PMID- 31210286
OWN - NLM
STAT- MEDLINE
DCOM- 20200918
LR  - 20200918
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 11
DP  - 2019 Jun
TI  - MiR-20b promotes osteocyte apoptosis in rats with steroid-induced necrosis of the 
      femoral head through BMP signaling pathway.
PG  - 4599-4608
LID - 18037 [pii]
LID - 10.26355/eurrev_201906_18037 [doi]
AB  - OBJECTIVE: To study the effect of micro-ribonucleic acid (miR)-20b on osteocyte 
      apoptosis in rats with steroid-induced necrosis of the femoral head (SNFH) and to 
      analyze whether the bone morphogenetic protein (BMP) signaling pathway is 
      involved in the regulation. MATERIALS AND METHODS: A total of 36 Sprague-Dawley 
      rats were randomly divided into control group (n=12), model group (n=12) and 
      intervention group (n=12). The rat model of SNFH was established in the model and 
      intervention groups, while the rats in the intervention group were 
      intraperitoneally injected with the bone morphogenetic protein (BMP) signaling 
      pathway inhibitor. After modeling, the femoral head in each group was taken, and 
      the morphology of osteocytes was observed via hematoxylin-eosin (HE) staining. 
      The apoptosis level of femoral head cells was detected via terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. 
      The miR-20b expression level in femoral head cells in each group was detected via 
      quantitative Polymerase Chain Reaction (qPCR). The expression levels of 
      inflammatory factors in femoral head cells in each group were detected via 
      enzyme-linked immunosorbent assay (ELISA). The expression levels of apoptotic 
      proteins and BMP signaling pathway-related proteins in femoral head cells in each 
      group were detected via Western blotting. RESULTS: Compared with those in the 
      control group, the bone trabecula was sparse, the number of osteocytes 
      significantly declined and the number of apoptotic osteocytes markedly increased 
      (p<0.01); the expression level of miR-20b in bone tissues remarkably increased 
      (p<0.01), the content of interleukin-1beta (IL-1beta), IL-6 and tumor necrosis factor-alpha 
      (TNF-alpha) in bone tissues increased (p<0.01), the content of IL-10 significantly 
      declined (p<0.01), the expression level of cleaved caspase-3 protein in bone 
      tissues markedly increased (p<0.01), the Bcl-2/Bax expression level evidently 
      declined (p<0.01) and the expression levels of anaplastic lymphoma kinase3 
      (ALK3), GATA4 and NKX2.5 in bone tissues remarkably increased (p<0.01) in the 
      model group. Compared with those in the model group, the necrosis of bone tissues 
      significantly decreased, the apoptosis level of osteocytes remarkably declined 
      (p<0.01), the content of IL-1beta, IL-6 and TNF-alpha in bone tissues markedly decreased 
      (p<0.01), the content of IL-10 increased (p<0.01), the expression level of 
      cleaved caspase-3 protein in bone tissues significantly declined (p<0.01), the 
      B-cell lymphoma 2/BCL2-Associated X (Bcl-2/Bax) expression level markedly 
      increased (p<0.01) and the expression levels of ALK3, GATA4 and NKX2.5 in bone 
      tissues significantly decreased (p<0.01) in the intervention group. CONCLUSIONS: 
      SNFH will significantly increase the expression level of miR-20b in bone tissues, 
      thereby activating the BMP signaling pathway, promoting the release of 
      inflammatory factors and leading to osteocyte apoptosis. Inhibiting the BMP 
      signaling pathway can effectively reduce the osteocyte apoptosis level.
FAU - Li, G-Q
AU  - Li GQ
AD  - Department of Orthopaedics, Caoxian People's Hospital, Heze, China. 
      robinjc@qq.com.
FAU - Wang, Z-Y
AU  - Wang ZY
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (MIRN20 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - EC 2.7.11.30 (Bone Morphogenetic Protein Receptors)
RN  - X4W7ZR7023 (Methylprednisolone)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Bone Morphogenetic Protein Receptors/metabolism
MH  - Disease Models, Animal
MH  - Femur Head
MH  - Femur Head Necrosis/chemically induced/*genetics/metabolism
MH  - Injections, Intraperitoneal
MH  - Methylprednisolone/*adverse effects
MH  - MicroRNAs/*genetics
MH  - Osteocytes/chemistry/*cytology/drug effects
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction/drug effects
EDAT- 2019/06/19 06:00
MHDA- 2020/09/20 06:00
CRDT- 2019/06/19 06:00
PHST- 2019/06/19 06:00 [entrez]
PHST- 2019/06/19 06:00 [pubmed]
PHST- 2020/09/20 06:00 [medline]
AID - 18037 [pii]
AID - 10.26355/eurrev_201906_18037 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Jun;23(11):4599-4608. doi: 
      10.26355/eurrev_201906_18037.