ライフサイエンスコーパス: AQP5

1 encoding water-channel protein aquaporin-5 (AQP5).

2 type I (AT1) cell-specific gene aquaporin-5 (Aqp5).

3 89 blocked the cpt-cAMP-mediated increase of AQP5.

4 ce and transgenic null mice lacking AQP1 and AQP5.

5 nvolved in Ca(2+)-dependent up-regulation of AQP5.

6 secretion in wild-type mice and mice lacking AQP5.

7 lacking (individually) AQP1, AQP3, AQP4, and AQP5.

8 type mice and knockout mice lacking AQP4 or AQP5.

9 1 carboxyl terminus that were not present in AQP5.

10 lecting duct, in addition to AQP0, AQP4, and AQP5.

11 kout mice lacking aquaporins AQP1, AQP3, and AQP5.

12 ithin the homologous p358P/E region of mouse Aqp5.

13 rway epithelial cell line without endogenous AQP5.

14 of the paracellular barrier in mice lacking AQP5.

15 ells and in the apical region of acini along AQP5.

16 0.03 nl min(-1) gland(-1)) vs. mice lacking AQP5 (0.19 +/- 0.04 nl min(-1) gland(-1)).

17 ation, and spacer length 5'-AQP2-5 kb spacer-AQP5-7 kb spacer-AQP6-3'.

18 corneal epithelial cell marker aquaporin 5 (AQP5), a water channel protein.

19 fter hypotonic stimulation; and reduction of AQP5 abundance after addition of the TRPV4 agonist 4alph

20 rgic agonist terbutaline produced changes in AQP5 abundance in mouse trachea and lung, consistent wit

21 er studies, these observations indicate that AQP5 abundance is tightly regulated along a range of osm

22 otonic medium, a dose-responsive decrease in AQP5 abundance was observed.

23 lead to a selective decrease in aquaporin-5 (AQP5) abundance because of protein internalization and d

24 HDAC3 overexpression inhibited Sp1-mediated Aqp5 activation, while HDAC3 knockdown augmented AQP5 pr

25 The predominant message is for AQP5, although the evidence was consistent with the pres

26 Importantly, AQP5, an acinar-specific protein critical for function,

27 Elevated levels of AQP5 and cleaved 120-kDa fragments of alpha-fodrin were

28 on of markers for alveolar epithelial cells (Aqp5 and Sftpc), Clara cells (Scgb1a1) and ciliated cell

29 ed the association and surface expression of AQP5 and TRPV4.

30 rn blotting for the presence of aquaporin 5 (AQP5) and 120-kDa fragments of alpha-fodrin.

31 0.3 (AQP3), 24 +/- 0.6 (AQP4), 5.0 +/- 0.4 (AQP5), and 0.25 +/- 0.05 (MIP); pf values were insensiti

32 , 8 +/- 2 (AQP3), 29 +/- 1 (AQP4), 10 +/- 1 (AQP5), and 1.3 +/- 0.2 (MIP), and they were relatively i

33 n of TMEM16A, the water channel aquaporin 5 (AQP5), and other regulators of sweat gland function was

34 ion and aqua channel genes (Ae2a, Car2, and Aqp5), and salivary gland markers.

35 the number of tight junction strands of both AQP5+/+ and AQP5-/- male mice after pilocarpine stimulat

36 lot analysis indicated the presence of AQP2, AQP5, and AQP6 genes, but not AQP0.

37 most closely related aquaporins (AQP0, AQP2, AQP5, and AQP6) have been mapped to chromosome band 12q1

38 R (Muscarinic Acetylcholine receptor M3) and AQP5 (Aquaporin 5) protein expression, b) decreased sali

39 ransient receptor potential vanalloid 4) and AQP5 (aquaporin 5), which is required for regulating wat

40 educed amino acid sequences of human and rat AQP5 are 91% identical with 6 substitutions in the 22-am

41 tion and serine/threonine phosphorylation of AQP5 are required for proper function.

42 These results show that cAMP regulates AQP5 at multiple levels, by increasing synthesis of AQP5

43 ar endothelia, AQP4 in airway epithelia, and AQP5 at the apical plasma membrane in type I cells of al

44 fic antibodies revealed strong expression of AQP5 at the luminal membrane of secretory epithelial cel

45 strong expression of aquaporin water channel AQP5 at the luminal membrane of serous epithelial cells

46 munofluorescence data reveal the presence of AQP5 at the plasma membrane in the stratum granulosum of

47 isolation and characterization of the human AQP5 cDNA and gene.

