ライフサイエンスコーパス: AQP3

1 investigate HDAC's role in the regulation of AQP3.

2 versed MPXR in cells lacking native AQP2 and AQP3.

3 uamous cell carcinoma strongly overexpresses AQP3.

4 x 10(-14)) 3.3 +/- 0.2 (AQP2), 2.1 +/- 0.3 (AQP3), 24 +/- 0.6 (AQP4), 5.0 +/- 0.4 (AQP5), and 0.25 +

5 , 19 +/- 2 (AQP1), 10 +/- 1 (AQP2), 8 +/- 2 (AQP3), 29 +/- 1 (AQP4), 10 +/- 1 (AQP5), and 1.3 +/- 0.2

6 nto the cell by transit through aquaporin-3 (AQP3), a plasma membrane H2O2-conducting channel.

7 Aquaporin 3 (AQP3), a water/glycerol channel protein, has been found

8 In keratinocytes aquaporin-3 (AQP3), an efficient glycerol transporter, is associated

9 langiocytes, AQP4 in gastric parietal cells, AQP3 and AQP4 in colonic surface epithelium, AQP5 in sal

10 Consistent with the known functions of Aqp3 and Aqp8 as H2O2 transporters, primitive, but not d

11 irectly demonstrates that aquaporin isoforms AQP3 and AQP8, but not AQP1, can promote uptake of H(2)O

12 our laboratory has shown co-localization of AQP3 and phospholipase D2 (PLD2) in caveolin-rich membra

13 ) in response to TNF-alpha is facilitated by AQP3 and required for NF-kappaB activation by regulation

14 re the same pathway with glycerol or urea in AQP3 and that this aquaporin, therefore, forms a water-s

15 psoriasis is reduced in AQP3 knockout mice (AQP3(-/-)), and is accompanied by impaired NF-kappaB act

16 icant decrease in protein abundance of AQP2, AQP3, and AQP4 in HT rats as compared with CTL and HT+T

17 cending limb of Henle, and vasa recta; AQP2, AQP3, and AQP4 in the collecting duct; AQP6 in the papil

18 of mice lacking kidney water channels AQP1, AQP3, and AQP4 indicates a critical role for AQP2 in neo

19 nd on knockout mice lacking aquaporins AQP1, AQP3, and AQP5.

20 an control rats despite an increase in AQP1, AQP3, and Na-K-2Cl co-transporter expression.

21 d increased abundance of aquaporin 1 (AQP1), AQP3, and Na-K-2Cl co-transporter proteins and a marked

22 genic null mice lacking (individually) AQP1, AQP3, AQP4, and AQP5.

23 edullary collecting-duct water channel AQP4, AQP3/AQP4 double-knockout mice were generated.

24 uaglyceroporins, encoded by the aquaporin 3 (Aqp3), Aqp7, and Aqp9 genes in mouse islets.

25 Multifunctional aquaglyceroporins AQP3, AQP7, and AQP9 are permeated by water, glycerol, a

26 AQP1 and AQP3 are also expressed in the kidney where their deleti

27 Recent data implicate AQP3 as an important determinant in epidermal proliferat

28 As AQP3 associates with Nox2, we propose that this interpla

29 addition, phloretin (0.1 mM) inhibited Pf of AQP3 by 35%, whereas it did not alter Pgly or Pur.

30 e report that the water channel Aquaporin-3 (AQP3) can facilitate the uptake of H(2)O(2) into mammali

31 The mouse AQP3 cDNA was isolated and encodes a 292-amino acid wate

32 ells irreversibly, while Ni (2+) blocked the AQP3 channels reversibly.

33 AQP3 coexpression decreased the promoter activity of ker

34 gged AQP3 (GLIP) and each of the four tagged AQP3 constructs; [3H]glycerol uptake was not increased i

35 d using polyclonal antibodies to rat AQP2 or AQP3 (courtesy of Dr. M.A. Knepper, National Institutes

36 AQP3 deficiency did not alter corneal epithelial thickne

37 glycerol-3-phosphate, and ATP were found in AQP3 deficiency without impairment of mitochondrial func

38 the reduced proliferation and ATP content in AQP3 deficiency, with cellular glycerol, ATP, and prolif

39 AQP3 deficient (AQP3(-/-)) mice exhibited significantly

40 Reduced AQP3-dependent glycerol transport in AQP3-deficient epidermis appears to be responsible for t

41 tion in proliferating BrdU-positive cells in AQP3-deficient mice during healing, and by reduced proli

42 mpairment in corneal re-epithelialization in AQP3-deficient mice results from distinct defects in cor

43 ) = 0.025 cm/s), slowing 3.6 +/- 0.7-fold in AQP3-deficient mice.

