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. 2016 May 26;7(5):e2235. doi: 10.1038/cddis.2016.144

Figure 6.

Figure 6

EPA, but not AA, therapy induces adaptive autophagy in Dex-induced apoptotic mBMMSCs and maintains the proliferative ability via GPR120-mediated AMPK-mTOR signaling pathway. Under the circumstance of Dex-induced apoptotic cell death, the downstream targets of GPR120 are highly involved in anti-apoptosis and autophagy-induction process when GPR120 is activated by EPA,. In detail, GPR120 activates Ras-Erk1/2 cascade to inhibit Dex-induced apoptosis and modulates AMPK/mTOR to induce cell autophagy. However, EPA treatment alone without Dex is unable to induce much autophagy, which indicates the effect of EPA in inducing adaptive autophagy when cells are suffering Dex-induced apoptotic cell death