ライフサイエンスコーパス: hypertonicity

1 action following exposures to extracellular hypertonicity.

2 ells from the deleterious effects of ambient hypertonicity.

3 of the modulation domains were stimulated by hypertonicity.

4 (AQP1) is a water channel that is induced by hypertonicity.

5 lactose-supplemented medium or extracellular hypertonicity.

6 heat inducible, only HSP70-2 was induced by hypertonicity.

7 asmid led to a complete loss of induction by hypertonicity.

8 ellular polyol accumulation or extracellular hypertonicity.

9 scription of the HSP70-2 gene in response to hypertonicity.

10 erase was markedly stimulated in response to hypertonicity.

11 human diabetic condition known as nonketotic hypertonicity.

12 mined the regulation of the gamma subunit by hypertonicity.

13 ation of the gamma subunit of Na-K-ATPase by hypertonicity.

14 tatively involved in long term adaptation to hypertonicity.

15 in renal cells in response to extracellular hypertonicity.

16 d in most renal cell lines unless induced by hypertonicity.

17 or cell survival under extreme conditions of hypertonicity.

18 eins from IMCD3 cells chronically adapted to hypertonicity.

19 ses in hypotonicity, whereas it increases in hypertonicity.

20 potonicity and nuclear import in response to hypertonicity.

21 sed S100A4 message in IMCD3 cells adapted to hypertonicity.

22 ed SLC26A7 were retained in the cytoplasm in hypertonicity.

23 reatine transporter mRNA in cells exposed to hypertonicity.

24 hway in regulating induction of RMIC COX2 by hypertonicity.

25 anglion and Muller cells and is regulated by hypertonicity.

26 ed chloride secretion in response to luminal hypertonicity.

27 gamma-subunit expression in cells adapted to hypertonicity.

28 Clinically relevant hypertonicity (10-25 mM) suppressed degranulation and su

29 Hypertonicity (200 %) evoked a large non-selective (PK /

30 Inhibition by tamoxifen (10 microm) and by hypertonicity (340 mosm) identified them as ICl(swell).

31 Apical hypertonicity (350 mOsm) reduced Jdw by approximately 12

32 Basolateral hypertonicity (450 mOsm), after permeabilization of the

33 vity during normotonicity (290 mosmol/kg) or hypertonicity (500 mosmol/kg, NaCl added) or both.

34 sults demonstrate that water deprivation and hypertonicity activate NF-kappaB.

35 Hypertonicity activated ERK, p38 kinase, and JNK in mIMC

36 These results define JNK2 as the primary hypertonicity-activated JNK isoform in IMCD-3 cells and

37 studies are consistent with a model whereby hypertonicity activates COX2-derived prostaglandin produ

38 In cultured renal cells, hypertonicity activates multiple mitogen-activated prote

39 Separate reports that hypertonicity activates p38 via a Rac1-OSM-MEKK3-MKK3-p3

40 Hypertonicity activates the transcription factor TonEBP/

41 In the absence of vasopressin, hypertonicity alone induced rapid (<10 min) plasma membr

42 Hypertonicity also resulted in the rapid tyrosine phosph

43 o intracellular water deficits stemming from hypertonicity and a disturbance in water metabolism.

44 ibition by acidic pH(i) and to activation by hypertonicity and NH(+)(4).

45 osm-9 worms restored avoidance responses to hypertonicity and nose touch, but not the response to od

46 to the basolateral membrane is increased in hypertonicity and potassium depletion.

47 Using BLECs initially maintained at hypertonicity and reacting to a decrease in medium osmol

48 and mitochondrial potential were reduced by hypertonicity and recovered after longer periods of time

49 Alternatively, BLECs acclimated to sodium hypertonicity and subsequently transferred to high sodiu

50 how these solutes help relieve the stress of hypertonicity and the nature of transporters and enzymes

51 the normal regulatory response mechanism to hypertonicity and to identify whether and how this respo

52 thasone become unresponsive to regulation by hypertonicity and vasopressin.

53 istically, NF-kappaB activity increased with hypertonicity and was necessary for hypertonic induction

54 However, hyperactive stretch reflexes, hypertonicity, and the Babinski reflex were observed soo

55 llular stress, including noxious heat, cold, hypertonicity, and tissue damage, the nematode Caenorhab

56 retch effect also show strong enhancement by hypertonicity, and vice versa.

