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17β-Estradiol promotes cell proliferation in rat osteoarthritis model chondrocytes via PI3K/Akt pathway

Abstract

Osteoarthritis (OA) is the most common cause of musculoskeletal pain and disability. The importance of chondrocytes in the pathogenesis of OA is unequivocal. 17β-estradiol (E2) has a potential protective effect against OA. However, the mechanism of E2 in OA chondrocytes remains unclear. In this study, we investigated the regulative effect of E2 on cell growth and the relationship between E2 and the PI3K/Akt pathway in rat OA model chondrocytes (pretreated with interleukin-1β). We found that E2 induced chondrocyte proliferation, and increased the expression level of Akt simultaneously, especially the expression level of P-Akt. Furthermore, the inhibition of P-Akt could block chondrocyte proliferation induced by E2. These results suggest that PI3K/Akt activation induced by E2 may be an important factor in the mechanism of E2 in cell proliferation in rat OA model chondrocytes, and help further understanding the role of E2 in OA progression.

Abbreviations

Akt:

protein kinase B

BrdU:

5-bromo-2′-deoxyuridine

DAPI:

4,6-diamidino-2-phenylindole

E2:

17β-estradiol

ER:

estrogen receptor

IL-1β:

interleukin-1β

OA:

osteoarthritis

P-Akt:

Akt phosphorylated

PI3K:

phosphoinositide-3-OH kinase

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Correspondence to Chun Xia or Bing Zhang.

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Huang, J.G., Xia, C., Zheng, X.P. et al. 17β-Estradiol promotes cell proliferation in rat osteoarthritis model chondrocytes via PI3K/Akt pathway. Cell Mol Biol Lett 16, 564 (2011). https://doi.org/10.2478/s11658-011-0023-y

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