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Rapamycin prevents the mutant huntingtin- suppressed GLT-1 expression in cultured astrocytes

Aim: To investigate the effects of rapamycin on glutamate uptake in cultured rat astrocytes expressing N-terminal 552 residues of mutant huntingtin (Htt-552). Methods: Primary astrocyte cultures were prepared from the cortex of postnatal rat pups. An astrocytes model of Huntington's disease was esta... Full description

Journal Title: Acta pharmacologica Sinica 2012, Vol.33 (3), p.385-392
Main Author: Chen, Lei-lei
Other Authors: Wu, Jun-chao , Wang, Lin-hui , Wang, Jin , Qin, Zheng-hong , Difiglia, Marian , Lin, Fang
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States: Nature Publishing Group
ID: ISSN: 1671-4083
Link: https://www.ncbi.nlm.nih.gov/pubmed/22266730
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4077128
title: Rapamycin prevents the mutant huntingtin- suppressed GLT-1 expression in cultured astrocytes
format: Article
creator:
  • Chen, Lei-lei
  • Wu, Jun-chao
  • Wang, Lin-hui
  • Wang, Jin
  • Qin, Zheng-hong
  • Difiglia, Marian
  • Lin, Fang
subjects:
  • 3-MA
  • Adenovirus
  • Animal models
  • Animals
  • Astrocytes
  • Astrocytes - drug effects
  • Astrocytes - metabolism
  • autophagy
  • Cortex
  • Enumeration
  • Excitatory Amino Acid Transporter 2 - antagonists & inhibitors
  • Excitatory Amino Acid Transporter 2 - biosynthesis
  • Excitatory Amino Acid Transporter 2 - genetics
  • Excitatory Amino Acid Transporter 2 - metabolism
  • Gene expression
  • GLT-1
  • glutamate uptake
  • Glutamic acid transporter
  • Huntingtin
  • Huntingtin Protein
  • huntingtin-552
  • Huntington Disease - genetics
  • Huntington Disease - metabolism
  • Huntington's disease
  • Microtubule-associated protein 1
  • Models
  • mRNA表达水平
  • Mutation
  • Nerve Tissue Proteins - genetics
  • Nerve Tissue Proteins - metabolism
  • Nuclear Proteins - genetics
  • Nuclear Proteins - metabolism
  • Original
  • Phagocytosis
  • Polymerase chain reaction
  • Rapamycin
  • Rats
  • Rats, Sprague-Dawley
  • Scintillation
  • Sirolimus - pharmacology
  • Western blotting
  • 微管相关蛋白
  • 星形胶质细胞
  • 液体闪烁计数
  • 突变体
  • 细胞摄取
  • 谷氨酸转运体
  • 雷帕霉素
ispartof: Acta pharmacologica Sinica, 2012, Vol.33 (3), p.385-392
description: Aim: To investigate the effects of rapamycin on glutamate uptake in cultured rat astrocytes expressing N-terminal 552 residues of mutant huntingtin (Htt-552). Methods: Primary astrocyte cultures were prepared from the cortex of postnatal rat pups. An astrocytes model of Huntington's disease was established using the astrocytes infected with adenovirus carrying coden gene of N-terminal 552 residues of Huntingtin. The protein levels of glutamate transporters GLT-1 and GLAST, the autophagic marker microtubule-associated protein 1A/1B-light chain 3 (LC3) and the autophagy substrate p62 in the astrocytes were examined using Western blotting. The mRNA expression levels of GLT-1 and GLAST in the astrocytes were determined using Real-time PCR. [3H]glutamate uptake by the astrocytes was measured with liquid scintillation counting. Results: The expression of mutant Htt-552 in the astrocytes significantly decreased both the mRNA and protein levels of GLT-1 but not those of GLAST. Furthermore, Htt-552 significantly reduced [3H]glutamate uptake by the astrocytes, Treatment with the autophagy inhibitor 3-MA (10 mmol/L) significantly increased the accumulation of mutant Htt-552, and reduced the expression of GLT-1 and [3H]glutamate uptake in the astrocytes. Treatment with the autophagy stimulator rapamycin (0.2 mg/mL) significantly reduced the accumulation of mutant Htt-552, and reversed the changes in GLT-1 expression and [3H]glutamate uptake in the astrocytes. Conclusion: Rapamcin, an autophagy stimulator, can prevent the suppression of GLT-1 expression and glutamate uptake by mutant Htt- 552 in cultured astrocytes.
