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Fig. 4. S1P signalling pathway involves the activation of RhoA and LIM kinase, a
degradation target. (A) S1P- and LPA-induced retinal growth cone
collapse are blocked by RhoA kinase inhibitor (Y-27632). Y-27632 was added
immediately prior to the addition of S1P in stage 32 retinal explants cultured
for 24 hours. *P<0.05, Mann-Whitney U test.
(B,C) Cumulative distribution of turning angles after Y-27632
treatment. The repulsive response elicited by S1P is inhibited by application
of Y-27632 prior to the start of the turning assay. (C) Mean turning graph
from data in B. ***P<0.005, Kolmogorov-Smirnov test.
(D) Quantitative immunofluorescence analysis of LIMK-P and LIMK
immunoreactivities. A 2-minute S1P treatment caused a significant increase in
LIMK-P, whereas LIMK signal remained unchanged. LIMK-P signal was not affected
by a 2-minute LPA treatment. At 5 minutes, S1P induced a significant decrease
of both LIMK-P and LIMK immunoreactivities within growth cones when compared
with control. This decrease is abolished by lactacystin treatment. (E)
Representative pictures of LIM kinase-P (LIMK-P) and LIM kinase (LIMK)
immunoreactivities within growth cones treated with S1P for 2 or 5 minutes, or
when lactacystin was applied 10 minutes before S1P application. Numbers inside
bars indicate growth cones tested. **P<0.01,
***P<0.005, Mann-Whitney U test. Scale bar in
D: 10 µm.
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