytes preincubated with

41 The adult heart lacks reserve cardiocytes and cannot regenerate.

42 on was determined in primary cultures of rat cardiocytes and in a murine C(2)C(12) myoblast cell line

43 cardiocytes impairs their removal by healthy cardiocytes and increases urokinase plasminogen activato

44 xin-deficient heart tissue, liver tissue and cardiocytes and observed a transcript down-regulation to

45 ocytosis of apoptotic cardiocytes by healthy cardiocytes and reverses the anti-Ro60-dependent impaire

46 c regions suggests that interactions between cardiocytes and their environment may contribute to hear

47 fflux was also found in primary hepatocytes, cardiocytes, and fibroblasts.

48 SPRY2 reproduced the branching morphology in cardiocytes, and vice versa, knockdown of miR-21 using a

49 at morphological and biochemical features of cardiocyte apoptosis exist in the left ventricular myoca

50 Electron microscopic features of cardiocyte apoptosis included (1) intact sarcolemma and

51 Evidence for cardiocyte apoptosis was based on transmission electron

52 Features of cardiocyte apoptosis were observed in dogs with heart fa

53 These opsonized cardiocytes are phagocytosed by macrophages, which secre

54 aprotinin prior to coculturing with healthy cardiocytes attenuated TGF-beta activation.

55 ultures of healthy cardiocytes and apoptotic cardiocytes bound by IgG from a mother whose child had C

56 cipate in physiologic clearance of apoptotic cardiocytes but that clearance is inhibited by opsonizat

57 crophages incubated with opsonized apoptotic cardiocytes (but not nonopsonized) dramatically increase

58 pertrophic response of cultured neonatal rat cardiocytes, but its role in the adult heart is controve

59 The cardiac promoter drives expression in cardiocytes, but not in mouse L cells.

60 tly by 3.7-fold in contracting vs. quiescent cardiocytes, but ODC/betaGal mRNA was unchanged.

61 ased threefold 1 hour after loading of adult cardiocytes, but this increased expression was not block

62 g of uPAR enhances phagocytosis of apoptotic cardiocytes by healthy cardiocytes and reverses the anti

63 and determined in nonapoptotic and apoptotic cardiocytes by indirect immunofluorescence.

64 In summary, the current model of cardiocyte Ca(2+) dynamics provides an integrated theore

65 In this study, cardiocyte Ca(2+) dynamics were modeled using a set of s

66 tures of healthy cardiocytes and apo-CHB-IgG cardiocytes compared with healthy cardiocytes and apopto

67 In early apoptotic cardiocytes, condensation of the PI- and Ro- or La-stain

68 tissue volume fraction, the number of other cardiocytes connected to an individual cardiocyte (4.60

69 After formalin fixation, the number of cardiocytes connected to an individual cardiocyte was co

70 constitutes primarily a viscous load on the cardiocyte contractile apparatus in pressure-overload ca

71 Thus, the microtubule-based cardiocyte contractile dysfunction characteristic of pre

72 Increased microtubule density causes cardiocyte contractile dysfunction in right ventricular

73 In contrast, cardiocyte contractile function in cells from failing LV

74 Cardiocyte contractile function was equivalent, and unaf

75 crotubule network forms that interferes with cardiocyte contraction and microtubule-based transport.

76 , which imposes a viscous load that inhibits cardiocyte contraction.

77 pplies cyclical strain (1 Hz) to ventricular cardiocytes cultured on collagen-coated silicone elastom

78 an atrial cell-specific enhancer in primary cardiocyte cultures.

79 intrinsic to the myofilament portion of the cardiocyte cytoskeleton but rather from an increased den

80 onent of the extramyofilament portion of the cardiocyte cytoskeleton.

81 hromatin immunoprecipitation assays in adult cardiocytes demonstrate that SRF and GATA4 are associate

82 Spontaneously contacting cardiocytes derived from the ES cells were used to evalu

83 a, the other major PKC isoform seen in adult cardiocytes, did not show a change in subcellular locali

84 aluated whether anti-Ro binding to apoptotic cardiocytes enhances plasmin-mediated activation of TGF-

85 Importantly, cardiocytes exposed to doxorubicin displayed reduced lev

86 Cultured fetal cardiocytes expressed phosphatidylserine receptors (PSRs

87 acrophages cultured with opsonized apoptotic cardiocytes expressed proinflammatory markers, supported

