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miR-223 contributes to the AGE-promoted apoptosis via down-regulating insulin-like growth factor 1 receptor in osteoblasts.

miR-223 inhibits the advanced glycation end product (AGE)-promoted apoptosis in osteoblasts. Advanced glycation end products (AGEs) have been confirmed to induce bone quality deterioration in diabetes mellitus (DM), and to associate with abnormal expression of miRNAs in DM patients or in vitro . Rec... Full description

Journal Title: Bioscience reports 2016, Vol.36(2)
Main Author: Qin, Yi
Other Authors: Ye, Jichao , Wang, Peng , Gao, Liangbin , Wang, Suwei , Shen, Huiyong
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1573-4935 ; DOI: 10.1042/BSR20150271
Link: http://search.proquest.com/docview/1786517783/?pq-origsite=primo
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title: miR-223 contributes to the AGE-promoted apoptosis via down-regulating insulin-like growth factor 1 receptor in osteoblasts.
format: Article
creator:
  • Qin, Yi
  • Ye, Jichao
  • Wang, Peng
  • Gao, Liangbin
  • Wang, Suwei
  • Shen, Huiyong
subjects:
  • 3' Untranslated Regions–Drug Effects
  • Animals–Genetics
  • Apoptosis–Drug Effects
  • Cell Line–Metabolism
  • Down-Regulation–Pharmacokinetics
  • Glycation End Products, Advanced–Genetics
  • Mice–Metabolism
  • Micrornas–Cytology
  • Osteoblasts–Metabolism
  • Receptor, IGF Type 1–Biosynthesis
  • Receptor, IGF Type 1–Genetics
  • 3' Untranslated Regions
  • Glycation End Products, Advanced
  • Mirn223 Microrna, Mouse
  • Micrornas
  • Receptor, IGF Type 1
  • Advanced Glycation End Products (Ages)
  • Apoptosis
  • Insulin-Like Growth Factor 1 Receptor (IGF-1r)
  • Mir-223
  • Osteoblasts
ispartof: Bioscience reports, 2016, Vol.36(2)
description: miR-223 inhibits the advanced glycation end product (AGE)-promoted apoptosis in osteoblasts. Advanced glycation end products (AGEs) have been confirmed to induce bone quality deterioration in diabetes mellitus (DM), and to associate with abnormal expression of miRNAs in DM patients or in vitro . Recently, miRNAs have been recognized to mediate the onset or progression of DM. In the present study, we investigated the regulation on miR-223 level by AGE-BSA treatment in osteoblast-like MC3T3-E1 cells, with real-time quantitative PCR assay. And then we examined the inhibition of insulin-like growth factor 1 receptor (IGF-1R) expression by miR-223 , via targeting of the 3′ UTR of IGF-1R with real-time quantitative PCR, western blotting and luciferase reporter assay. Then we explored the regulation of miR-223 and IGF-1R levels, via the lentivirus-mediated miR-223 inhibition and IGF-1R overexpression in the AGE-BSA-induced apoptosis in MC3T3-E1 cells. It was demonstrated that AGE-BSA treatment with more than 100 μg/ml significantly up-regulated miR-223 level, whereas down-regulated IGF-1R level in MC3T3-E1 cells. And the up-regulated miR-223 down-regulated IGF-1R expression in both mRNA and protein levels, via targeting the 3′ UTR of IGF-1R . Moreover, though the AGE-BSA treatment promoted apoptosis in MC3T3-E1 cells, the IGF-1R overexpression or the miR-223 inhibition significantly attenuated the AGE-BSA-promoted apoptosis in MC3T3-E1 cells. In summary, our study recognized the promotion of miR-223 level by AGE-BSA treatment in osteoblast-like MC3T3-E1 cells. The promoted miR-223 targeted IGF-1R and mediated the AGE-BSA-induced apoptosis in MC3T3-E1 cells. It implies that miR-223 might be an effective therapeutic target to antagonize the AGE-induced damage to osteoblasts in DM.
language: eng
source:
identifier: E-ISSN: 1573-4935 ; DOI: 10.1042/BSR20150271
fulltext: fulltext
issn:
  • 15734935
  • 1573-4935
url: Link


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titlemiR-223 contributes to the AGE-promoted apoptosis via down-regulating insulin-like growth factor 1 receptor in osteoblasts.
creatorQin, Yi ; Ye, Jichao ; Wang, Peng ; Gao, Liangbin ; Wang, Suwei ; Shen, Huiyong
contributorQin, Yi (correspondence author) ; Qin, Yi (record owner)
ispartofBioscience reports, 2016, Vol.36(2)
identifierE-ISSN: 1573-4935 ; DOI: 10.1042/BSR20150271
subject3' Untranslated Regions–Drug Effects ; Animals–Genetics ; Apoptosis–Drug Effects ; Cell Line–Metabolism ; Down-Regulation–Pharmacokinetics ; Glycation End Products, Advanced–Genetics ; Mice–Metabolism ; Micrornas–Cytology ; Osteoblasts–Metabolism ; Receptor, IGF Type 1–Biosynthesis ; Receptor, IGF Type 1–Genetics ; 3' Untranslated Regions ; Glycation End Products, Advanced ; Mirn223 Microrna, Mouse ; Micrornas ; Receptor, IGF Type 1 ; Advanced Glycation End Products (Ages) ; Apoptosis ; Insulin-Like Growth Factor 1 Receptor (IGF-1r) ; Mir-223 ; Osteoblasts
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descriptionmiR-223 inhibits the advanced glycation end product (AGE)-promoted apoptosis in osteoblasts. Advanced glycation end products (AGEs) have been confirmed to induce bone quality deterioration in diabetes mellitus (DM), and to associate with abnormal expression of miRNAs in DM patients or in vitro . Recently, miRNAs have been recognized to mediate the onset or progression of DM. In the present study, we investigated the regulation on miR-223 level by AGE-BSA treatment in osteoblast-like MC3T3-E1 cells, with real-time quantitative PCR assay. And then we examined the inhibition of insulin-like growth factor 1 receptor (IGF-1R) expression by miR-223 , via targeting of the 3′ UTR of IGF-1R with real-time quantitative PCR, western blotting and luciferase reporter assay. Then we explored the regulation of miR-223 and IGF-1R levels, via the lentivirus-mediated miR-223 inhibition and IGF-1R overexpression in the AGE-BSA-induced apoptosis in MC3T3-E1 cells. It was demonstrated that AGE-BSA treatment with more than 100 μg/ml significantly up-regulated miR-223 level, whereas down-regulated IGF-1R level in MC3T3-E1 cells. And the up-regulated miR-223 down-regulated IGF-1R expression in both mRNA and protein levels, via targeting the 3′ UTR of IGF-1R . Moreover, though the AGE-BSA treatment promoted apoptosis in MC3T3-E1 cells, the IGF-1R overexpression or the miR-223 inhibition significantly attenuated the AGE-BSA-promoted apoptosis in MC3T3-E1 cells. In summary, our study recognized the promotion of miR-223 level by AGE-BSA treatment in osteoblast-like MC3T3-E1 cells. The promoted miR-223 targeted IGF-1R and mediated the AGE-BSA-induced apoptosis in MC3T3-E1 cells. It implies that miR-223 might be an effective therapeutic target to antagonize the AGE-induced damage to osteoblasts in DM.
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titlemiR-223 contributes to the AGE-promoted apoptosis via down-regulating insulin-like growth factor 1 receptor in osteoblasts.
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