ライフサイエンスコーパス: anti-miR

1 ion modulates the transcriptomic response to anti-miR.

2 ithelial cells after knockdown of MIR29 with anti-MIRs.

3 Our results demonstrate that the anti-miR-10 inhibitor not only decreases RhoGTPase/survi

4 Weekly treatments of mice with MN-anti-miR-10b and low-dose doxorubicin resulted in comple

5 cells were also transfected with a specific anti-miR-10b inhibitor in order to silence miR-10b expre

6 Our results demonstrate that anti-miR-10b inhibitor not only enhances HOXD10 expressi

7 CSCs were also transfected with a specific anti-miR-10b inhibitor to silence miR-10b expression and

8 We found that combination treatments with anti-miR-122 and a DAA had additive or synergistic antiv

9 has been exploited for the development of an anti-miR-122 antagomir as a host-targeting antiviral, th

10 istration of 2 mg kg(-1) chemically modified anti-miR-122 complexed with iNOP-7 resulted in 83.2 +/-

11 systemic delivery of a chemically stabilized anti-miR-122 complexed with interfering nanoparticles (i

12 te targeted N-acetylgalactosamine conjugated anti-miR-122 oligonucleotide, was well tolerated and res

13 Intravenous injection of rAAV9 expressing anti-miR-122 or anti-let-7 TuDs depleted the correspondi

14 atment in HCV-replicating cells with DAA and anti-miR-122 sharply reduced HCV RNA amounts.

15 atasvir, and sofosbuvir) in combination with anti-miR-122 treatment against HCV genotype 1a in cell c

16 rAAV producing anti-miR-122 TuD but not anti-let-7 TuD reduced serum ch

17 and has implications for the development of anti-miR-122-based HCV drugs.

18 s was achieved by combining daclatasvir with anti-miR-122.

19 antly decreased by combining simeprevir with anti-miR-122.

20 n miR-124a levels with Ccl2 expression, with anti-miR-124a increasing Ccl2 mRNA levels in Klf2(+/+) m

21 Anti-miR-125b and anti-miR-155 prevented CD154-mediated

22 levated responsiveness to IFN-gamma, whereas anti-miR-125b treatment decreases CD80 surface expressio

23 Modulation of miR-126 by anti-miR-126 or miR-mimic-126 treatment resulted in sign

24 Anti-miR-126 transfection markedly impaired the capacity

25 Anti-miR 130a treatment led to reduced airway branching

26 In vivo studies revealed that LNA(TM) anti-miR-130a could up-regulate the AQP4 M1 transcript a

27 Introduction of anti-miR-130a in hepatocytes increased IFITM1 expression

28 tocytes upregulates miR-130a and that use of anti-miR-130a may have potential for restriction of HCV

29 ivo silencing of miR-132 by the provision of anti-miR-132 (antagomir-132) nanoparticles to HSV-infect

30 Notably, administration of anti-miR-132 inhibited angiogenesis in wild-type mice bu

31 ovascularization, whereas the application of anti-miR-132 inhibits neovascularization by maintaining

32 ly, vessel-targeted nanoparticle delivery of anti-miR-132 restored p120RasGAP expression in the tumor

33 injection of an antagomir targeting miR-132, anti-miR-132, reduced postnatal retinal vascular develop

34 However, overexpression of anti-miR-135a and anti-miR-199a-5p oligonucleotides led

35 onary hypertension in vivo in miR-143-/- and anti-miR-143-3p-treated mice exposed to chronic hypoxia

36 gh miR-145 silences the expression of c-Myc, anti-miR-145 enhances its expression.

37 Finally, the blockade of miR-145 by anti-miR-145 is able to reverse the p53-mediated c-Myc r

38 A locked nucleic acid-modified anti-miR-146a given before LPS treatment knocked down mi

39 Transfection of anti-miR-146a nucleotides reversed the inhibitory effect

40 Anti-miR-148a also reduced thrombus formation following

41 Within 18 h of transfection with an anti-miR-150 construct, primary B lymphocytes secrete ap

42 These results suggest that shuttling anti-miR-150 molecules from B lymphocytes to T cells req

43 ocytes secrete approximately 3,000 copies of anti-miR-150 molecules per cell.

44 Anti-miR-150 molecules released by B lymphocytes were in

45 Finally, anti-miR-150 synthesized in B cells were secreted both a

46 s, but only extracellular vesicle-associated anti-miR-150 were apparently taken up by CD8 T cells.

