MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR
Authors: Bo Xia
Li Feng
Gong-Biao Lu
Bao-Fang Tian
Journal: Pharmaceutical biology (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: MC3T3-E1 cells; MicroRNA; ovariectomized rat; primary osteoblasts.
Affiliations: Department of Traumatic Orthopedics, Jining No. 1 People's Hospital , Jining , China., Department of Spine Surgery, Jining No, 1 People's Hospital , Jining , China.

Abstract:  Context: Evidence suggests that microRNA (miRNA) regulate 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 blot were performed to detect the expressions 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 Control group, 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. 

Retracted: No

PubPeer comments:
 Figure 5A. * Blue boxes focus attention on a group of cells that appears to be shared between two different panels. ![file] , 
 Correction, April 2020: https: www.tandfonline.com doi full 10.1080 13880209.2020.1745479  The authors have found out that Figures 5 and 6, and the sentence starting as u201cHowever, miR-152 inhibitor + siRICTOR group showed no significant differenceu2026u201d coming under the sub-section u201cExpression of miR-152, RICTOR and downstream proteins in osteoblastsu201d of the Results section have some errors that need to be rectified. The revised Figure 5 would appear as below: [...] In the sub-section u201cExpression of miR-152, RICTOR and downstream proteins in osteoblastsu201d of the Results section, the sentence u201cHowever, miR-152 inhibitor + siRICTOR group showed no significant difference in miR-152 from miR-152 inhibitor group, with significantly increased levels of RICTOR and p-Akt (s473) Akt (all pu2009 u20090.05)u201d should read, u201cHowever, miR-152 inhibitor + siRICTOR group showed no significant difference in miR-152 from miR-152 inhibitor group, with significantly decreased levels of RICTOR and p-Akt (s473) Akt (all pu2009 u20090.05).u201d  ,