Insight into the possible role of miR-214 in primary osteoporosis via osterix.

Autor: Mohamad N; Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt., Nabih ES; Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt., Zakaria ZM; Orthopedic Surgery and Traumatology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt., Nagaty MM; Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt., Metwaly RG; Orthopedic Surgery and Traumatology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Jazyk: angličtina
Zdroj: Journal of cellular biochemistry [J Cell Biochem] 2019 Sep; Vol. 120 (9), pp. 15518-15526. Date of Electronic Publication: 2019 May 05.
DOI: 10.1002/jcb.28818
Abstrakt: Osteoporosis is a bone disease characterized by chronic pain and recurrent fractures. Osterix is a transcription factor regulating bone formation. miR-214 was found to have a role in skeletogenesis. Our goal was to investigate the possible role of miR-214 in primary osteoporosis through osterix. Their expression was determined in bone samples obtained from primary osteoporotic patients (n = 26) and age- and sex-matched controls (n = 14). Additionally, their expression was correlated to the laboratory and clinical parameters of the study participants. Differential expression of osterix and miR-214 was detected in the osteoporotic group compared to controls. While miR-214 was significantly higher, osterix was significantly lower. In primary osteoporotic patients, relative quantification value of osterix was positively correlated with sex, body mass index, and ionized calcium and negatively correlated with miR-214 and C-reactive protein. Thus, the role of miR-214 in primary osteoporosis could be through inhibiting osterix expression in bones and therefore both miR-214 and osterix could be targets for future therapeutic intervention.
(© 2019 Wiley Periodicals, Inc.)
Databáze: MEDLINE
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