language: eng
source:
identifier: ISSN: 1671-4083
fulltext: no_fulltext
issn:
  • 1671-4083
  • 1745-7254
url: Link


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titleRapamycin prevents the mutant huntingtin- suppressed GLT-1 expression in cultured astrocytes
creatorChen, Lei-lei ; Wu, Jun-chao ; Wang, Lin-hui ; Wang, Jin ; Qin, Zheng-hong ; Difiglia, Marian ; Lin, Fang
creatorcontribChen, Lei-lei ; Wu, Jun-chao ; Wang, Lin-hui ; Wang, Jin ; Qin, Zheng-hong ; Difiglia, Marian ; Lin, Fang
descriptionAim: To investigate the effects of rapamycin on glutamate uptake in cultured rat astrocytes expressing N-terminal 552 residues of mutant huntingtin (Htt-552). Methods: Primary astrocyte cultures were prepared from the cortex of postnatal rat pups. An astrocytes model of Huntington's disease was established using the astrocytes infected with adenovirus carrying coden gene of N-terminal 552 residues of Huntingtin. The protein levels of glutamate transporters GLT-1 and GLAST, the autophagic marker microtubule-associated protein 1A/1B-light chain 3 (LC3) and the autophagy substrate p62 in the astrocytes were examined using Western blotting. The mRNA expression levels of GLT-1 and GLAST in the astrocytes were determined using Real-time PCR. [3H]glutamate uptake by the astrocytes was measured with liquid scintillation counting. Results: The expression of mutant Htt-552 in the astrocytes significantly decreased both the mRNA and protein levels of GLT-1 but not those of GLAST. Furthermore, Htt-552 significantly reduced [3H]glutamate uptake by the astrocytes, Treatment with the autophagy inhibitor 3-MA (10 mmol/L) significantly increased the accumulation of mutant Htt-552, and reduced the expression of GLT-1 and [3H]glutamate uptake in the astrocytes. Treatment with the autophagy stimulator rapamycin (0.2 mg/mL) significantly reduced the accumulation of mutant Htt-552, and reversed the changes in GLT-1 expression and [3H]glutamate uptake in the astrocytes. Conclusion: Rapamcin, an autophagy stimulator, can prevent the suppression of GLT-1 expression and glutamate uptake by mutant Htt- 552 in cultured astrocytes.
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1EISSN: 1745-7254
2DOI: 10.1038/aps.2011.162
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languageeng
publisherUnited States: Nature Publishing Group
subject3-MA ; Adenovirus ; Animal models ; Animals ; Astrocytes ; Astrocytes - drug effects ; Astrocytes - metabolism ; autophagy ; Cortex ; Enumeration ; Excitatory Amino Acid Transporter 2 - antagonists & inhibitors ; Excitatory Amino Acid Transporter 2 - biosynthesis ; Excitatory Amino Acid Transporter 2 - genetics ; Excitatory Amino Acid Transporter 2 - metabolism ; Gene expression ; GLT-1 ; glutamate uptake ; Glutamic acid transporter ; Huntingtin ; Huntingtin Protein ; huntingtin-552 ; Huntington Disease - genetics ; Huntington Disease - metabolism ; Huntington's disease ; Microtubule-associated protein 1 ; Models ; mRNA表达水平 ; Mutation ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Original ; Phagocytosis ; Polymerase chain reaction ; Rapamycin ; Rats ; Rats, Sprague-Dawley ; Scintillation ; Sirolimus - pharmacology ; Western blotting ; 微管相关蛋白 ; 星形胶质细胞 ; 液体闪烁计数 ; 突变体 ; 细胞摄取 ; 谷氨酸转运体 ; 雷帕霉素
ispartofActa pharmacologica Sinica, 2012, Vol.33 (3), p.385-392
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0Chen, Lei-lei
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5Difiglia, Marian
6Lin, Fang
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0Rapamycin prevents the mutant huntingtin- suppressed GLT-1 expression in cultured astrocytes
1Acta pharmacologica Sinica
addtitleActa Pharmacologica Sinica
descriptionAim: To investigate the effects of rapamycin on glutamate uptake in cultured rat astrocytes expressing N-terminal 552 residues of mutant huntingtin (Htt-552). Methods: Primary astrocyte cultures were prepared from the cortex of postnatal rat pups. An astrocytes model of Huntington's disease was established using the astrocytes infected with adenovirus carrying coden gene of N-terminal 552 residues of Huntingtin. The protein levels of glutamate transporters GLT-1 and GLAST, the autophagic marker microtubule-associated protein 1A/1B-light chain 3 (LC3) and the autophagy substrate p62 in the astrocytes were examined using Western blotting. The mRNA expression levels of GLT-1 and GLAST in the astrocytes were determined using Real-time PCR. [3H]glutamate uptake by the astrocytes was measured with liquid scintillation counting. Results: The expression of mutant Htt-552 in the astrocytes significantly decreased both the mRNA and protein levels of GLT-1 but not those of GLAST. Furthermore, Htt-552 significantly reduced [3H]glutamate uptake by the astrocytes, Treatment with the autophagy inhibitor 3-MA (10 mmol/L) significantly increased the accumulation of mutant Htt-552, and reduced the expression of GLT-1 and [3H]glutamate uptake in the astrocytes. Treatment with the autophagy stimulator rapamycin (0.2 mg/mL) significantly reduced the accumulation of mutant Htt-552, and reversed the changes in GLT-1 expression and [3H]glutamate uptake in the astrocytes. Conclusion: Rapamcin, an autophagy stimulator, can prevent the suppression of GLT-1 expression and glutamate uptake by mutant Htt- 552 in cultured astrocytes.