88 and MAP4 decoration were assessed in normal cardiocytes following an equivalent level of MAP4 expres

89 Isolated cardiocytes from 16-24 wk abortuses were rendered apopto

90 Human fetal cardiocytes from 16-24-wk abortuses were cultured and in

91 ity causes decreased contractile function of cardiocytes from cats with hypertrophy produced by chron

92 Measurements were made in two groups of cardiocytes from cats with right ventricular (RV) hypert

93 m for staining of right and left ventricular cardiocytes from control cats and cats with right ventri

94 Cardiocytes from normal and pressure-hypertrophied cats

95 picuous in microtubules of right ventricular cardiocytes from pressure overloaded cats, i.e., the mic

96 Ro60 bound and inhibited uptake of apoptotic cardiocytes from wild-type but not Ro60-knockout mice.

97 increased IK+Ach activity in ES cell-derived cardiocytes from wild-type cells, in cells lacking alpha

98 We developed methods for culture of cardiocytes from zebrafish embryos and found that, even

99 Thus, the PKC signaling pathway in cardiocytes has different effects depending on the timin

100 hanced Na+-Ca2+ exchanger gene expression in cardiocytes; however, load induced c-fos expression is A

101 maternal anti-SSA/Ro Abs to fetal apoptotic cardiocytes impairs their removal by healthy cardiocytes

102 The increase in junctions per cardiocyte in concentrically hypertrophied hearts sugges

103 Cell membrane lesion sealing of hypoxic cardiocytes in culture with CSIL has been reported.

104 There was no evidence of apoptotic cardiocytes in normal dogs.

105 The role of cardiocytes in physiologic removal of apoptotic cells an

106 eases during growth of cardiac muscle cells (cardiocytes) in vitro.

107 cally stimulated contraction of adult feline cardiocytes increased eIF-4E phosphorylation to 34% afte

108 d with nonapoptotic cardiocytes or apoptotic cardiocytes incubated with normal sera, apoptotic cardio

109 One hour after loading of adult cardiocytes, induction of c-fos expression was increased

110 These data show that a nuclear factor in cardiocytes interacts with an enhancer element (+25 and

111 ajor PKC isoforms seen in the adult heart in cardiocytes isolated from diabetic rats and determined p

112 TnI phosphorylation was increased 5-fold in cardiocytes isolated from the hearts of diabetic animals

113 The contractile function of cardiocytes isolated from the ventricles at the end of t

114 ogenitor cells that can give rise to beating cardiocyte-like cells and vascular components, and the a

115 this study, we examined the possibility that cardiocyte loss in heart failure may be due, in part, to

116 We sought to determine whether the cardiocyte microtubule network densification characteris

117 ional corroborative data show that increased cardiocyte microtubule network density is an important m

118 lly, apparent viscosity in the two groups of cardiocytes, microtubule depolymerization by colchicine

119 ase protein synthesis after 4 hours in adult cardiocytes nor at 100 nmol/L in neonatal cardiocytes.

120 Cardiocytes obtained by biopsy before and after in vivo

121 ning was equal in right and left ventricular cardiocytes of control cats, but Glu-tubulin and Delta2-

122 e results suggest that direct stimulation of cardiocyte opioid delta(1) receptors leads to activation

123 ate and direct effect of load input into the cardiocyte or instead a concomitant of hypertrophic grow

124 protein synthesis in both adult and neonatal cardiocytes or 24-hour [3H]phenylalanine incorporation i

125 Compared with nonapoptotic cardiocytes or apoptotic cardiocytes incubated with norm

126 uclear DNA fragments showed that 11% were of cardiocyte origin confirmed by positive labeling with st

127 Our results suggest that resident cardiocytes participate in physiologic clearance of apop

128 n of SSA/Ro and SSB/La antigens to the fetal cardiocyte plasma membrane were common downstream events

129 ocytes incubated with normal sera, apoptotic cardiocytes preincubated with affinity-purified Abs to S

130 pared with healthy cardiocytes and apoptotic cardiocytes preincubated with IgG from a healthy donor,

131 ultures of healthy cardiocytes and apoptotic cardiocytes preincubated with IgG from a healthy donor.