48 The AQP5 cDNA from a human submaxillary gland library contai

49 porters and aquaporins, including AE3, AQP4, AQP5, CFTR, ClC2gamma, KCC1, NHE1, NKAalpha1, NKAbeta1,

50 ion barrier, were significantly decreased in AQP5-/- compared with AQP5+/+ salivary glands.

51 on cell swelling per se, and (ii) TRPV4 and AQP5 concertedly control regulatory volume decrease.

52 onally, administration of IGF-1 to Atg5(f/f);Aqp5-Cre mice did not preserve physiological function.

53 In this study, we utilized Atg5(f/f);Aqp5-Cre mice which harbor a conditional knockout of Atg

54 Collectively, Atg5(f/f);Aqp5-Cre mice would be a useful tool to enhance our unde

55 ory granules in salivary glands of Atg5(f/f);Aqp5-Cre mice.

56 phagy, in salivary acinar cells of Atg5(f/f);Aqp5-Cre mice.

57 rol of aquaporin 5 (Aqp5) promoter/enhancer (Aqp5-Cre) allows us to specifically inactivate Atg5, a p

58 Tear film hypertonicity in AQP5 deficiency is likely caused by reduced transcorneal

59 shown that the volume of saliva secreted by AQP5-deficient mice is decreased, indicating a role for

60 trations in urine and blood in wild-type and AQP5-deficient mice.

61 /s and decreased by greater than fivefold in AQP5-deficient mice.

62 wild-type mice, slowing 2.1 +/- 0.4-fold in AQP5-deficient mice; tau was 2.4 +/- 0.1 seconds in conj

63 /- 0.3 microm/min, wild type) was reduced by AQP5 deletion (2.7 +/- 0.1 microm/min).

64 P(f) was reduced 10-fold by AQP5 deletion and was further reduced by 2- to 3-fold in

65 AQP5 deletion did not affect lung morphology at the ligh

66 P5 knockout mice, nor was there an effect of AQP5 deletion when fluid absorption was maximally stimul

67 functional sweat glands was not affected by AQP5 deletion.

68 eal transparency was not impaired by AQP1 or AQP5 deletion.

69 resholds were not affected by AQP1, AQP3, or AQP5 deletion.

70 ulmonary artery pressure was not affected by AQP5 deletion.

71 salivary mucous cells, were not affected by AQP5 deletion.

72 lands, where fluid secretion is aquaporin-5 (AQP5) dependent, we postulated that aquaporin water chan

73 inar cells from mice lacking either TRPV4 or AQP5 displayed greatly reduced Ca2+ entry and loss of RV

74 duce distinct short and long term effects on AQP5 distribution and abundance that may contribute to r

75 We examined the effects of cAMP on AQP5 distribution and abundance.

76 was further reduced by 2- to 3-fold in AQP1/AQP5 double-knockout mice.

77 ncing, missense mutations were identified in AQP5, encoding water-channel protein aquaporin-5 (AQP5).

78 es expressing AmtB and RhAG, but not AQP4 or AQP5, exhibit greater DeltapH(S)(NH(3)) values.

79 -4.3- and -1.7-AQP5-luciferase constructs in AQP5-expressing lung (MLE-15) and salivary (Pa-4) cells

80 When AQP5-expressing mouse lung epithelial cells were treated

81 ed in control (water-injected) oocytes or in AQP5-expressing oocytes with osmotic water permeabilitie

82 roylanilide hydroxamic acid (SAHA) increased AQP5 expression and Sp1-mediated transcription of p358P/

83 soproternol also caused similar increases in AQP5 expression both in vitro and in mouse lung tissue s

84 n factors and histone modifications regulate Aqp5 expression during alveolar epithelial cell transdif

85 ion may permit molecular characterization of AQP5 expression during normal development and in clinica

86 d osmolarity; however, osmotic regulation of AQP5 expression has not been reported.