47 locking miR-155 expression using a synthetic anti-miR-155 after alloHSCT decreased aGVHD severity and

48 Moreover, anti-miR-155 delivered systemically showed uptake in the

49 -155 led to preferential accumulation of the anti-miR-155 in hepatocytes.

50 xperiments showed that miR-26a, miR-130a and anti-miR-155 increased apoptosis after in vitro and in v

51 n or by peripheral or centrally administered anti-miR-155 inhibitor in SOD1 mice.

52 ravenous injection of Lac-GLN containing Cy3-anti-miR-155 led to preferential accumulation of the ant

53 Intravenous administration of 1.5 mg/kg anti-miR-155 loaded Lac-GLN resulted in up-regulation of

54 y, we show that an 8-mer locked nucleic acid anti-miR-155 oligonucleotide targeting the seed region o

55 ene expression between B cells isolated from anti-miR-155 PNA-treated and miR-155-deficient mice.

56 Anti-miR-125b and anti-miR-155 prevented CD154-mediated repression of BCL2

57 Lac-GLN effectively delivered anti-miR-155 to HCC cells with a 16.1- and 4.1-fold up-r

58 Intraventricular anti-miR-155 treatment derepressed microglial miR-155 ta

59 glial miR-155 targeted genes, and peripheral anti-miR-155 treatment prolonged survival.

60 Finally, we found that anti-Mir-155 treatment reduced clinical severity of EAE

61 developed for delivery of anti-microRNA-155 (anti-miR-155) to hepatocellular carcinoma (HCC) cells.

62 sfected with an antisense miR-155 inhibitor, anti-miR-155, endogenous hAT(1)R expression and angioten

63 study highlight the therapeutic potential of anti-miR-155-mediated inhibition of miR-155 in the treat

64 Anti-miR-155-transfected AMs exhibited an increase in SR

65 tion of healthy PACs ex vivo-engineered with anti-miR-15a/16 improved postischemic blood flow recover

66 Treatment of mice with systemic delivery of anti-miR-17 and anti-miR-19 reduced tumor growth in flan

67 ition of miR-17 and miR-19a seed families by anti-miR-17 and anti-miR-19, respectively, resulted in d

68 Anti-miR-17 treatment attenuates cyst growth in short-te

69 L tumor cell proliferation and survival, and anti-miR-181a abrogates these effects.

70 Systemic delivery of anti-miR-181b in angiotensin II-infused Apoe(-/-) and Ld

71 n vivo administration of locked nucleic acid anti-miR-181b retarded both the development and the prog

72 ferase imaging showed that mice treated with anti-miR-182 had a lower burden of liver metastases comp

73 Our results demonstrate that the use of anti-miR-182 is a promising therapeutic strategy for met

74 Specifically, we assessed the effect of anti-miR-182 oligonucleotides synthesized with 2' sugar

75 scriptional profiling of tumors treated with anti-miR-182 or with control oligonucleotides revealed a

76 Anti-miR-182 treatment inhibits the hypertrophic respons

77 esion and migration modulated in response to anti-miR-182 treatment.

78 ce with systemic delivery of anti-miR-17 and anti-miR-19 reduced tumor growth in flank and brain allo

79 and miR-19a seed families by anti-miR-17 and anti-miR-19, respectively, resulted in diminished tumor

80 Furthermore, LNA-anti-miR-192 attenuated proteinuria in these diabetic mi

81 LNA-anti-miR-192 significantly reduced levels of miR-192, bu

82 odified inhibitor of miR-192, designated LNA-anti-miR-192, in mouse models of diabetic nephropathy.

83 Anti-miR-192-5p significantly blocked VAN-induced apopto

84 nuated HIF-1alpha and ET-1 expression, while anti-miR-199 reversed the effects, suggesting that ethan

85 (COMP), type II collagen, and Sox9, whereas anti-miR-199a(*) increased the expression of these chond

86 However, overexpression of anti-miR-135a and anti-miR-199a-5p oligonucleotides led to a several fold

87 metastases of MDA-MB-231 cells in vivo, and anti-miR-200 treatment in vivo resulted in increased met

88 ccelerated wound closure in vitro induced by anti-miR-200c was associated with upregulation of genes

89 he less aggressive Huh7 cell was enhanced by anti-miR-200c+141.

