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Leptin regulates disc cartilage endplate degeneration and ossification by way of activation of the MAPK-ERK signalling pathway in vivo and in vitro.
J Cell Mol Med. 2018 Jan 26;:
Authors: Han YC, Ma B, Guo S, Yang M, Li LJ, Wang SJ, Tan J
Summary
Latest findings exhibit that leptin performs a major position in chondrocyte and osteoblast differentiation. Nonetheless, the mechanisms by which leptin acts on cartilage endplate (CEP) cells to provide rise to calcification are nonetheless unclear. The purpose of this research was to guage the results of leptin that induced mineralization of CEP cells in vitro and in vivo. We constructed a rat mannequin of lumbar disc degeneration and decided that leptin was extremely expressed within the presence of CEP calcification. Rat CEP cells handled with or with out leptin have been used for in vitro evaluation utilizing RT-PCR and Western blotting to look at the expression of osteocalcin (OCN) and runt-related transcription issue 2 (Runx2). Each OCN and Runx2 expression ranges have been considerably elevated in a dose- and time-dependent method. Leptin activated ERK1/2 and STAT3 phosphorylation in a time-dependent method. Inhibition of phosphorylated ERK1/2 utilizing focused siRNA suppressed leptin-induced OCN and Runx2 expression and blocked the formation of mineralized nodules in CEP cells. We additional demonstrated that exogenous leptin induced matrix mineralization of CEP cells in vivo. We propose that leptin promotes the osteoblastic differentiation of CEP cells through the MAPK/ERK sign transduction pathway and could also be used to analyze the mechanisms of disc degeneration.
PMID: 29372627 [PubMed – as supplied by publisher]