87 Here we show that AQP5 expression in cultured lung epithelial cells is dec

88 g immunohistochemical staining, we show that AQP5 expression in mouse lung is not restricted to type

89 Bmla1 overexpression resulted in increased Aqp5 expression levels.

90 Modulation of gland AQP5 expression or function might provide a novel approa

91 We found that AQP5 expression was needed for shear-induced barrier enh

92 FGFR1b, Fgf1, and Spry1 as well as increased Aqp5 expression, a marker of end bud differentiation.

93 st antibody is sufficient to cause decreased AQP5 expression, demonstrating that the TNF-alpha effect

94 he nucleus blocks the effect of TNF-alpha on AQP5 expression, indicating that activation of NF-kappaB

95 tor/histone acetyltransferase p300 decreased AQP5 expression, while p300 overexpression enhanced p358

96 lls in vitro, as indicated by an increase in AQP5 expression.

97 siologic relevance for osmotic regulation of AQP5 expression.

98 medium produced a dose-dependent increase in AQP5 expression; AQP5 protein peaked by 24 h and returne

99 These results indicate that AQP5 facilitates fluid secretion in submucosal glands an

100 ockout (Aqp5(-/-)) mice were used to analyze AQP5 function in pulmonary physiology.

101 ithin the proximal 5'-flanking region of rat AQP5 gene dictates its restricted expression in both lun

102 compassing the 5'-flanking region of the rat AQP5 gene has been characterized in detail.

103 q and mouse chromosome 15, which contain the Aqp5 gene.

104 H(3))*, the sequence was AQP4 congruent with AQP5 > AQP1 > AmtB > RhAG.

105 o DeltapH(S)(CO(2))*/P(f)*, the sequence was AQP5 > AQP1 congruent with AQP4.

106 en demonstrated that overexpression of human AQP5 (hAQP5) induces cell proliferation in colon cancer

107 type distribution from intercross of founder AQP5 heterozygous mice was 70:69:29 wild-type:heterozygo

108 Oocytes expressing rat AQP4, rat AQP5, human RhAG, or the bacterial Rh homolog AmtB also

109 malian cornea, AQP1 in endothelial cells and AQP5 in epithelial cells.

110 These results implicate a key role for AQP5 in saliva fluid secretion and provide direct eviden

111 ent mice is decreased, indicating a role for AQP5 in saliva secretion; however, the mechanism by whic

112 AQP3 and AQP4 in colonic surface epithelium, AQP5 in salivary gland, AQP7 in small intestine, AQP8 in

113 These results indicate the expression of AQP5 in sweat gland secretory epithelium, but provide di

114 We demonstrate here a role for AQP5 in the palmoplantar epidermis and propose that the

115 Expression of human AQP5 in Xenopus oocytes conferred mercurial-sensitive os

116 TRPV4 participates in hypotonic reduction of AQP5, including a requirement for extracellular calcium

117 AQP5 induction was also observed in the lung, salivary,

118 AQP5 induction was observed only with relatively imperme

119 (MEK) inhibitors, U0126 and PD98059, blocked AQP5 induction.

120 These data suggest a novel pathway by which AQP5 influences bronchoconstriction.

121 Genomic Southern analysis indicated that AQP5 is a single copy gene which localized to human chro

122 ional and post-transcriptional regulation of AQP5 is accomplished.

123 This study demonstrates that AQP5 is induced by hypertonic stress and that induction

124 titative RT-PCR confirmed that expression of AQP5 is much lower in KC cornea than in non-KC cornea.

125 These results indicate that AQP5 is responsible for the majority of water transport

126 In the salivary gland, AQP5 is the major aquaporin expressed on the apical memb

127 These data show that AQP5 is the major pathway for regulating the water perme

128 Aquaporin-5 (AQP5) is a water channel protein expressed in lung, sali

129 Aquaporin-5 (AQP5) is a water channel protein that is selectively exp

130 Aquaporin-5 (AQP5) is a water-selective transporting protein expresse

131 Aquaporin-5 (AQP5) is expressed in epithelia of lung, cornea, and var

132 Aquaporin-5 (AQP5) is present on the apical membrane of epithelial ce

133 Although aquaporin 5 (AQP5) is the major water channel expressed in alveolar t

134 P)-3, but not the equivalent apical membrane AQP5, is delivered in post-Golgi structures directly to

135 Aqp5 knockout (Aqp5(-/-)) mice were used to analyze AQP5

136 absorption did not differ in litter-matched AQP5 knockout mice, nor was there an effect of AQP5 dele

137 Here, we examined the role of AQP5 using AQP5 knockout mice, which were recently shown to manifes

138 a production was reduced by more than 60% in AQP5 knockout mice.