57 exit with phloretin reestablishes vestibular hypertonicity, as it reequilibrates with the cytosolic g

58 peech processing, levels of irritability and hypertonicity, attention levels, ability to self-regulat

59 Moreover, hypertonicity blunted aldosterone-stimulated expression

60 ite volume changes produced by extracellular hypertonicity, but at the expense of a cellular capacity

61 Currents were not activated by bath hypertonicity, but were inhibited by acid pH.

62 al homologous cascades that are activated by hypertonicity, but whose osmoregulatory targets are not

63 sult urea causes is not simply the result of hypertonicity; but rather (3) that urea, via breakdown t

64 is up-regulated by amino acid starvation and hypertonicity by a mechanism dependent on both ATF4-medi

65 Renal medullary cells compensate for hypertonicity by accumulating variable amounts of compat

66 medullary epithelial (IME) cells respond to hypertonicity by G(2) arrest.

67 ns, respectively, they survive the stress of hypertonicity by raising the cellular concentration of m

68 range 2-10 mM maintaining the same degree of hypertonicity caused a progressive activation of the con

69 Acute hypertonicity causes cell cycle delay and apoptosis in m

70 Vestibular hypertonicity causes osmotic water inflow, which raises

71 Hypertonicity did not induce a change in cytosolic cAMP

72 Thus, activation of p38 isoforms by hypertonicity does not contribute to activation of TonEB

73 re exposed to a hyperosmolar salt condition (hypertonicity) due to the operation of urinary concentra

74 The hypertonicity effect is sharply reduced (but not elimina

75 KC3AC1 cells, and Tis11b knockdown prevented hypertonicity-elicited repression of MR.

76 in hypertonic medium reveal that exposure to hypertonicity elicits slow activation of TonEBP, which i

77 iated by mechanical tension on integrins.The hypertonicity enhancement, like the stretch effect, does

78 It was reported previously that hypertonicity exerted a dual, time-dependent effect on v

79 in large part through the following pathway: hypertonicity --> Jak2 phosphorylation and activation --

80 Hypertonicity has been shown to modulate the innate immu

81 in the renal medulla adapt to the stress of hypertonicity (hyperosmotic salt) by accumulating organi

82 Tear film hypertonicity in AQP5 deficiency is likely caused by red

83 Tissues experience hypertonicity in both physiological (kidney medullar cel

84 Pro-inflammatory targets were induced by hypertonicity in discs from wild-type but not TonEBP-hap

85 subunits of Na-K-ATPase are up-regulated by hypertonicity in inner-medullary collecting duct cells a

86 gated upstream components of the response to hypertonicity in lung epithelial cells and found that be

87 al membrane transporter that is activated by hypertonicity in many cells.

88 Aquaporin-1 (AQP1) expression is induced by hypertonicity in renal medullary cells.

89 ullary collecting duct (IMCD) contributes to hypertonicity in the medullary interstitium which, in tu

90 y flow external to the transporter caused by hypertonicity in the outer cytosolic layers.

91 Hypertonicity increased accumulation of the organic osmo

92 Hypertonicity increased p38, ERK1/2, and JNK MAPK activi

93 In addition, hypertonicity increased total cellular and plasma membra

94 Here, we report that hypertonicity increases expression of the mRNA-destabili

95 ments demonstrated that exposure of cells to hypertonicity increases the binding of tonicity-responsi

96 We previously showed that hypertonicity increases transactivating activity of TonE

97 cells, a cell line derived from mouse IMCDs, hypertonicity induced a marked increase in COX-2 protein

98 Hypertonicity induced by NaCl, but not by urea or mannit

99 Inhibiting MAPK activity abolished hypertonicity-induced accumulation of AQP2 at the cell s

100 ignaling molecules that could be involved in hypertonicity-induced activation of NHE-1 in CHO-K1 cell

101 ause inhibition of p38 is reported to reduce hypertonicity-induced activation of the osmoprotective t

102 tion under isotonic conditions, and augments hypertonicity-induced apoptosis.

103 eIF2alpha phosphorylation are protected from hypertonicity-induced apoptosis.