44 hanical, and biosynthetic defects in skin of AQP3-deficient mice.

45 AQP3 deletion did not affect erythrocyte glycerol permea

46 By electron microscopy AQP3 deletion did not affect the structure of the unpert

47 AQP3 deletion had little effect on AQP1 or AQP4 protein

48 a, lactic acid, glucose) was not affected by AQP3 deletion nor was the absolute amount or profile of

49 asal skin barrier function was not impaired, AQP3 deletion produced an approximately 2-fold delay in

50 However, AQP3 deletion produced significant reductions in glycero

51 AQP3 deletion resulted in a > 4-fold reduced osmotic wat

52 stinct defect in cell migration arising from AQP3 deletion.

53 iva was 0.0011 cm/s and was not sensitive to AQP3 deletion.

54 ng, was also approximately 2-fold delayed by AQP3 deletion.

55 and morphology were not grossly affected by AQP3 deletion.

56 tering optics method, was >3-fold reduced by AQP3 deletion.

57 components with E-cadherin, but each blocked AQP3 delivery to forming cell-cell contacts.

58 Reduced AQP3-dependent glycerol transport in AQP3-deficient epid

59 e burns accelerated their healing through an AQP3-dependent mechanism that activates angiogenesis, tr

60 In response to injury, AQP3-depleted colonic epithelial cells showed defective

61 Daily urine output in AQP1/AQP3 double knockout mice (15 ml) was 9-fold greater tha

62 Here AQP1/AQP3 double knockout mice were generated and analyzed to

63 Hg (2+) inhibited the water flux in AQP3-expressing cells irreversibly, while Ni (2+) blocke

64 C3 suggested a role for HDAC3 in suppressing AQP3 expression basally.

65 Thus, our study supports the regulation of AQP3 expression by HDAC3 and p53.

66 However, AQP3 expression has not been observed in mouse erythrocy

67 AQP3 expression in human skin is increased in response t

68 cells in the collecting duct, and increased AQP3 expression in the basolateral membrane.

69 Modulation of AQP3 expression or function may thus alter epidermal moi

70 be modulated up or down based on endogenous AQP3 expression, which in turn can influence downstream

71 nvolved in regulating HDAC inhibitor-induced AQP3 expression.

72 The contribution of AQP3-facilitated cell migration to corneal re-epithelial

73 Our data suggest involvement of AQP3-facilitated glycerol transport in epidermal cell pr

74 Collectively, these data indicate that AQP3-facilitated H2O2 transport is required for NF-kappa

75 Both AQP2 and AQP3 gained access to the surface plasma membrane in ins

76 esis was discovered using mice with targeted AQP3 gene disruption.

77 The mouse AQP3 gene was analyzed, and AQP3 null mice were generate

78 over control) in oocytes expressing untagged AQP3 (GLIP) and each of the four tagged AQP3 constructs;

79 Re-expression of AQP3 had no effect on the expression of the proliferatio

80 Thus, our results indicate that AQP3 has a pro-differentiative role in epidermal keratin

81 Aquaporin (AQP) water channel AQP3 has been proposed to be the major glycerol and non-

82 rmal water/glycerol transporter aquaporin-3 (AQP3) have reduced stratum corneum (SC) hydration and sk

83 These results imply a critical role of AQP3 in asthma, and AQP3 may be a novel therapeutic targ

84 udies indicate independent roles of AQP1 and AQP3 in countercurrent exchange and collecting duct osmo

85 Involvement of AQP3 in epithelial cell proliferation was investigated b

86 alyzed to investigate the functional role of AQP3 in erythrocytes and kidneys.

87 H2O2 in the colonic epithelium and implicate AQP3 in innate immunity at mucosal surfaces.

88 udies, controversy remains about the role of AQP3 in keratinocyte differentiation.

89 To test this idea, we re-expressed AQP3 in mouse keratinocytes derived from AQP3-knockout m

90 t functional evidence for the involvement of AQP3 in skin physiology.

