Fig. 4
From: The role of thrombospondin-1 in trehalose-induced autophagy and ocular hypertension in mice

Trehalose or THBS1 LSKL peptide upregulated autophagic flux in hTM cells. hTM cells were either incubated individually with trehalose (100 mM), SLLK or LSKL peptide (1 or 5 µM), or co-incubated with 100 mM trehalose and 5 µM LSKL peptide for 48 h. (a) 100 mM trehalose upregulated autophagic vacuoles in hTM cells by 32%. (b) THBS1 LSKL inhibitor peptide upregulated autophagic flux by 26% at 1 µM and 55% at 5 µM when compared with the SLLK control peptide. (c) Trehalose added to 5 µM LSKL peptide did not further upregulate autophagic vacuoles relative to cells treated with LSKL alone (51% and 53% upregulation, respectively). Data represent mean ± SEM (n = 3 different cell strains per group). Statistical significance relative to vehicle control (unpaired Student’s t-test) is indicated by **(P < 0.01), ***(P < 0.001) and ***(P < 0.0001). Tre: trehalose.