Fig. 3: Mechanisms underlying the dual role of TMEM16A in LPS induced cell barrier dysfunction. | Cell Death & Disease

Fig. 3: Mechanisms underlying the dual role of TMEM16A in LPS induced cell barrier dysfunction.

From: Dual role of Ca2+-activated Cl− channel transmembrane member 16A in lipopolysaccharide-induced intestinal epithelial barrier dysfunction in vitro

Fig. 3

a MTT and BrdU analysis was carried out to test the ration of cell proliferation and apoptosis (proliferation/apoptosis) at different time points. Effects of TMEM16A on IEC-6 cell proliferation/apoptosis incubated with relative low dose LPS (0.1 μg/mL LPS) (a1) and high dose LPS (10 μg/mL LPS) (a2). (n = 6/group). b Representative (b1) and statistical results of expression of cleave caspase3 (Cl-caspase3) (b2), occludin (b3), and MLCK (b4) in low and high dose LPS incubated IEC-6 cells. (n = 6/group). Data are expressed as the mean ± SD. Values in the normal control (NC) group are set to 100% and other values are given relative to those in the NC group, **p < 0.01 compared with NC group.

Back to article page