title: MicroRNA-335-5p inhibits osteoblast apoptosis induced by high glucose.
abstract: Diabetic osteoporosis represents a serious health condition with increasing incidence. Previous studies have shown that microRNA (miR)-335-5p is highly expressed in MC3T3-E1 osteoblasts and promotes their differentiation via downregulating the expression of dickkopf‑1 (DKK1). The present study investigated the effects of miR‑335‑5p on apoptosis of osteoblasts induced by high glucose (HG), as well as the underlying molecular mechanisms. MC3T3‑E1 osteoblasts were transfected with miR‑335‑5p mimics or control miR and cultured under HG conditions for seven days. Reverse‑transcription PCR and showed that, compared with the control group, the expression levels of miR‑335‑5p were significantly downregulated in the HG group. However, no significant differences were observed in the mRNA expression levels of DKK1 between these groups. Furthermore, flow cytometric analysis showed that the apoptotic rate was increased by >2‑fold in the HG group compared with that in the control group, while miR‑335‑5p overexpression significantly decreased the apoptotic rate in these model cells by ~40%. In addition, western blot analysis revealed that the protein expression levels of DKK1 and caspase‑3 were significantly elevated in the HG group, which was significantly inhibited by overexpression of miR‑335‑5p. These results may indicate that miR‑335‑5p overexpression inhibited HG‑induced apoptosis of MC3T3‑E1 osteoblasts through decreasing the protein expression levels of DKK1. The results of the present study suggested that miR‑335‑5p may represent a potential target for the treatment of diabetic osteoporosis.
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Jiling
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Zhengping
authors.initials: Z
authors.lastname: Feng
authors.affiliation: Laboratory Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Lixue
authors.initials: L
authors.lastname: Chen
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Xiaoju
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Huacong
authors.initials: H
authors.lastname: Deng
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D005786:Gene Expression Regulation / Q000187:drug effects*; D005947:Glucose / Q000494:pharmacology*; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis*; D051379:Mice; D035683:MicroRNAs / Q000096:biosynthesis*; D010006:Osteoblasts / Q000378:metabolism*
chemical_list: C501127:Dkk1 protein, mouse; D036341:Intercellular Signaling Peptides and Proteins; D035683:MicroRNAs; C541986:Mirn335 microRNA, mouse; D005947:Glucose