91 A novel role for AQP3 in skin tumorigenesis was discovered using mice wit

92 We studied the role of AQP3 in stratum corneum (SC) hydration by comparative me

93 -2 (AQP2), phosphorylated AQP2 (p-AQP2), and AQP3 in the inner medulla and in the outer medulla plus

94 rmal water/glycerol transporter aquaporin-3 (AQP3) in mice reduced superficial skin conductance by ap

95 in vivo and vitro experiments indicated that AQP3 induced the production of some chemokines such as C

96 aquaporin in cell proliferation and suggest AQP3 induction as a possible therapy to accelerate the r

97 rapy for skin diseases like psoriasis, where AQP3 is abnormally expressed.

98 Our data provide direct evidence that AQP3 is not functionally important in erythrocyte water

99 Finally, we establish that AQP3 is required for Nox-derived H(2)O(2) signaling upon

100 AQP3 is the AQP that is expressed in the skin where it f

101 AQP3 is thus a key player in epidermal biology and a pot

102 ; (b) AQP2 is unchanged in the base; and (c) AQP3 is unchanged.

103 Aquaporin-3 (AQP3) is a membrane transporter of water and glycerol ex

104 Aquaporin-3 (AQP3) is a small transmembrane water/glycerol channel th

105 Aquaporin-3 (AQP3) is a water and glycerol channel expressed in epide

106 Aquaporin-3 (AQP3) is a water channel expressed at the basolateral pl

107 Aquaporin-3 (AQP3) is a water channel found in the basolateral cell m

108 Aquaporin-3 (AQP3) is a water/glycerol-transporting protein expressed

109 Here, we show that H2O2, imported via AQP3, is involved in nuclear factor-kappaB (NF-kappaB) s

110 ediated induction of psoriasis is reduced in AQP3 knockout mice (AQP3(-/-)), and is accompanied by im

111 d [(3)H]glycerol uptake in normal but not in AQP3-knockout keratinocytes, confirming that the express

112 oliferation and skin tumorigenesis, in which AQP3-knockout mice are resistant to tumor formation by a

113 AQP3-knockout mice have reduced stratum corneum water co

114 content in epidermis and stratum corneum in AQP3-knockout mice, and correction of the phenotype abno

115 sed AQP3 in mouse keratinocytes derived from AQP3-knockout mice.

116 The SAHA-induced increase in AQP3 levels resulted in enhanced [(3)H]glycerol uptake i

117 imply a critical role of AQP3 in asthma, and AQP3 may be a novel therapeutic target.

118 AQP3 may thus be an important determinant in skin tumori

119 ce receiving OVA-sensitized splenocytes from AQP3(-/-) mice compared with wild-type mice after OVA ch

120 consistently with fewer CD4(+) T cells from AQP3(-/-) mice migrating to the lung than from wild-type

121 hogen Citrobacter rodentium Correspondingly, AQP3(-/-) mice showed impaired healing of superficial wo

122 AQP3 deficient (AQP3(-/-)) mice exhibited significantly reduced airway i

123 itor suberoylanilide hydroxamic acid induced AQP3 mRNA and protein expression in a dose- and time-dep

124 cells potentiated the expression of AQP2 and AQP3 mRNA, and cAMP production induced by dDAVP (desmopr

125 lly corrected the reduced skin elasticity in AQP3 null mice as measured by the kinetics of skin displ

126 The renal medulla in most AQP1/AQP3 null mice by age 4 weeks was atrophic and fluid-fil

127 by comparative measurements in wild-type and AQP3 null mice generated in a hairless SKH1 genetic back

128 The hairless AQP3 null mice had normal perinatal survival, growth, an

129 city, barrier recovery, and wound healing in AQP3 null mice in a hairless (SKH1) genetic background a

130 howed remarkably reduced SC water content in AQP3 null mice in the hairless genetic background (165 +

131 tion in epidermal and SC glycerol content in AQP3 null mice may account for these defects, providing

132 The impaired skin hydration in AQP3 null mice provides the first functional evidence fo

133 s that the residual concentrating ability of AQP3 null mice was due to the inner medullary collecting

134 Fluid consumption in AQP3 null mice was more than 10-fold greater than that i

135 SC hydration in hairless wild-type and AQP3 null mice was reduced to comparable levels (90-100

136 sin administration or water deprivation, the AQP3 null mice were able to concentrate their urine part

137 The mouse AQP3 gene was analyzed, and AQP3 null mice were generated by targeted gene disruptio

138 The growth and phenotype of AQP3 null mice were grossly normal except for polyuria.

139 ed by cutometry was significantly reduced in AQP3 null mice with approximately 50% reductions in elas

140 reduced blood-to-SC transport of glycerol in AQP3 null mice, resulting in slowed lipid biosynthesis.

