Author: Ma, J; Wan, J; Meng, J; Banerjee, S; Ramakrishnan, S; Roy, S
Title: Methamphetamine induces autophagy as a pro-survival response against apoptotic endothelial cell death through the Kappa opioid receptor Document date: 2014_3_6
ID: wu2mogfa_18
Snippet: Our study demonstrated that METH disrupted HBMECs and HUVECs barrier function in a time-dependent manner. Lowdose METH at early time points induced the conversion of LC3-I into LC3-II and increased LAMP1 in endothelial cells. Interestingly, METH upregulated Beclin1 expression through KOR and ERK1/2 pathways. Furthermore, METH-induced autophagy in endothelial cells was triggered by inactivation of the AKT/mTOR/p70S6K pathway and activation of the .....
Document: Our study demonstrated that METH disrupted HBMECs and HUVECs barrier function in a time-dependent manner. Lowdose METH at early time points induced the conversion of LC3-I into LC3-II and increased LAMP1 in endothelial cells. Interestingly, METH upregulated Beclin1 expression through KOR and ERK1/2 pathways. Furthermore, METH-induced autophagy in endothelial cells was triggered by inactivation of the AKT/mTOR/p70S6K pathway and activation of the ERK1/ 2 pathway ( Figure 6 ). METH-induced autophagy was regulated by the Bcl-2/Beclin1 complex. Changes in Bcl-2/Beclin1 complex have been observed in endothelial cell autophagy when treated with anti-angiogenic inhibitors. 27 METH also promoted caspase activity and suppression of autophagy accelerated METH-induced apoptosis.
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