Protein tyrosine phosphatase deficiency…
677
Figure 7A, APAP markedly increased the levels of phosphorylated JNK in wild-type
hepatocytes. Interestingly, the lack of PTP1B prevented JNK activation in response
to APAP.
Figure 5.- PTP1B-deficient hepatocytes are protected against APAP-induced arrest in the S
phase of the cell cycle. A.
PTP1B
+/+
and PTP1B
-/-
immortalized
hepatocytes were treated with
various doses of APAP for 16 h. The percentage of S phase cell population was measured by flow
cytometry.
B.
Images of flow cytomerty showing the effect of APAP treatment on G0/G1 and S
phases in both
PTP1B
+/+
and PTP1B
-/-
immortalized
hepatocytes.
*
P<0.05,
**
P<0.01 and
***
P<0.005 PTP1B
-/-
vs. PTP1B
+/+
cells (n=4 independent experiments).
Table 1.-
Effect of APAP treatment in the induction of both apoptosis and necrosis in PTP1B
+/+
PTP1B
-/-
hepatocytes.
Population
PI
PI+*
PI+dim**
PTP1B
+/+
C
99.5
10
10.8
PTP1B
+/+
0.5mM
98.5
22.7
24.1
PTP1B
+/+
1mM
98.7
23.1
24.6
PTP1B
-/-
C
99.9
4.5
3.9
PTP1B
-/-
0.5mM
99.5
7.2
5.7
PTP1B
-/-
1mM
99
10.2
6.7
PI*=Necrosis. PI**=Apoptosis
