Fig. 5: Effects of α7-nAChRs activation on phosphorylation of mTOR in primary cultured chondrocytes and human cartilage tissues. | Cell Death & Disease

Fig. 5: Effects of α7-nAChRs activation on phosphorylation of mTOR in primary cultured chondrocytes and human cartilage tissues.

From: Stimulation of α7-nAChRs coordinates autophagy and apoptosis signaling in experimental knee osteoarthritis

Fig. 5

Immunoblots of lysates obtained from cultured wild-type (WT) chondrocytes and α7-nAChR knockout (KO) chondrocytes probed with antibodies to p-mTOR or mTOR (A). Compared to that in WT chondrocytes, the phosphorylation of mTOR was increased in KO chondrocytes after MIA treatment (B). Immunoblots of lysates were obtained from cultured WT chondrocytes treated with nicotine (Nic) or Nic + MLA probed with antibodies to p-mTOR or mTOR (C). Nic reduced the intensity of MIA-induced phosphorylation of mTOR (B and D), which could be reversed by MLA (D). Immunoblots of lysates obtained from human cartilage tissues probed with antibodies to p-mTOR or mTOR (E). Phosphorylation of mTOR in tissues of OA patients was significantly increased (F). The results are represented as mean ± SEM of three independent experiments in (B and D), 4 samples/group in (F). **P < 0.01, *P < 0.05 versus corresponding control group; ##P < 0.01, #P < 0.05 versus corresponding MIA group; &P < 0.05 versus WT MIA group; $P < 0.05 versus WT MIA + 10 μM nicotine, using two-way ANOVA followed by Tukey’s test (B), one-way ANOVA followed by Tukey’s test (D), or Student’s unpaired t test (F).

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