Targeting Pin1 Protects Mouse Cardiomyocytes from High-Dose Alcohol-Induced Apoptosis

Figure 4

Pin1 enhanced alcohol-mediated mitochondria oxidative stress in cardiomyocytes. (a) Western blot of mCyt.C release in Pin1-knockdown cardiomyocytes treated or untreated with alcohol (200 mM) for 24 h. Relative mitochondrial membrane potential (b) and mROS levels (c) in cells are indicated. (d) mCyt.C levels in Pin1-overexpressed cardiomyocytes treated or untreated with alcohol (50 mM) for 24 h. Relative mitochondrial membrane potential (e) and mROS levels (f) in cells are indicated. and . Cell viability (g) and caspase-3 activity (h) assays in Pin1-overexpressed cells treated with alcohol (50 mM) and NAC (1 μM) or Mito-TEMPO (50 μM). and compared with cells untreated with alcohol; compared with Pin1 overexpression cells treated with alcohol only. (i) Western blot of mitochondrial p-p66Shc levels in control or Pin1-knockdown cardiomyocytes treated or untreated with alcohol (200 mM) for 24 h. (j) Western blot of mitochondrial p-p66Shc levels in Pin1-overexpressed cardiomyocytes treated or untreated with alcohol (50 mM) for 24 h.

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

(i)

(j)