MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR
Context: Evidence suggests that microRNA (miRNA) regulates gene expression and bone tissue homoeostasis of osteoporosis. MiR-152 has found to be abnormally expressed in osteoporosis, but its role in osteoblast differentiation has not been elucidated. Objective: To understand the potential mechanism...
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Taylor & Francis Group
2019
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oai:doaj.org-article:939e238c31bd43fdb5a34b7bfe6c09e72021-11-17T14:21:56ZMiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR1388-02091744-511610.1080/13880209.2019.1657153https://doaj.org/article/939e238c31bd43fdb5a34b7bfe6c09e72019-01-01T00:00:00Zhttp://dx.doi.org/10.1080/13880209.2019.1657153https://doaj.org/toc/1388-0209https://doaj.org/toc/1744-5116Context: Evidence suggests that microRNA (miRNA) regulates gene expression and bone tissue homoeostasis of osteoporosis. MiR-152 has found to be abnormally expressed in osteoporosis, but its role in osteoblast differentiation has not been elucidated. Objective: To understand the potential mechanism of miR-152 in osteoblast differentiation via regulation of RICTOR. Materials and methods: The expression of miR-152 and RICTOR were tested in ovariectomized rat models of osteoporosis. Primary osteoblasts and MC3T -E1 cells were assigned into four groups, namely Control, miR-152 inhibitor, miR-control and miR-152 inhibitor + siRICTOR groups. qRT PCR and Western blots were performed to detect the expression of miR-152 and RICTOR, respectively. MTT assay was used to evaluate cell viability, and ALP activity determination and mineralization analyses were also conducted. Results: In ovariectomy-induced osteoporotic rats, miR-152 (3.06 ± 0.35) in femoral tissues increased significantly, while RICTOR (0.31 ± 0.04) decreased. Compared with the Control group, the miR-152 inhibitor group presented appreciable reduction of miR-152 in primary osteoblasts and MC3T3-E1 cells, as well as remarkable increases in RICTOR, p-Akt(s473)/Akt ratio, and osteogenesis-related genes, with enhanced cell viability, ALP activity and mineralization. In comparison with cells in the miR-152 inhibitor group, those in the miR-152 inhibitor + siRICTOR group had no observable difference in miR-152, but were dramatically up-regulated in RICTOR, as well as the corresponding opposite tendencies of other factors. Conclusion: Inhibiting miR-152 promoted osteoblasts differentiation and alleviated osteoporosis by up-regulating RICTOR. Therefore, miR-152 may be an essential mediator of osteoblast differentiation and a new therapeutic strategy for osteoporosis.Li FengBo XiaBao-Fang TianGong-Biao LuTaylor & Francis Grouparticlemicrornaovariectomized ratprimary osteoblastsmc3t3-e1 cellsTherapeutics. PharmacologyRM1-950ENPharmaceutical Biology, Vol 57, Iss 1, Pp 586-594 (2019) |
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microrna ovariectomized rat primary osteoblasts mc3t3-e1 cells Therapeutics. Pharmacology RM1-950 |
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microrna ovariectomized rat primary osteoblasts mc3t3-e1 cells Therapeutics. Pharmacology RM1-950 Li Feng Bo Xia Bao-Fang Tian Gong-Biao Lu MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR |
description |
Context: Evidence suggests that microRNA (miRNA) regulates gene expression and bone tissue homoeostasis of osteoporosis. MiR-152 has found to be abnormally expressed in osteoporosis, but its role in osteoblast differentiation has not been elucidated. Objective: To understand the potential mechanism of miR-152 in osteoblast differentiation via regulation of RICTOR. Materials and methods: The expression of miR-152 and RICTOR were tested in ovariectomized rat models of osteoporosis. Primary osteoblasts and MC3T -E1 cells were assigned into four groups, namely Control, miR-152 inhibitor, miR-control and miR-152 inhibitor + siRICTOR groups. qRT PCR and Western blots were performed to detect the expression of miR-152 and RICTOR, respectively. MTT assay was used to evaluate cell viability, and ALP activity determination and mineralization analyses were also conducted. Results: In ovariectomy-induced osteoporotic rats, miR-152 (3.06 ± 0.35) in femoral tissues increased significantly, while RICTOR (0.31 ± 0.04) decreased. Compared with the Control group, the miR-152 inhibitor group presented appreciable reduction of miR-152 in primary osteoblasts and MC3T3-E1 cells, as well as remarkable increases in RICTOR, p-Akt(s473)/Akt ratio, and osteogenesis-related genes, with enhanced cell viability, ALP activity and mineralization. In comparison with cells in the miR-152 inhibitor group, those in the miR-152 inhibitor + siRICTOR group had no observable difference in miR-152, but were dramatically up-regulated in RICTOR, as well as the corresponding opposite tendencies of other factors. Conclusion: Inhibiting miR-152 promoted osteoblasts differentiation and alleviated osteoporosis by up-regulating RICTOR. Therefore, miR-152 may be an essential mediator of osteoblast differentiation and a new therapeutic strategy for osteoporosis. |
format |
article |
author |
Li Feng Bo Xia Bao-Fang Tian Gong-Biao Lu |
author_facet |
Li Feng Bo Xia Bao-Fang Tian Gong-Biao Lu |
author_sort |
Li Feng |
title |
MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR |
title_short |
MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR |
title_full |
MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR |
title_fullStr |
MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR |
title_full_unstemmed |
MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR |
title_sort |
mir-152 influences osteoporosis through regulation of osteoblast differentiation by targeting rictor |
publisher |
Taylor & Francis Group |
publishDate |
2019 |
url |
https://doaj.org/article/939e238c31bd43fdb5a34b7bfe6c09e7 |
work_keys_str_mv |
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_version_ |
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