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. 2015 Dec 28;10(12):e0145523. doi: 10.1371/journal.pone.0145523

Fig 5. TGRL lipolysis activates apoptosis both in vitro and vivo.

Fig 5

A) Lipolysis activates caspase-3 activity in HAEC at 3h. B) Caspase-3 protein expression was blocked by TGF-β receptor inhibitor, ALK. Western blots (a) and densitometry quantification (b) for caspase-3. Treatment with lipolysis products increases expression of the active fragment of caspase-3 at 3 h. Additional treatment with 10 μM of inhibitor ALK (TL3+ALK) abrogated the expression of the active caspase-3 fragment. N = 3/treatment group, P≤0.05,* = TL compared to TL + ALK. C) TGRL lipolysis products activate apoptosis in mouse carotid artery. (a) Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining of mouse carotid artery. (b) Percentage of apoptosis of endothelial cells based on FITC and nuclear staining. TGRL lipolysis (TL) significantly induced apoptosis (65%) compare to control in mouse carotid artery. Positive control: DNAse I treated; negative control: without rTdT enzyme. N = 4 mice/group, P≤0.05 as significant, * = T or TL compare to media control group, # = TL compare to T. Original magnification ×60, Bar = 20 μm.