139 he mechanisms that underlie this decrease in AQP5 levels are therefore of considerable interest.

140 nsient transfection assays of -4.3- and -1.7-AQP5-luciferase constructs in AQP5-expressing lung (MLE-

141 ies of 5' --> 3' deletion constructs of -4.3-AQP5-luciferase suggest that a common salivary and lung

142 ns in the expression of Sftpa, Sftpb, Abca3, Aqp5, Lzp-s, Scd2, and Aytl2 in lungs misexpressing MIA.

143 f tight junction strands of both AQP5+/+ and AQP5-/- male mice after pilocarpine stimulation but no c

144 Compared with Aqp5(+/+) mice, Aqp5(-/-) mice show a significantly incr

145 otid and 77% in sublingual acinar cells from Aqp5(-)/- mice in response to hypertonicity-induced cell

146 increased tonicity of the saliva secreted by Aqp5(-)/- mice in response to pilocarpine stimulation ar

147 id and sublingual acinar cells isolated from Aqp5(-)/- mice is decreased significantly.

148 oconstriction, was significantly enhanced in Aqp5(-/-) mice challenged with aerosolized methacholine

149 Compared with Aqp5(+/+) mice, Aqp5(-/-) mice show a significantly increased concentrat

150 ivity to bronchoconstriction observed in the Aqp5(-/-) mice was not due to differences in tracheal sm

151 Aqp5 knockout (Aqp5(-/-)) mice were used to analyze AQP5 function in pu

152 liva of AQP5-/- mice is half that in matched AQP5+/+ mice, indicating a 2-fold decrease in permeabili

153 tion of FITC-D into either AQP5 wild-type or AQP5-/- mice and saliva collection for fixed time interv

154 mount of FITC-D transported in the saliva of AQP5-/- mice is half that in matched AQP5+/+ mice, indic

155 sed by approximately 1.4-fold in glands from AQP5-/- mice, suggesting an alteration in the volume-sen

156 multiple levels, by increasing synthesis of AQP5 mRNA and by triggering translocation of AQP5 to the

157 These data show that TNF-alpha decreases AQP5 mRNA and protein expression and that the molecular

158 oncentration- and time-dependent decrease in AQP5 mRNA and protein expression.

159 -cAMP (cpt-cAMP) causes a 4-fold increase in AQP5 mRNA and protein levels and induces translocation o

160 in D abolished the cAMP-mediated increase in AQP5 mRNA and showed that there was no increase in the h

161 at there was no increase in the half-life of AQP5 mRNA, and inhibition of protein kinase A by H-89 bl

162 de blocked the cpt-cAMP-mediated increase of AQP5 mRNA, indicating that de novo protein synthesis is

163 tivation of TRPV4 by hypotonicity depends on AQP5, not on cell swelling per se, and (ii) TRPV4 and AQ

164 )] was increased by approximately twofold in AQP5 null mice (230 +/- 20 mM) and was greatly reduced a

165 QP4 null mice, and 1.9 +/- 0.3 microl/min in AQP5 null mice (p < 0.001).

166 .3 +/- 0.2-fold increase in total protein in AQP5 null mice and a smaller increase in [Cl(-)], sugges

167 We generated AQP5 null mice by targeted gene disruption.

168 land morphology was similar in wild-type and AQP5 null mice.

169 y reduced in AQP1 null mice and increased in AQP5 null mice.

170 a 57 +/- 4% reduced fluid secretion rate in AQP5 null mice.

171 not differ significantly in wild type versus AQP5 null mice.

172 type), 101 +/- 2 (AQP1 null), and 144 +/- 2 (AQP5 null).

173 The unimpaired alveolar fluid clearance in AQP5-null mice indicates that high alveolar water permea

174 P(f)(tiss) in AQP5-null mice was restored to 0.0015 cm/s after removal

175 exposure to cAMP produced internalization of AQP5 off of the membrane and a decrease in protein abund

176 The lack of effect of AQP5 on sweat secretion rate was confirmed by microcapil

177 not different in lungs of mice lacking AQP1, AQP5 or AQP1/AQP5 together, despite an up to 30-fold red

178 ased in oocytes expressing AQP1, AQP2, AQP4, AQP5, or MIP.

