ライフサイエンスコーパス: AQP5

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

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

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

4 89 blocked the cpt-cAMP-mediated increase of AQP5.

5 ce and transgenic null mice lacking AQP1 and 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 oting endolysosomal degradation of NKCC1 and AQP5.

12 w potential recombinant antibodies targeting AQP5.

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

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

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

16 rway epithelial cell line without endogenous AQP5.

17 of the paracellular barrier in mice lacking AQP5.

18 0.03 nl min(-1) gland(-1)) vs. mice lacking AQP5 (0.19 +/- 0.04 nl min(-1) gland(-1)).

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

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

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

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

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

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

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

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

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

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

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

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

31 AQP5 and the isoforms AQP1 and AQP4 decreased, whereas A

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

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

34 tic stress on two transporters, aquaporin 5 (AQP5) and the transient receptor potential cation channe

35 0.3 (AQP3), 24 +/- 0.6 (AQP4), 5.0 +/- 0.4 (AQP5), and 0.25 +/- 0.05 (MIP); pf values were insensiti

36 , 8 +/- 2 (AQP3), 29 +/- 1 (AQP4), 10 +/- 1 (AQP5), and 1.3 +/- 0.2 (MIP), and they were relatively i

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

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

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

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

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

42 11 was also potently down-regulated, whereas Aqp5/AQP5 expression persisted, resulting in the inhibit

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

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

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

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

47 functionally validate, the membrane protein AQP5 as a marker that enriches for mouse and human adult

48 lens water fluxes, with a specific focus on AQP5 as a regulated water channel in the lens.

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

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

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

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

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

54 Anti-AQP5 autoantibodies have been observed in patients with

55 annels expressed on the plasma membrane with AQP5 being the major channel expressed in several human

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

57 The AQP5 cDNA from a human submaxillary gland library contai

58 We also showed that the new CHO-K1/AQP5 cell line can be used to study molecular mechanisms

59 Additionally, tumour-resident AQP5(+) cells can selectively initiate organoid growth i

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

61 e-transfected cell line overexpressing human AQP5 (CHO-K1/AQP5) to perform primarily cell-based phage

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

63 We show that stem cells within the AQP5(+) compartment are a source of WNT-driven, invasive

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

65 d hypofunction, we developed an aquaporin 5 (AQP5) Cre mouse line to produce genetic recombination pr

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

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

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

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

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

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

72 The resulting AQP5-Cre/TNF-alphaglo mice display severe inflammation i

73 astric cancer in vivo, using newly generated Aqp5-creERT2 mouse models.

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

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

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

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

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

79 /- 0.3 microm/min, wild type) was reduced by AQP5 deletion (2.7 +/- 0.1 microm/min).

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

81 AQP5 deletion did not affect lung morphology at the ligh

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

83 functional sweat glands was not affected by AQP5 deletion.

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

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

86 ulmonary artery pressure was not affected by AQP5 deletion.

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

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

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

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

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

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

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

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

95 -4.3- and -1.7-AQP5-luciferase constructs in AQP5-expressing lung (MLE-15) and salivary (Pa-4) cells

96 When AQP5-expressing mouse lung epithelial cells were treated

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

98 mbedded in collagen gel (3D) decreased their AQP5 expression and exhibited a reduction in intra-cellu

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

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

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

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

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

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

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

106 Bmla1 overexpression resulted in increased Aqp5 expression levels.

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

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

109 AQP5 expression was reduced in the salivary glands, whil

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

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

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

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

114 siologic relevance for osmotic regulation of AQP5 expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 m also modulates the membrane trafficking of AQP5 in the anterior influx pathway and equatorial efflu

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

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

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

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

137 AQP5 induction was observed only with relatively imperme

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

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

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

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

142 AQP5 is formed by six transmembrane helices linked with

143 In humans, AQP5 is frequently expressed in primary intestinal and d

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

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

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

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

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

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

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

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

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

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

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

155 eased expression of several AQPs, especially AQP5, is associated with increased cancer cell migration

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

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

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

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

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

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

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

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

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

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

166 Since both lens pressure and AQP5-mediated water permeability ( PH2O ) can be altered

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 real-time PCR demonstrated the reduction of AQP5 mRNA expression by the transfection of miR-1226-3p

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

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

187 3p, and miR-19b-3p as putative regulators of AQP5 mRNA.

188 8), KRT1 (n = 3), DSP (n = 2), KRT9 (n = 2), AQP5 (n = 2), KRT16 (n = 1), SERPINA12 (n = 1), ABCA12 (

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

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

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

192 .3 +/- 0.2-fold increase in total protein in AQP5 null mice and a smaller increase in [Cl(-)], sugges

193 We generated AQP5 null mice by targeted gene disruption.

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

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

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

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

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

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

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

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

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

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

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

205 We found that AQP5 overexpression in normal epithelial cells induced c

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

207 Aquaporin-5 (AQP5) plays a role in breast cancer cell migration.

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

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

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

211 Immunoblotting revealed a decrease of AQP5 protein abundance when each of these miRNAs was tra

212 ioengineered and their inhibitory effects on AQP5 protein expression and cell migration were demonstr

213 activation, while HDAC3 knockdown augmented AQP5 protein expression.

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

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

216 Purified AQP5 protein was phosphorylated by protein kinase A but

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

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

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

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

221 AQP5 reduced both cell-cell coordination during collecti

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

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

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

225 Taken together, AQP5-regulating miRNAs are identified, which could be ex

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

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

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

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

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

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

232 can be used to study molecular mechanisms of AQP5 sub-cellular trafficking making these cells a usefu

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

234 This study aimed to identify AQP5-targeting miRNAs and examine their effects on breas

235 For the efficient delivery of AQP5-targeting miRNAs to breast cancer cells, exosomes e

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

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

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

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

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

241 cell line overexpressing human AQP5 (CHO-K1/AQP5) to perform primarily cell-based phage display biop

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

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

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

245 protein synthesis is essential for increased AQP5 transcription.

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

247 ase reporter assay revealed the reduction of AQP5 translation after the transfection of miR-19b-3p in

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

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

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

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

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

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

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

255 ide cotransporter-1 (NKCC1) and aquaporin 5 (AQP5), which are membrane proteins involved in salivatio

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

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

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

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