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03-MA
1Adenovirus
2Animal models
3Animals
4Astrocytes
5Astrocytes - drug effects
6Astrocytes - metabolism
7autophagy
8Cortex
9Enumeration
10Excitatory Amino Acid Transporter 2 - antagonists & inhibitors
11Excitatory Amino Acid Transporter 2 - biosynthesis
12Excitatory Amino Acid Transporter 2 - genetics
13Excitatory Amino Acid Transporter 2 - metabolism
14Gene expression
15GLT-1
16glutamate uptake
17Glutamic acid transporter
18Huntingtin
19Huntingtin Protein
20huntingtin-552
21Huntington Disease - genetics
22Huntington Disease - metabolism
23Huntington's disease
24Microtubule-associated protein 1
25Models
26mRNA表达水平
27Mutation
28Nerve Tissue Proteins - genetics
29Nerve Tissue Proteins - metabolism
30Nuclear Proteins - genetics
31Nuclear Proteins - metabolism
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34Polymerase chain reaction
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36Rats
37Rats, Sprague-Dawley
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titleRapamycin prevents the mutant huntingtin- suppressed GLT-1 expression in cultured astrocytes
authorChen, Lei-lei ; Wu, Jun-chao ; Wang, Lin-hui ; Wang, Jin ; Qin, Zheng-hong ; Difiglia, Marian ; Lin, Fang
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34Polymerase chain reaction
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38Scintillation
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42星形胶质细胞
43液体闪烁计数
44突变体
45细胞摄取
46谷氨酸转运体
47雷帕霉素
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notes
0Aim: To investigate the effects of rapamycin on glutamate uptake in cultured rat astrocytes expressing N-terminal 552 residues of mutant huntingtin (Htt-552). Methods: Primary astrocyte cultures were prepared from the cortex of postnatal rat pups. An astrocytes model of Huntington's disease was established using the astrocytes infected with adenovirus carrying coden gene of N-terminal 552 residues of Huntingtin. The protein levels of glutamate transporters GLT-1 and GLAST, the autophagic marker microtubule-associated protein 1A/1B-light chain 3 (LC3) and the autophagy substrate p62 in the astrocytes were examined using Western blotting. The mRNA expression levels of GLT-1 and GLAST in the astrocytes were determined using Real-time PCR. [3H]glutamate uptake by the astrocytes was measured with liquid scintillation counting. Results: The expression of mutant Htt-552 in the astrocytes significantly decreased both the mRNA and protein levels of GLT-1 but not those of GLAST. Furthermore, Htt-552 significantly reduced [3H]glutamate uptake by the astrocytes, Treatment with the autophagy inhibitor 3-MA (10 mmol/L) significantly increased the accumulation of mutant Htt-552, and reduced the expression of GLT-1 and [3H]glutamate uptake in the astrocytes. Treatment with the autophagy stimulator rapamycin (0.2 mg/mL) significantly reduced the accumulation of mutant Htt-552, and reversed the changes in GLT-1 expression and [3H]glutamate uptake in the astrocytes. Conclusion: Rapamcin, an autophagy stimulator, can prevent the suppression of GLT-1 expression and glutamate uptake by mutant Htt- 552 in cultured astrocytes.
1Huntington's disease; huntingtin-552; GLT-1; glutamate uptake; autophagy; rapamycin; 3-MA
231-1347/R
abstractAim: To investigate the effects of rapamycin on glutamate uptake in cultured rat astrocytes expressing N-terminal 552 residues of mutant huntingtin (Htt-552). Methods: Primary astrocyte cultures were prepared from the cortex of postnatal rat pups. An astrocytes model of Huntington's disease was established using the astrocytes infected with adenovirus carrying coden gene of N-terminal 552 residues of Huntingtin. The protein levels of glutamate transporters GLT-1 and GLAST, the autophagic marker microtubule-associated protein 1A/1B-light chain 3 (LC3) and the autophagy substrate p62 in the astrocytes were examined using Western blotting. The mRNA expression levels of GLT-1 and GLAST in the astrocytes were determined using Real-time PCR. [3H]glutamate uptake by the astrocytes was measured with liquid scintillation counting. Results: The expression of mutant Htt-552 in the astrocytes significantly decreased both the mRNA and protein levels of GLT-1 but not those of GLAST. Furthermore, Htt-552 significantly reduced [3H]glutamate uptake by the astrocytes, Treatment with the autophagy inhibitor 3-MA (10 mmol/L) significantly increased the accumulation of mutant Htt-552, and reduced the expression of GLT-1 and [3H]glutamate uptake in the astrocytes. Treatment with the autophagy stimulator rapamycin (0.2 mg/mL) significantly reduced the accumulation of mutant Htt-552, and reversed the changes in GLT-1 expression and [3H]glutamate uptake in the astrocytes. Conclusion: Rapamcin, an autophagy stimulator, can prevent the suppression of GLT-1 expression and glutamate uptake by mutant Htt- 552 in cultured astrocytes.
copUnited States
pubNature Publishing Group
pmid22266730
doi10.1038/aps.2011.162
oafree_for_read