104 Heat shock treatment promoted hypertonicity-induced AQP1 and heat shock protein 70 (HS

105 urea, betaine, and heat shock that regulate hypertonicity-induced AQP1 expression are potentially im

106 On the contrary, urea inhibited hypertonicity-induced AQP1 expression in a dose-dependen

107 ide (NaCl), urea, betaine, and heat shock on hypertonicity-induced AQP1 expression in cultured murine

108 inhibitor SP600125 significantly attenuated hypertonicity-induced AQP1 expression in mIMCD-3 cells.

109 element in the AQP1 promoter are involved in hypertonicity-induced AQP1 expression in mIMCD-3 cells.

110 hen cells were exposed continuously to N100, hypertonicity-induced AQP1 expression was elevated, wher

111 In addition, hypertonicity-induced AQP1 expression was significantly

112 of organic osmolyte betaine in N150 enhanced hypertonicity-induced AQP1 expression, whereas it decrea

113 50, suggesting an effect on the stability of hypertonicity-induced AQP1 expression.

114 nteract hypertonic stress and thus attenuate hypertonicity-induced AQP1 expression.

115 profoundly alters AQP2 trafficking and that hypertonicity-induced AQP2 accumulation at the cell surf

116 er vasopressin-dependent AQP2 trafficking or hypertonicity-induced AQP2 accumulation in the TGN.

117 Hypertonicity-induced binding of the transcription facto

118 nar cells from Aqp5(-)/- mice in response to hypertonicity-induced cell shrinkage and hypotonicity-in

119 OX2 gene significantly reduced both IKK1 and hypertonicity-induced COX2 reporter activity (p < 0.01).

120 Hypertonicity-induced EGF receptor (EGFR) transactivatio

121 blocked either regulatory volume increase or hypertonicity-induced enhancement of uptake of inositol,

122 The expression of mRNA for hypertonicity-induced genes (aldose reductase, betaine/g

123 Hypertonicity-induced increase in activity of the transc

124 endent protein kinase A activity blunted the hypertonicity-induced increase of AQP2 cell surface expr

125 QP2 transcriptional start site abolished the hypertonicity-induced increase of luciferase activity in

126 Hypertonicity-induced increases in IL-6 and IL-8 release

127 NK2 (HA-JNK2-APF) in stable clones inhibited hypertonicity-induced JNK activation by 40-70%, whereas

128 opanebetaine, in which a combination of NaCl hypertonicity-induced macropinocytosis and a transductio

129 Furthermore, hypertonicity-induced NFAT5/TonEBP transcriptional activ

130 chondria, but not NADPH oxidase, mediate the hypertonicity-induced phosphorylation of MAPK and the st

131 protein phosphatase 1 inhibitor, blocked the hypertonicity-induced PIP5KIbeta dephosphorylation/activ

132 noteworthy that luteolin strongly suppresses hypertonicity-induced release of the pro-inflammatory in

133 its regulation and the physiological role of hypertonicity-induced SGK1 gene expression remain unclea

134 tudies have documented MAPK mediation of the hypertonicity-induced stimulation of COX-2 expression in

135 1 and 3 sec during 30 Hz action potential or hypertonicity-induced stimulation.

136 sponsive enhancers (TonE) play a key role in hypertonicity-induced transcriptional stimulation of SMI

137 e amplitudes, frequency and velocity of such hypertonicity-induced waves closely resembled those of C

138 Hypertonicity induces a group of genes that are responsi

139 Thus, we propose that hypertonicity induces activation of NHE-1 in CHO-K1 cell

140 Hypertonicity induces an adaptive gene expression progra

141 In renal cells, hypertonicity induces genes for heat shock proteins (HSP

142 In mammalian cells, hypertonicity induces three mitogen-activated protein ki

143 recipitates from the HA-JNK2 cells displayed hypertonicity-inducible JNK activity.

144 tive TonEBP, IL6 and NOS2 promoters were not hypertonicity-inducible.

145 To determine whether activation of JNKs by hypertonicity is isoform-specific, renal inner medullary

146 induction of creatine transport activity by hypertonicity is not confined to muscle cells: a similar

147 ive and shrink when exposed to extracellular hypertonicity, it is not yet clear if these processes ar

148 ased AQP2 cell surface expression induced by hypertonicity largely resulted from a reduction in endoc

149 r gene is markedly stimulated in response to hypertonicity, leading to an increase in the activity of

150 Under external hypertonicity, loss of ine in the hindgut epithelium res

151 ic conditions was approximately 4 h, whereas hypertonicity markedly increased its half-life.

