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Tytuł pozycji:

Leptin regulates disc cartilage endplate degeneration and ossification through activation of the MAPK‐ERK signalling pathway in vivo and in vitro.

Tytuł :
Leptin regulates disc cartilage endplate degeneration and ossification through activation of the MAPK‐ERK signalling pathway in vivo and in vitro.
Autorzy :
Han, Ying‐Chao
Ma, Bin
Guo, Song
Yang, Mingjie
Li, Li‐Jun
Wang, Shan‐Jin
Tan, Jun
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Temat :
OSTEOBLASTS
CELL differentiation
MITOGEN-activated protein kinases
DEGENERATION (Pathology)
OSTEOCALCIN
LEPTIN
CELLULAR signal transduction
Źródło :
Journal of Cellular & Molecular Medicine; Apr2018, Vol. 22 Issue 4, p2098-2109, 12p
Czasopismo naukowe
Abstract: Recent findings demonstrate that leptin plays a significant role in chondrocyte and osteoblast differentiation. However, the mechanisms by which leptin acts on cartilage endplate (CEP) cells to give rise to calcification are still unclear. The aim of this study was to evaluate the effects of leptin that induced mineralization of CEP cells in vitro and in vivo. We constructed a rat model of lumbar disc degeneration and determined that leptin was highly expressed in the presence of CEP calcification. Rat CEP cells treated with or without leptin were used for in vitro analysis using RT‐PCR and Western blotting to examine the expression of osteocalcin (OCN) and runt‐related transcription factor 2 (Runx2). Both OCN and Runx2 expression levels were significantly increased in a dose‐ and time‐dependent manner. Leptin activated ERK1/2 and STAT3 phosphorylation in a time‐dependent manner. Inhibition of phosphorylated ERK1/2 using targeted siRNA suppressed leptin‐induced OCN and Runx2 expression and blocked the formation of mineralized nodules in CEP cells. We further demonstrated that exogenous leptin induced matrix mineralization of CEP cells in vivo. We suggest that leptin promotes the osteoblastic differentiation of CEP cells via the MAPK/ERK signal transduction pathway and may be used to investigate the mechanisms of disc degeneration. [ABSTRACT FROM AUTHOR]
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