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TY - JOUR
JO - Advances in Clinical and Experimental Medicine
J2 - Adv Clin Exp Med
SN - 1899-5276
PB - Wroclaw Medical University
VL - 30
IS - 5
PY - 2021
ID - Liu2021-05-31
TI - Silencing Hoxa2 reverses dexamethasone-induced dysfunction of MC3T3-E1 osteoblasts and osteoporosis in rats
AB - Background. Osteoporosis is damaging the health of women worldwide. Osteoporosis results from the imbalance between bone resorption and formation, which may be regulated by homeobox A2 (Hoxa2). However, the specific role and mechanism of Hoxa2 in osteogenesis and dexamethasone (Dex)-induced osteoporosis remain unknown.Objectives. The present study investigated the effect of Hoxa2 on differentiation and osteoblastogenesis.Material and Methods. Alkaline phosphatase staining and immunofluorescence staining were performed to evaluate the differentiation of MC3T3-E1 cells. Runt-related transcription factor 2 (Runx2), osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa B ligand (RANKL) in Dex stimulated osteoblastic MC3T3-E1 cells, and Dex-induced osteoporotic rats were estimated using western blot and quantitative polymerase chain reaction (qPCR). Serum markers of bone turnover were determined using enzyme-linked immunosorbent assay (ELISA). Trabecular bones of femur tissues were observed using hematoxylin and eosin (H&E) staining.Results. Hoxa2 short hairpin RNA significantly promoted the differentiation of MC3T3-E1 cells and expression of Runx2 and OPG in Dex-treated MC3T3-E1 cells and osteoporotic rats but inhibited the expression of RANKL. Furthermore, silencing Hoxa2 resulted in the upregulation of bone alkaline phosphatase but suppressed the expression of tartrate-resistant acid phosphatase and C-terminal cross-linked telopeptides of type I collagen.Conclusion. Silencing Hoxa2 reversed the Dex-induced inhibition of osteoblastogenesis by modulating Runx2 and RANK–RANKL–OPG axis.
AU - Liu, Yuan
AU - Wang, Le
AU - Yang, Youguo
AU - Xiong, Jianbin
SP - 525
EP - 534
DA - 2021-05-31
DO - 10.17219/acem/133495
UR - http://dx.doi.org/10.17219/acem/133495
ER -