152 Hypertonicity markedly induced COX2 expression in cultur

153 Na+-independent, Cl--dependent mechanism for hypertonicity-mediated activation of the JNK and the sub

154 nyl)-5-(4-pyridyl) imidazole), abolishes the hypertonicity-mediated induction of mRNAs for HSP70 and

155 Hypertonicity (most often present as high salinity) is s

156 In healthy subjects, systemic hypertonicity normally excites osmoreceptor neurons in t

157 ease in apoptosis in the renal medulla where hypertonicity normally prevails.

158 from inhibition of the adaptive responses to hypertonicity occurring during the urinary concentrating

159 than do wild-type mice, indicating that the hypertonicity of the mutants is likely to be caused by d

160 Adaptation of cells to hypertonicity often involves changes in gene expression.

161 nthine oxidase system mimicked the effect of hypertonicity on COX-2 expression and prostaglandin E(2)

162 his study investigated the effect of chronic hypertonicity on the OKP cell Na/H antiporter, encoded b

163 which enables organisms to tolerate external hypertonicity or desiccation.

164 IkappaB mutant reduced COX2 expression after hypertonicity or IKKalpha induction.

165 orylation of TonEBP increased in response to hypertonicity, phosphorylation of the activation and mod

166 These results indicate that hypertonicity plays an important role in AQP1 induction,

167 These data indicate that acute hypertonicity profoundly alters AQP2 trafficking and tha

168 initiation of G(2) delay by p38 kinase after hypertonicity protects the cells by decreasing the level

169 Hypertonicity rapidly activated NHE-1 in a concentration

170 Previously, it was found that hypertonicity rapidly causes nuclear translocation and p

171 goal of this study was to determine whether hypertonicity regulates iNOS expression and function in

172 Hypertonicity regulates the activity of NF-kappaB in dif

173 s epithelial cells (BLECs) exposed to sodium hypertonicity respond with an accumulation of intracellu

174 of ERK, p38 kinase, and JNK pathways and the hypertonicity response element in the AQP1 promoter are

175 activity of AQP1 promoter, which contains a hypertonicity response element, was attenuated in the pr

176 transcription initiation site that mediates hypertonicity-responsive enhancer activity.

177 Hypertonicity-stimulated COX-2 protein expression was si

178 We have previously shown that hypertonicity stimulates cyclooxygenase-2 (COX-2) expres

179 Immunoprecipitation studies showed that hypertonicity stimulates the assembly of a signaling com

180 understand the molecular mechanisms by which hypertonicity stimulates transcription, we analyzed the

181 tivity associated with amino acid starvation/hypertonicity that depends upon processing/maturation an

182 ibed for the treatment of the synkinesis and hypertonicity that often develop.

183 This suggests that when stimulated by hypertonicity, the cotransporter mediates K(+)/K(+) and

184 role of molecular crowding on the effects of hypertonicity, the effects of ionic imbalance on cellula

185 Due to local hypoxia and hypertonicity, the renal medulla is subject to extreme o

186 However, after hours of constant hypertonicity, the slow accumulation in the cytoplasm of

187 In response to hypertonicity, the up-regulation of claudin-4 (Cldn4) ex

188 In line with this, when cells are exposed to hypertonicity to accumulate a large amount of compatible

189 of the transcription factor associated with hypertonicity, TonEBP.

190 se, the transcription factor associated with hypertonicity, tonicity enhancer-binding protein (TonEBP

191 me properties from control (alpha1beta1) and hypertonicity-treated cultures (alpha1beta1gammaa) revea

192 XYD2b but not FXYD2a from both untreated and hypertonicity-treated NRK-52E cells.

193 inant-negative JNK-2-expressing cells during hypertonicity treatment.

194 TonEBP is stimulated by hypertonicity via several pathways: increased expression

195 ar induction of endogenous gammaa because of hypertonicity was seen in rat cell lines of other than r

196 Whole-disc response to hypertonicity was studied in an ex vivo organ culture mo

197 t, responses evoked by action potentials and hypertonicity were severely impaired after the same trea

198 RMICs failed to survive hypertonicity when COX2 was downregulated using a COX2-s

199 Cultured HLECs and BLECs responded to hypertonicity with an inducible but transitory upregulat

200 lpighian tubule/hindgut requires a region of hypertonicity within the organ.