90 The anti-miR-204-induced decrease in Kir7.1 protein levels s

91 rotein) consistent with our observation that anti-miR-204/211 decreased transepithelial resistance by

92 MT markers and cell migration is reverted by anti-miR-205.

93 Moreover, anti-miR-206* inhibitor treatment substantially rescued

94 ning the wild-type 3'-UTR or when a specific anti-miR-206* inhibitor was added.

95 nt of RASA1- or SPRED1-suppressed cells with anti-miR-206/21 had little or no impact on the level of

96 ce injected with LM7 stably transfected with anti-miR-20a had fewer metastases than those with contro

97 onal MI rats were then randomized to receive anti-miR-21 (KD21) or scrambled control sequence (Scr21)

98 n-gel electrophoresis of tumors treated with anti-mir-21 and identified the tumor suppressor tropomyo

99 Administration of anti-miR-21 blocked RI-induced cell proliferation and si

100 lly, knockdown of TSG101 increased uptake of anti-miR-21 by cancer cells in vivo following systemic d

101 Anti-miR-21 enhanced PPARalpha/retinoid X receptor (PPAR

102 r ESCRT-I protein, VPS28, improved uptake of anti-miR-21 in parental SKHEP1 cells and restored produc

103 cells were also transfected with a specific anti-miR-21 inhibitor in order to silence miR-21 express

104 cells were also transfected with a specific anti-miR-21 inhibitor in order to silence miR-21 express

105 Our results indicate that anti-miR-21 inhibitor not only enhances PDCD4 expression

106 Our results demonstrate that anti-miR-21 inhibitor not only upregulates PDCD4 express

107 , we found that treatment of WT mice with an anti-miR-21 oligonucleotide reduced the clinical severit

108 e transfected breast cancer MCF-7 cells with anti-miR-21 oligonucleotides and found that anti-miR-21

109 evaluated the therapeutic potential of these anti-miR-21 oligonucleotides in chronic kidney disease.

110 anti-miR-21 oligonucleotides and found that anti-miR-21 suppressed both cell growth in vitro and tum

111 r-21 down-regulated the luciferase activity, anti-mir-21 up-regulated it.

112 roductive free uptake of a miR-21 inhibitor (anti-miR-21).

113 Uptake of anti-miR-21, but not a mismatch (MM) control, induces ex

114 lucidate mechanisms of SKHEP1 sensitivity to anti-miR-21, we conducted an unbiased shRNA screen that

115 In addition, anti-miR-21-induced suppression of cell migration was re

116 Furthermore, this anti-miR-21-mediated cell growth inhibition was associat

117 downregulation of the antiapoptotic Bcl-2 in anti-miR-21-treated tumor cells.

118 poor uptake resulted in improved activity of anti-miR-21.

119 determinant of anti-proliferative effects of anti-miR-21.

120 to SKHEP1 clones with acquired resistance to anti-miR-21.

121 Intracolonic anti-miR-210 also reduced colitis in response to TNBS (2

122 entary locked nucleic acid oligonucleotides (anti-miR-210).

123 ne differentiation was largely unaffected by anti-miR-210.

124 ed intracolonically with locked nucleic acid anti-miR-210.

125 ce, or mice pretreated intracolonically with anti-miR-210.

126 vo biodistribution studies demonstrated that anti-miR-214 accumulated at the highest levels in the ki

127 Silencing of miR-214 by anti-miR-214 in whole AV leaflets with the fibrosa expos

128 e with an anti-miR directed against miR-214 (anti-miR-214) before UUO resulted in similar antifibroti

129 Anti-miR 221 treated lungs had more distal branch genera

130 A cholesterol-modified isoform of anti-miR-221 (chol-anti-miR-221) exhibited improved phar

131 fer a preclinical proof of efficacy for chol-anti-miR-221 in a valid orthotopic mouse model of HCC, s

132 bicin resistance with higher efficiency than anti-miR-221 in human breast cancer cells.

133 that a 2'-O-methyl phosphorothioate-modified anti-miR-221 oligonucleotide was most effective at reduc

134 miR-221, we showed that in vivo delivery of anti-miR-221 oligonucleotides leads to a significant red

135 Within the same period, chol-anti-miR-221 reduced tumor cell proliferation and increa

136 Chol-anti-miR-221 significantly reduced miR-221 levels in liv

137 terol-modified isoform of anti-miR-221 (chol-anti-miR-221) exhibited improved pharmacokinetics and li

138 Further, anti-miR-222 or -181b in combination with tamoxifen supp

139 LV-anti-miR-23b also significantly increased the hydroxylat

140 Furthermore, LV-anti-miR-23b significantly decreased endogenous levels o

141 of an miR-26a inhibitor, locked nucleic acid-anti-miR-26a, increased SMAD1 expression and rapidly ind

