Abstract:
:PI3K/AKT signaling is essential in regulating pathophysiology of osteoarthritis (OA). However, its potential modulatory role in early OA progression has not been investigated yet. Here, a mouse destabilization OA model in the tibia was used to investigate roles of PI3K/AKT signaling in the early subchondral bone changes and OA pathological process. We revealed a significant increase in PI3K/AKT signaling activation which was associated with aberrant bone formation in tibial subchondral bone following destabilizing the medial meniscus (DMM), which was effectively prevented by treatment with PI3K/AKT signaling inhibitor LY294002. PI3K/AKT signaling inhibition attenuated articular cartilage degeneration. Serum and bone biochemical analyses revealed increased levels of MMP-13, which was found expressed mainly by osteoblastic cells in subchondral bone. However, this MMP-13 induction was attenuated by LY294002 treatment. Furthermore, PI3K/AKT signaling was found to enhance preosteoblast proliferation, differentiation, and expression of MMP-13 by activating NF-κB pathway. In conclusion, inhibition of PI3K/AKT/NF-κB axis was able to prevent aberrant bone formation and attenuate cartilage degeneration in OA mice.
journal_name
J Cell Physioljournal_title
Journal of cellular physiologyauthors
Lin C,Shao Y,Zeng C,Zhao C,Fang H,Wang L,Pan J,Liu L,Qi W,Feng X,Qiu H,Zhang H,Chen Y,Wang H,Cai D,Xian CJdoi
10.1002/jcp.26460subject
Has Abstractpub_date
2018-08-01 00:00:00pages
6135-6147issue
8eissn
0021-9541issn
1097-4652journal_volume
233pub_type
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