141 SC glycerol content is reduced 3-fold in AQP3 null mice, whereas SC structure, protein/lipid comp

142 replacement corrects each of the defects in AQP3 null mice.

143 d reduced water content throughout the SC in AQP3 null mice.

144 content was reduced by approximately 50% in AQP3 null mice.

145 reduced water holding capacity in the SC of AQP3 null mice.

146 QP1 deletion but not further reduced in AQP1/AQP3 null mice.

147 e and 3H2O accumulation, was 3-fold lower in AQP3 null vs. wild-type mice, but became similar after t

148 ll proliferation was greatly impaired in the AQP3-null epidermis.

149 ization in vivo was significantly delayed in AQP3-null mice compared to wild-type mice.

150 d restoration of full-thickness epithelia of AQP3-null mice over days after scraping suggested a sepa

151 lities were measured in living wild-type and AQP3-null mice using calcein fluorescence-quenching and

152 We found that AQP3-null mice were remarkably resistant to the developm

153 parable apoptotic responses in wild-type and AQP3-null mice, promoter-induced cell proliferation was

154 rneal epithelial cells from wild-type versus AQP3-null mice.

155 ry cultures of corneal epithelial cells from AQP3-null mice.

156 e found expression of Aqp7 only, not that of Aqp3 or Aqp9, in the endocrine pancreas at both the mRNA

157 sfection experiments were performed in which AQP3 or empty vector was introduced into keratinocytes s

158 as ABR thresholds were not affected by AQP1, AQP3, or AQP5 deletion.

159 293) cells were transiently transfected with AQP3- or AQP4-encoding genes to express AQPs in plasma m

160 Here we report that AQP3 potentiates ovalbumin (OVA)-induced murine asthma b

161 l trafficking of AQP2, p-AQP2, and increased AQP3 protein expression.

162 2 (AQP2, the AVP-regulated water channel) or AQP3 protein was altered.

163 sphatidylglycerol (PG), we hypothesized that AQP3 provides glycerol to PLD2 for PG synthesis, which t

164 ot a LD PLD1 mutant, significantly inhibited AQP3 re-expression-induced differentiation marker expres

165 with 6.0 and 2.3 for water channels AQP1 and AQP3, respectively.

166 genes coding for the channel proteins Aqp2, Aqp3, Scnn1b (ENaCbeta), and Scnn1g (ENaCgamma), which a

167 Interestingly, overexpression of AQP1 and AQP3 showed no differences in extracellular signal-regul

168 f urinary-concentrating ability than did the AQP3 single-knockout mice.

169 Thus, our results support the idea that AQP3 supplies PLD2 with glycerol for synthesizing PG, a

170 For AQP3 the Arrhenius energy of activation for Pf was 3 kca

171 To examine the selectivity of AQP3, the permeability to water (Pf), urea (Pur), and gl

172 ferentiative signal, such that the action of AQP3 to induce differentiation should require PLD2.

173 estigation that examined the contribution of AQP3 to the mechanism of EPO action on the healing of bu

174 Acidic medium inhibits AQP3 transport activity; both glycerol uptake and PG syn

175 We hypothesized that AQP3 transports glycerol and "funnels" this primary alco

176 keratinocytes, confirming that the expressed AQP3 was functional.

177 e uptake of glycerol into oocytes expressing AQP3 was linear up to 165 mM.

178 Xenopus oocytes injected with cRNA encoding AQP3 was measured.

179 it water flow across the cell membrane, only AQP3 was permeable to glycerol and urea (Pgly > Pur).

180 all solute-transporting protein aquaporin-3 (AQP3) was found by immunofluorescence and immunogold ele

181 closely related aquaglyceroporins, AQP2 and AQP3, was linked to MPXR in a high-throughput loss-of-fu

182 ercuriphenylsulfonate (1 mM) abolished Pf of AQP3, whereas it did not affect Pgly.

183 The re-expression of AQP3, which increased [3H]glycerol uptake, also induced