PKCβ regulates ischemia/reperfusion injury in the lung
J. Clin. Invest. Tomoyuki Fujita, et al. 113:1615 doi:10.1172/JCI19225 [
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Figure 3Ischemia/reperfusion-mediated activation of MAPKs in the lung.
PKCβ
+/+ and
PKCβ
–/– mice underwent the indicated period of left-lung I/R. Animals were sacrificed and protein extracts from the I/R and uninstrumented lung were prepared and subjected to SDS-PAGE (12%, 50 ∝g of protein/lane). Immunoblotting with phospho-p44/42 MAPK antibody or total p44/42 MAPK antibody (
B), phospho-p38 MAPK antibody, or total p38 MAPK antibody (
I), and phospho-SAPK/JNK antibody or total SAPK/JNK antibody (
J) was performed. Data are shown as mean ± SEM of five experiments. Immunohistochemical analysis of phospho-p44/42 expression in murine lung from uninstrumented (
B) or I/R (
C)
PKCβ
+/+ mice, and from uninstrumented (
D) or I/R (
E)
PKCβ
–/– mice was performed. Scale bar: 50 ∝m. I/R lungs from
PKCβ
+/+ mice were subjected to immunofluorescence microscopy and double stained with an anti–phospho-p44/42 antibody (red) (
F) and an anti-macrophage antibody (F4/80, green) (
G). The merging of
F (pERK1/2) and
G (F4/80) is shown in
H. Arrows in
F and arrowheads in
G indicate dually stained cells Original magnification in
F–
H, ∞1,000. *
P < 0.001; **
P = 0.0041.