132 ulated that in vivo such opsonized apoptotic cardiocytes promote an inflammatory response by resident

133 To evaluate whether opsonized apoptotic cardiocytes promote inflammation, cells were cocultured

134 tures of healthy cardiocytes and apo-CHB-IgG cardiocytes promoted Smad2 phosphorylation and fibroblas

135 3H]phenylalanine incorporation into neonatal cardiocyte protein over a 24-hour period by 10%, whereas

136 by anti-Ro60 binding to the apoptotic fetal cardiocyte provide a molecular basis by which these anti

137 opy, coculturing of healthy cardiocytes with cardiocytes rendered apoptotic via extrinsic pathways re

138 of the sarcolemmal surface in myofibers and cardiocytes, respectively.

139 Binding of anti-Ro60 antibodies to apoptotic cardiocytes results in increased uPAR expression, as wel

140 summary, induction of apoptosis in cultured cardiocytes results in surface translocation of Ro/La an

141 ocal microscopy analyses at the level of the cardiocyte revealed that p70(S6K) is present predominant

142 nostaining of nonpermeabilized myofibers and cardiocytes revealed that some obscurin kinase isoforms

143 In permeabilized nonapoptotic cardiocytes, Ro and La were predominantly nuclear, and p

144 ransfection of reporter gene constructs into cardiocytes showed that deletion of the region between -

145 ects were assessed in protocol C by defining cardiocyte sigma versus epsilon during an increase in si

146 in protocol B from the loop area between the cardiocyte sigma-versus-epsilon relationship during an i

147 In protocol A, the cardiocyte sigma-versus-epsilon relationship was similar

148 agarose gel at a constant rate to define the cardiocyte sigma-versus-epsilon relationship.

149 mice and in in vitro systems of neonatal rat cardiocytes stimulated with peptide growth factors.

150 a pathologic cascade involving apoptosis of cardiocytes, surface translocation of Ro and La antigens

151 ve shown the levels of the sarcomere and the cardiocyte that a persistent increase in microtubule den

152 protein synthesis in both adult and neonatal cardiocytes; this response was unaltered by 1 mumol/L [S

153 ures enclose sarcomeres and connect adjacent cardiocytes through functional gap junctions.

154 The genetic response of the cardiocyte to load was examined by assessing c-fos and N

155 +/- 0.77 dyne/cm2 in the normally loaded LV cardiocytes to 16.46 +/- 1.32 dyne/cm2 in the hypertroph

156 .97 +/- 1.92 poise in the normally loaded LV cardiocytes to 87.85 +/- 6.95 poise in the hypertrophied

157 introduced an improved model of loaded adult cardiocytes to address a proposed requirement for angiot

158 r has been isolated and characterized in rat cardiocytes to investigate the role of MMP-13 in cardiac

159 combination may cause pressure-hypertrophied cardiocytes to resist changes in shape during diastole a

160 arent viscosity values of normally loaded LV cardiocytes to the abnormal values given above for press

161 ted that binding of anti-Ro Abs to apoptotic cardiocytes triggers TGF-beta activation, by virtue of i

162 Whereas cardiocytes under both conditions showed RGD-stimulated

163 stiffness and apparent viscosity in isolated cardiocytes via magnetic twisting cytometry, a technique

164 er of cardiocytes connected to an individual cardiocyte was counted in tissues from the middle portio

165 gma-versus-epsilon relation in hypertrophied cardiocytes was shifted to the left compared with normal

166 Subsequently, cardiocytes were electrically stimulated to contract at

167 Apoptotic cardiocytes were incubated with affinity-purified Abs to

168 The isolated cardiocytes were subjected to passive load by step incre

169 Isolated adult feline cardiocytes were treated with a 14-mer phosphorothioate

170 understand its role, we overexpressed it in cardiocytes where it revealed a unique type of cell-to-c

171 immunofluorescent staining of chicken embryo cardiocytes with anti-C-RZF antibodies demonstrated that

172 Treatment of apo-CHB-IgG cardiocytes with anti-uPAR or anti-uPA Abs or plasmin in

173 confocal microscopy, coculturing of healthy cardiocytes with cardiocytes rendered apoptotic via extr

174 hibited following preincubation of apoptotic cardiocytes with chicken and murine anti-SSA/Ro and -SSB

175 Treatment of adult cardiocytes with either 0.1 microM insulin or 0.1 microM

176 by the treatment of transfected primary rat cardiocytes with interleukin-1 (IL-1) and basic fibrobla

177 e used embryonic stem cell (ES cell)-derived cardiocytes with targeted inactivations of specific PT-s

178 w intercellular junctions developing between cardiocytes within developed myocardium.