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Atzin Robles-Contreras, Claudia Palacio, Marilu Arredondo-Flores, Jacqueline Oliva-Ramirez, Hector Perez-Cano, PhD in eye immunology; Human apoptotic proteome of senile cataract. Invest. Ophthalmol. Vis. Sci. 2013;54(15):2973.
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Various studies in murine models have suggested alterations in apoptosis of epithelial cells of the lens to cause cataract. Apoptotic proteins have not been described in human, so we consider apoptotic proteome study of senile cataract for a greater understanding of its pathogenesis.
Lens epithelium was obtained through a continuous curvilinear capsulorhexis patients who underwent phacoemulsification, both patients with senile cataract patients as well as healthy crystalline underwent surgery phacorefractive. Two membranes of each group were extracted DNA, which was run on an agarose gel to check DNA fragmentation. Remaining samples were placed in a lysis buffer. Once all the samples collected, we proceeded to perform the microarray 36 apoptotic proteins, as suggested by the vendor (R&D systems) adjusting to a protein concentration of 300mg. After processing the microarray membrane were visualized with iBOX and analyzed the density of each point with Vision Works LS software. Data were normalized relative to the positive control and the negative control. We considered as a biological significance more than 2-fold change.
Apoptotic proteome analysis in senile cataract showed that apoptotic and anti-apoptotic proteins were differentially expressed. By analyzing the proteins with which were greater increases, we found that the profile type is found antiapoptotic and survival: clusterin (7.3-fold change, fc), XIAP (7.1-fc), cIAP2 (4.3-fc), survivin (6.4-fc) and Livin (4.2-fc). By analyzing the DNA extracted from the lens epithelium (healthy or cataract) shows partial DNA damage.
Considering that there is a partial damage to the DNA of the cataract, and that was mainly the proteomic profile of antiapoptotic type, suggesting that cells although are suffering damage DNA, leading to a process of survival. We did not find an increase in biologically significance major apoptotic proteins (Bad, caspase 3), which says that these cells are not dying, but there is a survival response, so perhaps if there was a signal to start apoptosis, but not cell responds to die. Another protein was found to increase the TNFR1A which is a TNF receptor, which tells us that there is probably an inflammatory microenvironment signal to initiate apoptosis. Further studies are required to determine which factors trigger apoptosis and that turn the survival mechanisms, as well as analyzing the proteome apoptotic behaves in other types of cataract.
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