179 To determine whether AQP5 plays a role in mediating the shear effects on para

180 The membrane water channel aquaporin 5 (AQP5) plays an important role in transporting water acro

181 entified critical NFAT binding motifs in the AQP5 promoter that are involved in Ca(2+)-dependent up-r

182 recombinase through control of aquaporin 5 (Aqp5) promoter/enhancer (Aqp5-Cre) allows us to specific

183 activation, while HDAC3 knockdown augmented AQP5 protein expression.

184 immunochemistry, we have found expression of AQP5 protein in 62.8% (59/94) of resected colon cancer t

185 dose-dependent increase in AQP5 expression; AQP5 protein peaked by 24 h and returned to baseline lev

186 Purified AQP5 protein was phosphorylated by protein kinase A but

187 almar epidermis, indicating that the altered AQP5 proteins are trafficked in the normal manner.

188 antar epidermis and propose that the altered AQP5 proteins retain the ability to form open channels i

189 Our data indicate that AQP1 and AQP5 provide the principal routes for corneal water tran

190 , whereas the suppression of transcripts for AQP5 provides the first clear evidence of a molecular de

191 lated along a range of osmolalities and that AQP5 reduction by extracellular hypotonicity can be medi

192 irement for extracellular calcium to achieve AQP5 reduction; an increase in intracellular calcium in

193 a secretion; however, the mechanism by which AQP5 regulates water transport in salivary acinar cells

194 a-adrenergic agonist terbutaline, a biphasic AQP5 response was observed.

195 ificantly decreased in AQP5-/- compared with AQP5+/+ salivary glands.

196 Nfib only in mesenchyme results in decreased Aqp5, Sftpc and Foxj1 expression, increased cell prolife

197 The expression levels of clock genes and Aqp5 showed regular oscillatory patterns under both ligh

198 ith cpt-cAMP showed a significantly stronger AQP5 signal at the plasma membrane as compared with untr

199 The human AQP5 structural gene resides within a 7.4-kilobase SalI-

200 Expression of N terminus-deleted AQP5 suppressed TRPV4 activation and RVD but not cell sw

201 der-influenced molecular mechanism involving AQP5 that allows transcellular and paracellular routes o

202 ed whether targeted deletion of Aquaporin 5 (AQP5), the major transcellular water transporter in sali

203 Aquaporin 5 (AQP5), the major water channel expressed in alveolar, tr

204 protein levels and induces translocation of AQP5 to the apical plasma membrane.

205 AQP5 mRNA and by triggering translocation of AQP5 to the plasma membrane.

206 ee principal lung aquaporins, AQP1, AQP4 and AQP5, to test the hypothesis that aquaporins are importa

207 in lungs of mice lacking AQP1, AQP5 or AQP1/AQP5 together, despite an up to 30-fold reduction in wat

208 esults indicate that GATA6 and HDAC3 control Aqp5 transcription via modulation of H3 acetylation/deac

209 protein synthesis is essential for increased AQP5 transcription.

210 and/or interacts with GATA6/Sp1 to regulate Aqp5 transcription.

211 kinase-1/2 phosphorylation, suggesting that AQP5, unlike AQP1, may be involved in signal transductio

212 Here, we examined the role of AQP5 using AQP5 knockout mice, which were recently shown

213 tein-structure analysis indicates that these AQP5 variants have the potential to elicit an effect on

214 Hypotonic reduction of AQP5 was blocked by ruthenium red, methanandamide, and m

215 To confirm a functional interaction, AQP5 was expressed in control or TRPV4-expressing human

216 Hypotonic reduction of AQP5 was observed only in the presence of TRPV4 and was

217 The cDNA for the fifth mammalian aquaporin (AQP5) was isolated from rat, and expression was demonstr

218 After i.v. injection of FITC-D into either AQP5 wild-type or AQP5-/- mice and saliva collection for

219 cer tissue samples as well as association of AQP5 with liver metastasis.

220 tonic PBS to mouse trachea in vivo decreased AQP5 within 1 h, an effect blocked by ruthenium red.

221 decreased expression of TTF-1, aquaporin-5 (AQP5), zonula occludens-1 (ZO-1), and cytokeratins.