Abstract
Peroxiredoxin (PRX), a family of peroxidases, is associated with various biological processes such as the detoxification of oxidants and cell apoptosis. Besides, the anti-apoptosis effect of estrogen results partially from its anti-oxidant function. The purpose of this study was to investigate the expression of PRXs in ovariectomy (OVX) mice and the related anti-oxidative mechanism of estrogen. Eight-week-old mice were subjected to ovariectomy. MC3T3-E1 cells were pretreatment with 17b-estradiol and N-acetyl cysteine followed by oxidative injury induced with H2O2. Western blot and real time-PCR were applied to clarify the expressions of PRX1 and caspase-3, with both wild-type and PRX1 knockout MC3T3-E1 cells generated by CRISPR/Cas9 technology. The results showed PRX1 and PRX5 were upregulated in osteoblasts in the proximal tibial metaphysis of ovariectomy mice. Interestingly, PRX1 and PRX5 showed different distribution patterns, with PRX1 mainly accumulated in cell nuclei and PRX5 in the cytoplasm. Gene expression analysis showed significantly reduced expressions of PRX1 and caspase-3 in the pretreatment groups when compared with cells treated with H2O2 alone. Also, a decrease of caspase-3 expressions was observed in PRX1 knockout MC3T3-E1 cells with or without H2O2 in comparison to wild-type cells. These findings suggested that PRX may play important roles in estrogen-deficient osteoporosis. (200 words).
Highlights
Over the last 60 years estrogen deficiency has been highlighted as a key factor of osteoporosis in both women and men[1]
The stimulatory effects of gonadectomy on oxidative stress, osteoclastogenesis and osteoblast apoptosis, as well as the loss of bone mass were attenuated by treatment with antioxidants such as N-Acetyl Cysteine (NAC) or ascorbate, which were similar to estrogens and androgens[3,4,5]
hematoxylin and eosin (HE) staining showed no significant difference in the width of cortical bone between the OVX and SHAM groups (Fig. 2)
Summary
Over the last 60 years estrogen deficiency has been highlighted as a key factor of osteoporosis in both women and men[1]. Members of the typical 2Cys subgroup, including PRX1 through PRX4, contain an additional conserved cysteine in the carboxyl-terminal region, whereas PRX5 and PRX6, which are members of the atypical 2Cys and 1Cys subgroups, respectively, lack this second conserved cysteine[12] In addition to their roles as peroxidases, a body of evidence has begun to accumulate to suggest that individual members serve divergent functions associated with various biological processes, such as the cell functions, apoptosis and gene expression[8]. Despite these advances, it remains unclear how estrogen deficiency may contribute to osteoporosis and whether PRXs are involved in this disease process. We aimed to investigate the expression of PRX1 and PRX5 in estrogen deficient mice and any potential anti-oxidative role that they may exert (Fig. 1)
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