Session Title: AMD III
Session Date/Time: Sunday 29/09/2013 | 11:00-13:00
Paper Time: 11:48
Venue: Hall G1 (Level 2)
First Author: A.Pollack ISRAEL
Co Author(s): Z. Dvashi
Transforming growth factor beta (TGF-beta1) was previously reported to be involved in the regulation of RPE proliferation on one hand, and possible regulation of cell death, on the other. Upon TGF-beta1 stimulation of RPE cells, several cascades of mitogen-activated protein kinases (MAPKs) are been activated, such as: ERK, c-Jun N-terminal kinases (JNK) and p38. Earlier reports have demonstrated that p38 inhibition enhanced growth factor activation and alter the process of apoptosis and cell cycle. This study focused on the role of p38 as regulator of programmed cell death on RPE cells for better understanding diseases associated with RPE atrophy
Kaplan Medical Center, Rehovot, affiliated to the Hadassah Medical School, Hebrew University Jerusalem
ARPE-19 cells were subjected to FACS analysis, immunofluorescence staining, XTT analysis and real time PCR. Cells were treated with either TGF-1 or p38 inhibitor (SB203580) or in combination. Cells were harvested and subjected to analysis in the different methods
Inhibition of p38 reduces proliferation and increases ARPE-19 cell-cycle-arrest. Untreated cells demonstrated moderated increase of cells proliferation in serum starvation medium. However, RPE cells treated with p38 inhibitor (SB203580) display reduction in cell proliferation after two days- 2 followed by cell-cycle-arrest.
The progression of AMD is known to be involved with RPE cells programmed cell death. This study demonstrates that RPE cells apoptosis is mediated through p38 activation. This study demonstrated that p38 may be a pivotal regulator of RPE cell-cycle-arrest and cell death. This data may imply a potential novel approach to reduce RPE cell death by activating p38, thus may halt the progression of dry AMD.