142 = 0.046), and inhibition of miR-26a-2 using anti-miR-26a-2 substantially upregulated HOXA5 expressio

143 Because anti-miR-27b compounds that suppress miR-27b inhibit tum

144 Moreover, intraperitoneally delivered anti-miR-27b restored Nischarin expression and decreased

145 t suppress miR-27b inhibit tumor growth, the anti-miR-27b seems to be a good candidate for the develo

146 Bmpr2 mice treated with anti-miR-29 (20-mg/kg injections for 6 weeks) had improv

147 chondrial abnormalities, which improved with anti-miR-29 transfection in vitro; endothelial-like cell

148 em cell lines were similar and improved with anti-miR-29 treatment.

149 Treatment with locked nucleic acid anti-miR-29a significantly improved survival in a mouse

150 V)-transduced BEAS-2B cells, introduction of anti-miR-29b constructs increased the sensitivity to apo

151 n vivo administration of locked nucleic acid anti-miR-29b greatly increased collagen expression, lead

152 miR-29b decreased and anti-miR-29b increased activity of COL1A1, COL5A3, and C

153 ic delivery of locked nucleic acid-modified, anti-miR-29b-reduced endogenous miR-29b levels in the sm

154 Our results demonstrate that the anti-miR-302 inhibitor not only enhances the expression

155 These CSCs were transfected with a specific anti-miR-302 inhibitor to silence miR-302 expression and

156 urthermore, inhibition of hepatic miR-30c by anti-miR-30c increased hyperlipidemia and atherosclerosi

157 onflicting reports exist about the impact of anti-miR-33 therapy on the levels of very low-density li

158 nd suggest that caution should be taken with anti-miR-33-based therapies because they might raise pro

159 and point to a potential therapeutic use for anti-miR-34 as a radiosensitizing agent in p53-mutant br

160 Conversely, locked nucleic acid-based anti-miR-34a treatment diminished post-MI miR-34a upregu

161 Further, anti-miR-34a treatment in primary hepatocytes of obese m

162 Importantly, anti-miR-34a-mediated beneficial effects, including decr

163 ct of Tat was neutralized in the presence of anti-miR-34a.

164 hypertrophic marker type X collagen, whereas anti-miR-365 inhibits the expression of these genes.

165 We found overexpressed siFas and anti-miR-375 in plasmid encoding shFas and anti-miR-375

166 d anti-miR-375 in plasmid encoding shFas and anti-miR-375 transfected hBMSC-derived exosomes, which s

167 Knockdown of miR-423-5p with anti-miR-423-5p reversed training-induced bradycardia vi

168 R-433 but were induced by miR-433 antagomir (anti-miR-433).

169 l proliferation, which was not influenced by anti-miR-433.

170 n and invasion and antagonized the effect of anti-miR-433.

171 HCC97H cell migration, which was reversed by anti-miR-433.

172 lines decreases cellular transformation, and anti-miR-494 treatment of primary MYC-driven liver tumor

173 and transfection of PBC cholangiocytes with anti-miR-506 was able to improve their AE2 activity.

174 Treatment with the combination of anti-miR-630 and anti-vascular endothelial growth factor

175 The anti-miR-663 reduced OXPHOS complex activity and increas

176 Oligonucleotides anti-miR-7 inhibited the exendin-4-induced proliferation

177 Furthermore, silencing miR-712 by anti-miR-712 rescues TIMP3 expression and prevents ather

178 herapeutic approach to this disease using an anti-miR-886-3p.

179 Remarkably, administration of anti-miR-9 or JAK inhibitors suppressed MV-induced cell

180 Administration of an anti-miR-92a after disease initiation prevented albuminu

181 Conversely, anti-miR-93 inhibitors increased VEGF release.

182 Treatment of anti-miR-99b-transfected DCs with anti-TNF-alpha antibod

183 for efficient miRNA targeting and show that anti-miR activity is enhanced substantially by the prese

184 We show that anti-miR activity of a Cys-containing PNA is achieved by

185 Nebulized anti-miRs against miR-25 and miR-138 restore MCU express

186 of PNAs and other oligonucleotides as potent anti-miR agents.

187 data indicate that in vivo administration of anti-miRs allows for efficient miRNA targeting and conco

188 explored the subcellular localization of PNA anti-miRs and our data suggest that anti-miR targeting o

189 the regulation of productive free uptake of anti-miRs and reveal potential avenues for improving oli

190 oblastoma cells) passively took up 8-mer LNA-anti-miRs and specifically inhibited targeted microRNA s

191 Anti-miRs are oligonucleotide inhibitors complementary t

192 microRNA-155 by a systemically delivered LNA-anti-miR attenuated cardiac infiltration by monocyte-mac

193 by down-regulating TIMP3, and corresponding anti-miRs can be used to render these tumors responsive

194 d whether locked nucleic acid (LNA)-modified anti-miR chemistries can target cardiac expressed miRNAs

195 by using antisense oligonucleotides, called anti-miRs, complimentary to the miRNA sequences.

196 d previously that peptide nucleic acid (PNA) anti-miRs containing a few attached Lys residues were po

197 he miPSA has additional utility in assessing anti-miR cross-reactivity with miRNAs sharing similar se

198 in the study, use of DOPC nanoliposomes for anti-miR delivery serves as a better alternative approac

199 ects of LXA4 in renal epithelia; conversely, anti-miR directed against let-7c attenuated the effects

200 Treatment of wild-type mice with an anti-miR directed against miR-214 (anti-miR-214) before

201 Correspondingly, systemic delivery of miR-15 anti-miRs dose-dependently represses miR-15 in cardiac t

202 ion changes in these genes following in vivo anti-miR dosing, suggesting that derepression of these t

203 diameter of 73 nm, zeta potential of +3.5mV, anti-miR encapsulation efficiency of 88%, and excellent

204 e inhibited miRNAs are sterically blocked by anti-miRs from forming this interaction.

205 In contrast, miR-143 anti-miR had no effect.

206 An miR-138 anti-miR had the opposite effects.

207 et-7 family with a locked nucleic acid (LNA)-anti-miR has the opposite effect.

208 Indeed, down-regulation of miR-29 with anti-miRs in vitro and in vivo induces the expression of

209 ly dissociate from AGO2-miRNA complexes when anti-miR is spiked into liver lysates.

210 Selective reduction in miR-886-3p by an anti-miR led to elevation of FXN message and protein lev

211 miR-145 deficiency and anti-miR-mediated reduction resulted in significant prot

212 of the miR-17~92 cluster family by 8-mer LNA-anti-miRs might be considered for the treatment of SHH m

213 e of miR-338-3p in beta cells using specific anti-miR molecules mimicked gene expression changes occu

214 rdiac fibroblasts were transfected with pre-/anti-miR of miR-29b and miR-30c, and their conditioned m

215 Anti-miRNA (anti-miR) oligonucleotide drugs are being developed to i

216 nal inhibition of the respective miRNAs with anti-miR oligonucleotides resulted in induction of ICAM-

217 Conversely, the transfection of synthetic anti-miR oligonucleotides that inhibit miR-338 increases

218 targeting locked nucleic acid (LNA)-modified anti-miR oligonucleotides, termed tiny LNAs, that inhibi

219 e E14 whole lungs cultured for 48 hours with anti-miRs or mimics to miR-130a and miR-221.

220 nous miR-140 by locked nucleic acid-modified anti-miR partially sensitized resistant colon cancer ste

221 The inhibition of miR-378 by its anti-miR protected cardiomyocytes against H(2)O(2) and h

222 ition studies were performed with pre-miR or anti-miR, respectively.

223 Antisense-mediated knockdown (anti-miR) revealed that miR-206/21 coordinately promote

224 n of PNA anti-miRs and our data suggest that anti-miR targeting of miR-122 may take place in or assoc

225 GLN as a liver-specific delivery vehicle for anti-miR therapy.

226 poorly reflect the binding stoichiometry of anti-miR to miRNA.

227 onstrate that iNOPs can successfully deliver anti-miR to specifically target and silence miRNA in cli

228 e effectively downregulated in the tumors of anti-miR-treated mice compared with tumors of control-tr

229 Accordingly, anti-miR treatment causes a specific shift of cognate mi

230 rs that can be upregulated in tumor cells by anti-miR treatment.

231 We developed a novel method for delivering anti-miRs using liposomes for the functional knockdown o

232 ed in miR-145 knockout and mice treated with anti-miRs via measurement of systolic right ventricular

233 In vivo, nebulized anti-miRs were administered to rats with monocrotaline-i

234 or direct measurement of miRNA engagement by anti-miR, which is more robust than conventional pharmac